VEGF deficit is involved in endothelium dysfunction in preeclampsia
Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normote...
Ausführliche Beschreibung
Autor*in: |
Zhou, Qiong [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2010 |
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Anmerkung: |
© Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 |
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Übergeordnetes Werk: |
Enthalten in: Journal of Huazhong University of Science and Technology - Wuhan : Huazhong Univ. of Science and Technology, 2002, 30(2010), 3 vom: Juni, Seite 370-374 |
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Übergeordnetes Werk: |
volume:30 ; year:2010 ; number:3 ; month:06 ; pages:370-374 |
Links: |
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DOI / URN: |
10.1007/s11596-010-0359-y |
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Katalog-ID: |
SPR020999798 |
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245 | 1 | 0 | |a VEGF deficit is involved in endothelium dysfunction in preeclampsia |
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520 | |a Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. | ||
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700 | 1 | |a Qiao, Fuyuan |4 aut | |
700 | 1 | |a Wu, Yuanyuan |4 aut | |
700 | 1 | |a Xu, Jingjing |4 aut | |
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10.1007/s11596-010-0359-y doi (DE-627)SPR020999798 (SPR)s11596-010-0359-y-e DE-627 ger DE-627 rakwb eng Zhou, Qiong verfasserin aut VEGF deficit is involved in endothelium dysfunction in preeclampsia 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. Liu, Haiyi aut Qiao, Fuyuan aut Wu, Yuanyuan aut Xu, Jingjing aut Enthalten in Journal of Huazhong University of Science and Technology Wuhan : Huazhong Univ. of Science and Technology, 2002 30(2010), 3 vom: Juni, Seite 370-374 (DE-627)537444408 (DE-600)2376511-2 1993-1352 nnns volume:30 year:2010 number:3 month:06 pages:370-374 https://dx.doi.org/10.1007/s11596-010-0359-y 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_121 GBV_ILN_138 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 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_2056 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_2700 GBV_ILN_2817 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_4277 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_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 30 2010 3 06 370-374 |
spelling |
10.1007/s11596-010-0359-y doi (DE-627)SPR020999798 (SPR)s11596-010-0359-y-e DE-627 ger DE-627 rakwb eng Zhou, Qiong verfasserin aut VEGF deficit is involved in endothelium dysfunction in preeclampsia 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. Liu, Haiyi aut Qiao, Fuyuan aut Wu, Yuanyuan aut Xu, Jingjing aut Enthalten in Journal of Huazhong University of Science and Technology Wuhan : Huazhong Univ. of Science and Technology, 2002 30(2010), 3 vom: Juni, Seite 370-374 (DE-627)537444408 (DE-600)2376511-2 1993-1352 nnns volume:30 year:2010 number:3 month:06 pages:370-374 https://dx.doi.org/10.1007/s11596-010-0359-y 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_121 GBV_ILN_138 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 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_2056 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_2700 GBV_ILN_2817 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_4277 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_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 30 2010 3 06 370-374 |
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10.1007/s11596-010-0359-y doi (DE-627)SPR020999798 (SPR)s11596-010-0359-y-e DE-627 ger DE-627 rakwb eng Zhou, Qiong verfasserin aut VEGF deficit is involved in endothelium dysfunction in preeclampsia 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. Liu, Haiyi aut Qiao, Fuyuan aut Wu, Yuanyuan aut Xu, Jingjing aut Enthalten in Journal of Huazhong University of Science and Technology Wuhan : Huazhong Univ. of Science and Technology, 2002 30(2010), 3 vom: Juni, Seite 370-374 (DE-627)537444408 (DE-600)2376511-2 1993-1352 nnns volume:30 year:2010 number:3 month:06 pages:370-374 https://dx.doi.org/10.1007/s11596-010-0359-y 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_121 GBV_ILN_138 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 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_2056 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_2700 GBV_ILN_2817 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_4277 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_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 30 2010 3 06 370-374 |
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10.1007/s11596-010-0359-y doi (DE-627)SPR020999798 (SPR)s11596-010-0359-y-e DE-627 ger DE-627 rakwb eng Zhou, Qiong verfasserin aut VEGF deficit is involved in endothelium dysfunction in preeclampsia 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. Liu, Haiyi aut Qiao, Fuyuan aut Wu, Yuanyuan aut Xu, Jingjing aut Enthalten in Journal of Huazhong University of Science and Technology Wuhan : Huazhong Univ. of Science and Technology, 2002 30(2010), 3 vom: Juni, Seite 370-374 (DE-627)537444408 (DE-600)2376511-2 1993-1352 nnns volume:30 year:2010 number:3 month:06 pages:370-374 https://dx.doi.org/10.1007/s11596-010-0359-y 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_121 GBV_ILN_138 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 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_2056 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_2700 GBV_ILN_2817 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_4277 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_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 30 2010 3 06 370-374 |
