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논문 기본 정보

자료유형
학술저널
저자정보
Pan Yibin (Zhejiang University School of Medicine) Yan Lili (Zhejiang University School of Medicine) Chen Qiaoqiao (Zhejiang University School of Medicine) Wei Cheng (Zhejiang University School of Medicine) Dai Yongdong (Zhejiang University School of Medicine) Tong Xiaomei (Zhejiang University School of Medicine) Zhu Haiyan (Zhejiang University School of Medicine) Lu Meifei (Zhejiang University School of Medicine) Zhang Yanling (Zhejiang University School of Medicine) Jin Xiaoying (Zhejiang University School of Medicine) Zhang Tai (Zhejiang University School of Medicine) Lin Xiaona (Zhejiang University School of Medicine) Zhou Feng (Zhejiang University School of Medicine) Zhang Songying (Zhejiang University School of Medicine)
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제53권
발행연도
2021.1
수록면
1 - 15 (15page)
DOI
10.1038/s12276-020-00530-6

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In early pregnancy, the placenta anchors the conceptus and supports embryonic development and survival. This study aimed to investigate the underlying functions of Shh signaling in recurrent miscarriage (RM), a serious disorder of pregnancy. In the present study, Shh and Gli2 were mainly observed in cytotrophoblasts (CTBs), Ptch was mainly observed in syncytiotrophoblasts (STBs), and Smo and Gli3 were expressed in both CTBs and STBs. Shh signaling was significantly impaired in human placenta tissue from recurrent miscarriage patients compared to that of gestational age-matched normal controls. VEGF-A and CD31 protein levels were also significantly decreased in recurrent miscarriage patients. Furthermore, inhibition of Shh signaling impaired the motility of JAR cells by regulating the expression of Gli2 and Gli3. Intriguingly, inhibition of Shh signaling also triggered autophagy and autolysosome accumulation. Additionally, knockdown of BECN1 reversed Gant61-induced motility inhibition. In conclusion, our results showed that dysfunction of Shh signaling activated autophagy to inhibit trophoblast motility, which suggests the Shh pathway and autophagy as potential targets for RM therapy.

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