Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars
Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in ep...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Lee, Joon Seok [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Schlagwörter: |
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| Anmerkung: |
© Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 |
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| Übergeordnetes Werk: |
Enthalten in: Aesthetic plastic surgery - New York, NY : Springer, 1976, 43(2019), 5 vom: 25. Juli, Seite 1371-1380 |
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| Übergeordnetes Werk: |
volume:43 ; year:2019 ; number:5 ; day:25 ; month:07 ; pages:1371-1380 |
| Links: |
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| DOI / URN: |
10.1007/s00266-019-01434-1 |
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| Katalog-ID: |
SPR003359212 |
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| 520 | |a Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. | ||
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| 650 | 4 | |a Hypertrophic scar |7 (dpeaa)DE-He213 | |
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10.1007/s00266-019-01434-1 doi (DE-627)SPR003359212 (SPR)s00266-019-01434-1-e DE-627 ger DE-627 rakwb eng Lee, Joon Seok verfasserin aut Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. Myofibroblast (dpeaa)DE-He213 Fibroblast (dpeaa)DE-He213 Keratinocyte (dpeaa)DE-He213 Hypertrophic scar (dpeaa)DE-He213 Kim, Jong Seong aut Lee, Jeong Woo aut Choi, Kang Young aut Yang, Jung Dug aut Cho, Byung Chae aut Oh, Eun Jung aut Kim, Tae Jung aut Ko, Ung Hyun aut Shin, Jennifer H. aut Jeon, Sewha aut Lee, Yong Jig aut Chung, Ho Yun (orcid)0000-0002-1580-0487 aut Enthalten in Aesthetic plastic surgery New York, NY : Springer, 1976 43(2019), 5 vom: 25. Juli, Seite 1371-1380 (DE-627)254630758 (DE-600)1462126-5 1432-5241 nnns volume:43 year:2019 number:5 day:25 month:07 pages:1371-1380 https://dx.doi.org/10.1007/s00266-019-01434-1 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_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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2019 5 25 07 1371-1380 |
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10.1007/s00266-019-01434-1 doi (DE-627)SPR003359212 (SPR)s00266-019-01434-1-e DE-627 ger DE-627 rakwb eng Lee, Joon Seok verfasserin aut Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. Myofibroblast (dpeaa)DE-He213 Fibroblast (dpeaa)DE-He213 Keratinocyte (dpeaa)DE-He213 Hypertrophic scar (dpeaa)DE-He213 Kim, Jong Seong aut Lee, Jeong Woo aut Choi, Kang Young aut Yang, Jung Dug aut Cho, Byung Chae aut Oh, Eun Jung aut Kim, Tae Jung aut Ko, Ung Hyun aut Shin, Jennifer H. aut Jeon, Sewha aut Lee, Yong Jig aut Chung, Ho Yun (orcid)0000-0002-1580-0487 aut Enthalten in Aesthetic plastic surgery New York, NY : Springer, 1976 43(2019), 5 vom: 25. Juli, Seite 1371-1380 (DE-627)254630758 (DE-600)1462126-5 1432-5241 nnns volume:43 year:2019 number:5 day:25 month:07 pages:1371-1380 https://dx.doi.org/10.1007/s00266-019-01434-1 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_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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2019 5 25 07 1371-1380 |
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10.1007/s00266-019-01434-1 doi (DE-627)SPR003359212 (SPR)s00266-019-01434-1-e DE-627 ger DE-627 rakwb eng Lee, Joon Seok verfasserin aut Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. Myofibroblast (dpeaa)DE-He213 Fibroblast (dpeaa)DE-He213 Keratinocyte (dpeaa)DE-He213 Hypertrophic scar (dpeaa)DE-He213 Kim, Jong Seong aut Lee, Jeong Woo aut Choi, Kang Young aut Yang, Jung Dug aut Cho, Byung Chae aut Oh, Eun Jung aut Kim, Tae Jung aut Ko, Ung Hyun aut Shin, Jennifer H. aut Jeon, Sewha aut Lee, Yong Jig aut Chung, Ho Yun (orcid)0000-0002-1580-0487 aut Enthalten in Aesthetic plastic surgery New York, NY : Springer, 1976 43(2019), 5 vom: 25. Juli, Seite 1371-1380 (DE-627)254630758 (DE-600)1462126-5 1432-5241 nnns volume:43 year:2019 number:5 day:25 month:07 pages:1371-1380 https://dx.doi.org/10.1007/s00266-019-01434-1 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_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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2019 5 25 07 1371-1380 |
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10.1007/s00266-019-01434-1 doi (DE-627)SPR003359212 (SPR)s00266-019-01434-1-e DE-627 ger DE-627 rakwb eng Lee, Joon Seok verfasserin aut Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. Myofibroblast (dpeaa)DE-He213 Fibroblast (dpeaa)DE-He213 Keratinocyte (dpeaa)DE-He213 Hypertrophic scar (dpeaa)DE-He213 Kim, Jong Seong aut Lee, Jeong Woo aut Choi, Kang Young aut Yang, Jung Dug aut Cho, Byung Chae aut Oh, Eun Jung aut Kim, Tae Jung aut Ko, Ung Hyun aut Shin, Jennifer H. aut Jeon, Sewha aut Lee, Yong Jig aut Chung, Ho Yun (orcid)0000-0002-1580-0487 aut Enthalten in Aesthetic plastic surgery New York, NY : Springer, 1976 43(2019), 5 vom: 25. Juli, Seite 1371-1380 (DE-627)254630758 (DE-600)1462126-5 1432-5241 nnns volume:43 year:2019 number:5 day:25 month:07 pages:1371-1380 https://dx.doi.org/10.1007/s00266-019-01434-1 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_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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2019 5 25 07 1371-1380 |
