Exosome-LncPICALM-AU1 regulates endothelial–mesenchymal transition in hepatopulmonary syndrome

Author:

Yang Congwen,Yang Yihui,Chen Yang,Huang Jian,Li Yujie,Zhi Hongyu,Tang Xi,Wang Xiaobo,Belguise Karine,Xia Zhengyuan,Ning Jiaoling,Gu Jianteng,Yi Bin,Lu KaizhiORCID

Abstract

AbstractAs important mediators of intercellular communication, exosome have can modulate various cellular functions by transferring a variety of intracellular components to target cells. However, little is known about the role of exosome-mediated communication between distant organs. Hepatopulmonary syndrome (HPS) is a severe lung injury caused by chronic liver disease. A new long noncoding RNA (lncRNA) PICALM-AU1 was found and upregulated in the liver of HPS. It was located in the cholangiocytes of liver and then, secreted as exosome into the serum. PICALM-AU1 carrying serum exosomes induced endothelial-mesenchymal transition (EndMT) of PMVECs and promoted lung injury in vivo and in vitro. Furthermore, overexpression of PICALM-AU1 significantly suppressed miR144-3p and subsequently induced ZEB1 expression. Taken together, our findings identified cholangiocyte-derived exosomal lncRNA PICALM-AU1 plays a critical role in the EndMT of HPS lung. And PICALM-AU1 represents a noninvasive biomarker and potential therapeutic target for HPS.

Publisher

Cold Spring Harbor Laboratory

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