Transforming growth factor-β pathway is activated in cholecystolithiasis
Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are invo...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Köninger, Jörg [verfasserIn] di Mola, Fabio F. [verfasserIn] Di Sebastiano, Pierluigi [verfasserIn] Gardini, Andrea [verfasserIn] Brigstock, David R. [verfasserIn] Innocenti, Paolo [verfasserIn] Büchler, Markus W. [verfasserIn] Friess, Helmut [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2004 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Langenbeck's archives of surgery - Berlin : Springer, 1948, 390(2004), 1 vom: 20. Nov., Seite 21-28 |
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| Übergeordnetes Werk: |
volume:390 ; year:2004 ; number:1 ; day:20 ; month:11 ; pages:21-28 |
| Links: |
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| DOI / URN: |
10.1007/s00423-004-0517-4 |
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| Katalog-ID: |
SPR005571871 |
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| 520 | |a Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. | ||
| 650 | 4 | |a TGF-β |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a CTGF |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cholecystolithiasis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Fibrogenesis |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a di Mola, Fabio F. |e verfasserin |4 aut | |
| 700 | 1 | |a Di Sebastiano, Pierluigi |e verfasserin |4 aut | |
| 700 | 1 | |a Gardini, Andrea |e verfasserin |4 aut | |
| 700 | 1 | |a Brigstock, David R. |e verfasserin |4 aut | |
| 700 | 1 | |a Innocenti, Paolo |e verfasserin |4 aut | |
| 700 | 1 | |a Büchler, Markus W. |e verfasserin |4 aut | |
| 700 | 1 | |a Friess, Helmut |e verfasserin |4 aut | |
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10.1007/s00423-004-0517-4 doi (DE-627)SPR005571871 (SPR)s00423-004-0517-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Köninger, Jörg verfasserin aut Transforming growth factor-β pathway is activated in cholecystolithiasis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. TGF-β (dpeaa)DE-He213 CTGF (dpeaa)DE-He213 Cholecystolithiasis (dpeaa)DE-He213 Fibrogenesis (dpeaa)DE-He213 di Mola, Fabio F. verfasserin aut Di Sebastiano, Pierluigi verfasserin aut Gardini, Andrea verfasserin aut Brigstock, David R. verfasserin aut Innocenti, Paolo verfasserin aut Büchler, Markus W. verfasserin aut Friess, Helmut verfasserin aut Enthalten in Langenbeck's archives of surgery Berlin : Springer, 1948 390(2004), 1 vom: 20. Nov., Seite 21-28 (DE-627)253770440 (DE-600)1459390-7 1435-2451 nnns volume:390 year:2004 number:1 day:20 month:11 pages:21-28 https://dx.doi.org/10.1007/s00423-004-0517-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2339 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.65 ASE AR 390 2004 1 20 11 21-28 |
| spelling |
10.1007/s00423-004-0517-4 doi (DE-627)SPR005571871 (SPR)s00423-004-0517-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Köninger, Jörg verfasserin aut Transforming growth factor-β pathway is activated in cholecystolithiasis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. TGF-β (dpeaa)DE-He213 CTGF (dpeaa)DE-He213 Cholecystolithiasis (dpeaa)DE-He213 Fibrogenesis (dpeaa)DE-He213 di Mola, Fabio F. verfasserin aut Di Sebastiano, Pierluigi verfasserin aut Gardini, Andrea verfasserin aut Brigstock, David R. verfasserin aut Innocenti, Paolo verfasserin aut Büchler, Markus W. verfasserin aut Friess, Helmut verfasserin aut Enthalten in Langenbeck's archives of surgery Berlin : Springer, 1948 390(2004), 1 vom: 20. Nov., Seite 21-28 (DE-627)253770440 (DE-600)1459390-7 1435-2451 nnns volume:390 year:2004 number:1 day:20 month:11 pages:21-28 https://dx.doi.org/10.1007/s00423-004-0517-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2339 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.65 ASE AR 390 2004 1 20 11 21-28 |