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10.1007/s11596-010-0359-y doi (DE-627)SPR020999798 (SPR)s11596-010-0359-y-e DE-627 ger DE-627 rakwb eng Zhou, Qiong verfasserin aut VEGF deficit is involved in endothelium dysfunction in preeclampsia 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. Liu, Haiyi aut Qiao, Fuyuan aut Wu, Yuanyuan aut Xu, Jingjing aut Enthalten in Journal of Huazhong University of Science and Technology Wuhan : Huazhong Univ. of Science and Technology, 2002 30(2010), 3 vom: Juni, Seite 370-374 (DE-627)537444408 (DE-600)2376511-2 1993-1352 nnns volume:30 year:2010 number:3 month:06 pages:370-374 https://dx.doi.org/10.1007/s11596-010-0359-y 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_121 GBV_ILN_138 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 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_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2036 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_2056 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_2700 GBV_ILN_2817 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_4277 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_4346 GBV_ILN_4367 GBV_ILN_4392 GBV_ILN_4393 GBV_ILN_4700 GBV_ILN_4753 AR 30 2010 3 06 370-374 |
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Zhou, Qiong @@aut@@ Liu, Haiyi @@aut@@ Qiao, Fuyuan @@aut@@ Wu, Yuanyuan @@aut@@ Xu, Jingjing @@aut@@ |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR020999798</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519104734.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201006s2010 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s11596-010-0359-y</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR020999798</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s11596-010-0359-y-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Zhou, Qiong</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">VEGF deficit is involved in endothelium dysfunction in preeclampsia</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2010</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Haiyi</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Qiao, Fuyuan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wu, Yuanyuan</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xu, Jingjing</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Journal of Huazhong University of Science and Technology</subfield><subfield code="d">Wuhan : Huazhong Univ. of Science and Technology, 2002</subfield><subfield code="g">30(2010), 3 vom: Juni, Seite 370-374</subfield><subfield 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Zhou, Qiong |
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Zhou, Qiong VEGF deficit is involved in endothelium dysfunction in preeclampsia |
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VEGF deficit is involved in endothelium dysfunction in preeclampsia |
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VEGF deficit is involved in endothelium dysfunction in preeclampsia |
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VEGF deficit is involved in endothelium dysfunction in preeclampsia |
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Zhou, Qiong Liu, Haiyi Qiao, Fuyuan Wu, Yuanyuan Xu, Jingjing |
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vegf deficit is involved in endothelium dysfunction in preeclampsia |
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VEGF deficit is involved in endothelium dysfunction in preeclampsia |
abstract |
Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 |
abstractGer |
Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 |
abstract_unstemmed |
Summary This study examined the association of expression of vascular endothelial growth factor (VEGF), a promoter of angiogenesis, with endothelium dysfunction in preeclampsia. The level of VEGF protein and mRNA in the placenta and peripheral blood samples of 30 preeclampsia patients and 30 normotensive pregnant women was measured by immunohistochemistry, real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. VEGF expression in the human umbilical vein endothelial cells (HUVECs) was blocked by small interfering RNAs (siRNAs). The monolayer barrier function of HUVECs was determined by measuring the fluorescence intensity of BSA that crossed the HUVEC monolayers. The cell proliferation and cell-secreted nitric oxide (NO) level were detected by MTT method and nitrate reductase assay, respectively. The results showed that VEGF was expressed in the syncytiotrophoblasts and endothelial cells of vessels and capillaries in the placenta tissue. The serum level of VEGF in the preeclampsia patients was significantly decreased as compared with that in normal pregnant subjects, although VEGF mRNA expression in the placenta tissue of preeclampsia patients remained still high. Moreover, VEGF deficit could lead to endothelium cell dysfunction, and the administration of VEGF could protect endothelium cells from injury. It was concluded that lack of VEGF contributes to endothelium dysfunction, which may lead to the occurrence and development of preeclampsia. © Huazhong University of Science and Technology and Springer-Verlag Berlin Heidelberg 2010 |
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container_issue |
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title_short |
VEGF deficit is involved in endothelium dysfunction in preeclampsia |
url |
https://dx.doi.org/10.1007/s11596-010-0359-y |
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Liu, Haiyi Qiao, Fuyuan Wu, Yuanyuan Xu, Jingjing |
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up_date |
2024-07-03T19:38:23.467Z |
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score |
7.4018974 |