期刊
SCIENTIFIC REPORTS
卷 5, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep16859
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资金
- Wellbeing of Women research grant [R42533]
- MRC Centre Grant [G1002033]
- Federation of Women Graduates [134225]
- College of Medicine and Veterinary Medicine at the University of Edinburgh
- MRC [G1002033] Funding Source: UKRI
- Chief Scientist Office [SCD/02] Funding Source: researchfish
- Medical Research Council [G0500717, G1002033] Funding Source: researchfish
- Wellbeing of Women [RG1436] Funding Source: researchfish
VEGF-A, an angiogenic factor, is increased in the peritoneal fluid of women with endometriosis. The cytokine TGF-beta 1 is thought to play a role in the establishment of endometriosis lesions. Inhibitor of DNA binding (ID) proteins are transcriptional targets of TGF-beta 1 and ID1 has been implicated in VEGF-A regulation during tumor angiogenesis. Herein, we determined whether peritoneal expression of VEGF-A is regulated by TGF-beta 1 through the ID1 pathway in women with endometriosis. VEGF-A was measured in peritoneal fluid by ELISA (n = 16). VEGF-A and ID1 expression was examined in peritoneal biopsies (n = 13), and primary peritoneal and immortalized mesothelial cells (MeT5A) by immunohistochemistry, qRT-PCR and ELISA. VEGF-A was increased in peritoneal fluid from women with endometriosis and levels correlated with TGF-beta 1 concentrations (P < 0.05). VEGF-A was immunolocalized to peritoneal mesothelium and TGF-beta 1 increased VEGFA mRNA (P < 0.05) and protein (P < 0.05) in mesothelial cells. ID1 was increased in peritoneum from women with endometriosis and TGF-beta 1 increased concentrations of ID1 mRNA (P < 0.05) in mesothelial cells. VEGF-A regulation through ID1 was confirmed by siRNA in MeT5A cells (P < 0.05). Our data supports role for ID1 in the pathophysiology of endometriosis, as an effector of TGF beta 1 dependent upregulation of VEGF-A, and highlights a novel potential therapeutic target.
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