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10.1007/s00423-004-0517-4 doi (DE-627)SPR005571871 (SPR)s00423-004-0517-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Köninger, Jörg verfasserin aut Transforming growth factor-β pathway is activated in cholecystolithiasis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. TGF-β (dpeaa)DE-He213 CTGF (dpeaa)DE-He213 Cholecystolithiasis (dpeaa)DE-He213 Fibrogenesis (dpeaa)DE-He213 di Mola, Fabio F. verfasserin aut Di Sebastiano, Pierluigi verfasserin aut Gardini, Andrea verfasserin aut Brigstock, David R. verfasserin aut Innocenti, Paolo verfasserin aut Büchler, Markus W. verfasserin aut Friess, Helmut verfasserin aut Enthalten in Langenbeck's archives of surgery Berlin : Springer, 1948 390(2004), 1 vom: 20. Nov., Seite 21-28 (DE-627)253770440 (DE-600)1459390-7 1435-2451 nnns volume:390 year:2004 number:1 day:20 month:11 pages:21-28 https://dx.doi.org/10.1007/s00423-004-0517-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2339 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.65 ASE AR 390 2004 1 20 11 21-28 |
| allfieldsGer |
10.1007/s00423-004-0517-4 doi (DE-627)SPR005571871 (SPR)s00423-004-0517-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Köninger, Jörg verfasserin aut Transforming growth factor-β pathway is activated in cholecystolithiasis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. TGF-β (dpeaa)DE-He213 CTGF (dpeaa)DE-He213 Cholecystolithiasis (dpeaa)DE-He213 Fibrogenesis (dpeaa)DE-He213 di Mola, Fabio F. verfasserin aut Di Sebastiano, Pierluigi verfasserin aut Gardini, Andrea verfasserin aut Brigstock, David R. verfasserin aut Innocenti, Paolo verfasserin aut Büchler, Markus W. verfasserin aut Friess, Helmut verfasserin aut Enthalten in Langenbeck's archives of surgery Berlin : Springer, 1948 390(2004), 1 vom: 20. Nov., Seite 21-28 (DE-627)253770440 (DE-600)1459390-7 1435-2451 nnns volume:390 year:2004 number:1 day:20 month:11 pages:21-28 https://dx.doi.org/10.1007/s00423-004-0517-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2339 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.65 ASE AR 390 2004 1 20 11 21-28 |
| allfieldsSound |
10.1007/s00423-004-0517-4 doi (DE-627)SPR005571871 (SPR)s00423-004-0517-4-e DE-627 ger DE-627 rakwb eng 610 ASE 44.65 bkl Köninger, Jörg verfasserin aut Transforming growth factor-β pathway is activated in cholecystolithiasis 2004 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. TGF-β (dpeaa)DE-He213 CTGF (dpeaa)DE-He213 Cholecystolithiasis (dpeaa)DE-He213 Fibrogenesis (dpeaa)DE-He213 di Mola, Fabio F. verfasserin aut Di Sebastiano, Pierluigi verfasserin aut Gardini, Andrea verfasserin aut Brigstock, David R. verfasserin aut Innocenti, Paolo verfasserin aut Büchler, Markus W. verfasserin aut Friess, Helmut verfasserin aut Enthalten in Langenbeck's archives of surgery Berlin : Springer, 1948 390(2004), 1 vom: 20. Nov., Seite 21-28 (DE-627)253770440 (DE-600)1459390-7 1435-2451 nnns volume:390 year:2004 number:1 day:20 month:11 pages:21-28 https://dx.doi.org/10.1007/s00423-004-0517-4 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2339 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.65 ASE AR 390 2004 1 20 11 21-28 |
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English |
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Enthalten in Langenbeck's archives of surgery 390(2004), 1 vom: 20. Nov., Seite 21-28 volume:390 year:2004 number:1 day:20 month:11 pages:21-28 |
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Enthalten in Langenbeck's archives of surgery 390(2004), 1 vom: 20. Nov., Seite 21-28 volume:390 year:2004 number:1 day:20 month:11 pages:21-28 |
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TGF-β CTGF Cholecystolithiasis Fibrogenesis |
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Köninger, Jörg @@aut@@ di Mola, Fabio F. @@aut@@ Di Sebastiano, Pierluigi @@aut@@ Gardini, Andrea @@aut@@ Brigstock, David R. @@aut@@ Innocenti, Paolo @@aut@@ Büchler, Markus W. @@aut@@ Friess, Helmut @@aut@@ |
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Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">TGF-β</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">CTGF</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Cholecystolithiasis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Fibrogenesis</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">di Mola, Fabio F.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Di Sebastiano, Pierluigi</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gardini, Andrea</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brigstock, David R.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Innocenti, Paolo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Büchler, Markus W.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Friess, Helmut</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Langenbeck's archives of surgery</subfield><subfield code="d">Berlin : Springer, 1948</subfield><subfield code="g">390(2004), 1 vom: 20. 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Köninger, Jörg |
