Preeklamptik ve normotansif plasentalarda VEGF ve Vimentin ekspresyon
düzeylerinin immunohistokimya ve Western Blot yöntemleri ile incelenmesi
Amaç: Bu çalışmada anjiogenezi stimule eden vasküler endotel büyüme faktörü (VEGF) ve bir mezenşimal markır olan vimentin proteinlerinin preeklamptik ve normotansif plasentalardaki ekspresyon düzeylerini araştırmayı amaçladık. Yöntemler: Çalışmaya 35-38. haftalardaki doğum sonrası plasentalar dahil edildi. 10 adet preeklamptik ve 10 adet normal plasenta kullanıldı. %10’ luk formaldehit solüsyonuna atılan doku parçaları rutin parafin takiplerinden sonra histopatolojik olarak incelendi. VEGF ve vimentin protein düzeyleri Western Blot yöntemiyle ölçüldü. Bulgular: Preeklamptik plasentalarda sinsisyal proliferasyonun artmış olduğu izlendi. İntravillous sinsityal düğümler, sinsityal ödem, kollajen artışı ve damarlarda endotel hasar gözlendi. Preeklampsi (PE) sonucu plasentadaki VEGF ve vimentin protein düzeylerinin artış gösterdiği gözlendi. Sonuç: Preeklamptik plasenta dokusunda fonksiyonel olmayan VEGF ligandının reseptörüne bağlanamadığı için VEGF miktarının arttığı ve bu durumun yetersiz anjiogeneze neden olduğu olasıdır. Ayrıca preeklamptik plasentadaki vimentin artışının vasküler permeabilitenin azalmasına neden olabileceği düşünülmektedir.
Examining the expression level of VEGF and vimentin by immunohistochemistry and Western Blot in preeclamptic and normotensive placentas
Objective: In this study, we aimed to investigate the expression levels of vascular endothelial growth factor (VEGF) which stimulates angiogenesis and vimentin, an intermediate cytoskeleton filaments, in both preeclamptic and normotensive placentas. Methods: In this study, placentas after birth in 35-38 weeks were included. Ten preeclamptic placentas and ten normal placentas were used. Tissue pieces which had been soaked in 10% formaldehyde solution were examined histologically after routine paraffin follow. The expression levels of VEGF and vimentin were measured by Western Blot. Results: It was found that syncytial proliferation was increased in preeclamptic placentas. Intervillous syncytial knots, syncytial edema, collagen increase and vascular endothelial damage were observed. It was observed that VEGF and vimentin expression levels were increased as a result of preeclampsia. Conclusion: Nonfunctional VEGF which could not bind to its receptor leading to increased VEGF level may lead to inadequate angiogenesis in preeclamptic placenta. In addition, it is thought that an increase in vimentin level in preeclamptic placenta may cause reduced vascular permeability.
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