exosome-LncPICALM-AU1 regulates endothelial-mesenchymal transition in hepatopulmonary syndrome

Yang, C.; Yang, Y.; Chen, Y.; Huang, J.; Li, Y.; Zhi, H.; Tang, X.; Wang, X.; Belguise, K.; Xia, Z.; Ning, J.; Gu, J.; Yi, B.; lu, K.

doi:10.1101/2020.10.06.327874

bioRxiv · 10.1101/2020.10.06.327874

exosome-LncPICALM-AU1 regulates endothelial-mesenchymal transition in hepatopulmonary syndrome

Yang, C.·Yang, Y.·Chen, Y.·Huang, J.·Li, Y.·Zhi, H.·Tang, X.·Wang, X.·Belguise, K.·Xia, Z.·Ning, J.·Gu, J.·Yi, B.·lu, K.

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Abstract

As 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.

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Yang, C., Yang, Y., Chen, Y., Huang, J., Li, Y., Zhi, H., Tang, X., Wang, X., Belguise, K., Xia, Z., Ning, J., Gu, J., Yi, B., lu, K.. 2020-10-09. exosome-LncPICALM-AU1 regulates endothelial-mesenchymal transition in hepatopulmonary syndrome. https://doi.org/10.1101/2020.10.06.327874

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