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Köninger, Jörg ddc 610 bkl 44.65 misc TGF-β misc CTGF misc Cholecystolithiasis misc Fibrogenesis Transforming growth factor-β pathway is activated in cholecystolithiasis |
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610 ASE 44.65 bkl Transforming growth factor-β pathway is activated in cholecystolithiasis TGF-β (dpeaa)DE-He213 CTGF (dpeaa)DE-He213 Cholecystolithiasis (dpeaa)DE-He213 Fibrogenesis (dpeaa)DE-He213 |
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ddc 610 bkl 44.65 misc TGF-β misc CTGF misc Cholecystolithiasis misc Fibrogenesis |
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ddc 610 bkl 44.65 misc TGF-β misc CTGF misc Cholecystolithiasis misc Fibrogenesis |
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Transforming growth factor-β pathway is activated in cholecystolithiasis |
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Transforming growth factor-β pathway is activated in cholecystolithiasis |
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Köninger, Jörg |
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Köninger, Jörg di Mola, Fabio F. Di Sebastiano, Pierluigi Gardini, Andrea Brigstock, David R. Innocenti, Paolo Büchler, Markus W. Friess, Helmut |
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transforming growth factor-β pathway is activated in cholecystolithiasis |
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Transforming growth factor-β pathway is activated in cholecystolithiasis |
| abstract |
Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. |
| abstractGer |
Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. |
| abstract_unstemmed |
Background The etiopathogenesis of cholecystolithiasis is not well defined. Primary dysmotility of the organ, due to fibrosis of the gallbladder wall or muscular dysfunction, is suggested as a crucial factor. Transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) are involved in several fibrotic disorders and play a critical role in fibrogenesis, thereby changing the physiological function of the organs. In the present study we analyzed the role of TGF-β and its downstream target CTGF in patients with cholecystolithiasis. Methods Gallbladders were obtained from 16 individuals undergoing surgery for symptomatic cholecystolithiasis. Normal human gallbladder tissue samples from five individuals without any history of gallbladder disease were obtained through an organ donor transplantation program. Northern blot analysis, in situ hybridization, and immunohistochemistry were used to analyze the expression of TGF-β1 and CTGF in the gallbladder tissue samples. Results By northern blot analysis there was an enhanced TGF-β1 mRNA expression (eightfold increase; P<0.04) in the cholecystolithiasis tissue samples in comparison with normal controls. There was also a concomitant increase in CTGF (41-fold increase; P<0.01). By in situ hybridization and immunohistochemistry, CTGF mRNA was localized mainly in the mucosa layer, while intensive staining of the smooth muscle cells with TGF-β1 and CTGF was observed. In addition, TGF-β1 immunoreactivity was also localized in the fibroblasts and inflammatory cells. TGF-β1 m-RNA levels showed a significant relationship with the degree of fibrosis in the tissue samples (P<0.04, r=0.5). Conclusion Our data indicate that TGF-β and CTGF are involved in ultrastructural tissue changes in patients with cholecystolithiasis. Activation of the “TGF-β pathway,” predominantly in the remaining mucosa and submucosal layer, indicates that extracellular matrix (ECM) synthesis with subsequent gallbladder wall fibrosis is an important step in gallbladder dysfunction in this disorder. |
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| score |
7.400584 |