Title of article :
Pigment epithelial-derived factor expression in endometriotic lesions in a rat model of endometriosis
Author/Authors :
Fu، نويسنده , , Guofang and Che، نويسنده , , Xuan and Sun، نويسنده , , Yanmei and Huang، نويسنده , , Xiufeng and Xu، نويسنده , , Hong and Zhou، نويسنده , , Caiyun and Zhang، نويسنده , , Xinmei، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2013
Pages :
7
From page :
301
To page :
307
Abstract :
Angiogenesis is a prerequisite for endometriotic lesion formation and development. Pigment epithelium-derived factor (PEDF) is a potential inhibitor of angiogenesis. The objective of this study was to detect PEDF immunolocalization in endometriotic lesions and the correlation with vascular endothelial growth factor (VEGF) and microvascular density (MVD) in a rat model of endometriosis. A subcutaneous endometriosis rat model was established by using auto-transplantation. Expression of PEDF, VEGF and MVD labeled by von Willebrand factor (v-WF) in endometriotic lesions and endometrial tissues was evaluated using immunohistochemical staining. We detected lower PEDF immunostaining and higher VEGF and MVD immunostaining in active lesions in a rat model of endometriosis than that in endometriosis endometrium or control endometrium (P < 0.05), but no differences between endometriosis and control endometrium were found (P > 0.05). In lesions, PEDF expression was negatively correlated with VEGF expression, MVD or sizes of cysts (P < 0.01). On the contrary, both VEGF expression and MVD were positively correlated with lesion sizes (P < 0.05). In addition, VEGF expression was positively correlated with MVD (P < 0.01). Our results suggest that PEDF might be involved in the pathogenesis of endometriosis and may lead to novel treatment for this disease.
Keywords :
Pigment epithelium-derived factor , Angiogenesis , Animal model , Vascular endothelial growth factor , Rat , Endometriosis
Journal title :
Acta Histochemica
Serial Year :
2013
Journal title :
Acta Histochemica
Record number :
1760168
Link To Document :
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