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YAP activates pancreatic stellate cells and enhances pancreatic fibrosis

Hepatobiliary & Pancreatic Diseases International 2022年第6期21卷 583-589页

作者： lennard spanehl Denis Revskij Karen Bannert Luise Ehlers Robert Jaster Department of Medicine Ⅱ Division of GastroenterologyRostock University Medical CenterErnst-Heydemann-Str.618057 RostockGermany

Background:Pancreatic stellate cells(PSCs)foster the progression of pancreatic adenocarcinoma and chronic pancreatitis(CP)by producing a dense fibrotic ***,the incomplete knowledge of PSCs biology hampers the exploration of antifibrotic ***,we explored the role of the Hippo pathway in the context of PSCs activation and experimental ***:CP model was created in rats with the tail vein injection of dibutyltin dichloride(DBTC).The expression of Yes-associated protein(YAP)in CP tissue was *** and immortalized rats PSCs were treated with the YAP-inhibitor ***,YAP siRNA was ***,DNA synthesis,cell survival,levels ofα-smooth muscle actin(α-SMA)protein,presence of lipid droplets and PSCs gene expression were *** regulators of YAP signaling were studied by reporter gene ***:In DBTC-induced CP,pronounced expression of YAP in areas of tubular structures and periduc-tal fibrosis was *** diminished DNA replication in PSCs in a dose-dependent *** of YAP reduced cell *** cultures of PSCs were characterized by a de-crease of lipid droplets and increased synthesis ofα-SMA *** processes were not affected by *** the non-cytotoxic concentration of 100 nmol/L,verteporfin significantly reduced mRNA levels of transforming growth factor-β1(Tgf-β1)and Ccn family member 1(Ccn1).YAP signaling was acti-vated by TGF-β1,but repressed by interferon-γ.Conclusions:Activated YAP enhanced PSCs *** antifibrotic potential of Hippo pathway in-hibitors warrants further investigation.

关键词： Hippo pathway Pancreatic stellate cells Fibrosis Pancreatic cancer Chronic pancreatitis

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