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10.1007/s00266-019-01434-1 doi (DE-627)SPR003359212 (SPR)s00266-019-01434-1-e DE-627 ger DE-627 rakwb eng Lee, Joon Seok verfasserin aut Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. Myofibroblast (dpeaa)DE-He213 Fibroblast (dpeaa)DE-He213 Keratinocyte (dpeaa)DE-He213 Hypertrophic scar (dpeaa)DE-He213 Kim, Jong Seong aut Lee, Jeong Woo aut Choi, Kang Young aut Yang, Jung Dug aut Cho, Byung Chae aut Oh, Eun Jung aut Kim, Tae Jung aut Ko, Ung Hyun aut Shin, Jennifer H. aut Jeon, Sewha aut Lee, Yong Jig aut Chung, Ho Yun (orcid)0000-0002-1580-0487 aut Enthalten in Aesthetic plastic surgery New York, NY : Springer, 1976 43(2019), 5 vom: 25. Juli, Seite 1371-1380 (DE-627)254630758 (DE-600)1462126-5 1432-5241 nnns volume:43 year:2019 number:5 day:25 month:07 pages:1371-1380 https://dx.doi.org/10.1007/s00266-019-01434-1 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_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_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 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_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2019 5 25 07 1371-1380 |
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Lee, Joon Seok @@aut@@ Kim, Jong Seong @@aut@@ Lee, Jeong Woo @@aut@@ Choi, Kang Young @@aut@@ Yang, Jung Dug @@aut@@ Cho, Byung Chae @@aut@@ Oh, Eun Jung @@aut@@ Kim, Tae Jung @@aut@@ Ko, Ung Hyun @@aut@@ Shin, Jennifer H. @@aut@@ Jeon, Sewha @@aut@@ Lee, Yong Jig @@aut@@ Chung, Ho Yun @@aut@@ |
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Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. 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Lee, Joon Seok |
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Lee, Joon Seok misc Myofibroblast misc Fibroblast misc Keratinocyte misc Hypertrophic scar Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars |
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Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars Myofibroblast (dpeaa)DE-He213 Fibroblast (dpeaa)DE-He213 Keratinocyte (dpeaa)DE-He213 Hypertrophic scar (dpeaa)DE-He213 |
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Lee, Joon Seok Kim, Jong Seong Lee, Jeong Woo Choi, Kang Young Yang, Jung Dug Cho, Byung Chae Oh, Eun Jung Kim, Tae Jung Ko, Ung Hyun Shin, Jennifer H. Jeon, Sewha Lee, Yong Jig Chung, Ho Yun |
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effect of keratinocytes on myofibroblasts in hypertrophic scars |
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Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars |
| abstract |
Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 |
| abstractGer |
Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 |
| abstract_unstemmed |
Abstract Myofibroblasts play a central role in matrix formation and wound contraction during wound healing and undergo apoptosis at the end of the healing. Hypertrophic scarring is a pathologic condition in which myofibroblasts persist in the tissue. It has been hypothesized that abnormalities in epidermal–dermal crosstalk underlie this pathology. Therefore, in this study, we investigated whether myofibroblasts are affected by keratinocytes. Transforming growth factor beta-induced myofibroblasts (Imyo) and myofibroblasts from hypertrophic scar tissue (Hmyo) were characterized using microarrays. Keratinocytes were co-cultured with myofibroblasts, and quantitative PCR analysis was performed. We found that numerous extracellular matrix- and smooth muscle cell-associated genes were upregulated in Imyo and Hmyo respectively, and these findings suggest that Hmyo are fully differentiated myofibroblasts and that Imyo are less differentiated than Hmyo. Decreased collagen type 1 gene expression was found in keratinocytes co-cultured with Imyo and Hmyo; further, α-smooth muscle actin expression in Imyo increased in the presence of keratinocytes. These observations indicate that keratinocytes play a role in the development of pathological fibrosis in hypertrophic scar tissue by regulating the behavior of dermal fibroblasts and myofibroblasts. We believe that this study provides the basis for understanding the pathophysiology of hypertrophic scarring and identifying new therapeutic approaches for this dysfunction. No Level Assigned This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors -www.springer.com/00266. © Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery 2019 |
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Effect of Keratinocytes on Myofibroblasts in Hypertrophic Scars |
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Kim, Jong Seong Lee, Jeong Woo Choi, Kang Young Yang, Jung Dug Cho, Byung Chae Oh, Eun Jung Kim, Tae Jung Ko, Ung Hyun Shin, Jennifer H. Jeon, Sewha Lee, Yong Jig Chung, Ho Yun |
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Kim, Jong Seong Lee, Jeong Woo Choi, Kang Young Yang, Jung Dug Cho, Byung Chae Oh, Eun Jung Kim, Tae Jung Ko, Ung Hyun Shin, Jennifer H. Jeon, Sewha Lee, Yong Jig Chung, Ho Yun |
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| score |
7.4008837 |