ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2023
Gelsolin inhibits autophagy by regulating actin depolymerization in pancreatic ductal epithelial cells in acute pancreatitis.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- MCU-Mediated SIRT3 Inhibition Drives Oxidative Stress-Induced Cytoskeletal Disruption in Pancreatic Ductal Epithelium: A Mechanism of Hypertriglyceridemic Acute Pancreatitis.International journal of general medicine · 2025Article
- Caftaric acid attenuates kidney and remote organ damage induced by renal ischemia-reperfusion injury.Scientific reports · 2024Article
- Mitochondrial calcium uniporter promotes mitophagy by regulating the PINK1/Parkin pathway in caerulein‑treated pancreatic ductal epithelial cellsExperimental and therapeutic medicine · 2024Article
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7 authors at 1 institution in 1 country.
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Abstract
Gelsolin (GSN) can sever actin filaments associated with autophagy. This study investigated how GSN-regulated actin filaments control autophagy in pancreatic ductal epithelial cells (PDECs) in acute pancreatitis (AP). AP was produced in a rat model and PDECs using caerulein (CAE). Rat pancreatic duct tissue and HPDE6-C7 cells were extracted at 6, 12, 24, and 48 h after CAE treatment. HPDE6-C7 cells in the presence of CAE were treated with cytochalasin B (CB) or silenced for GSN for 24 h. Pancreatic histopathology and serum amylase levels were analyzed. Cellular ultrastructure and autophagy in PDECs were observed by transmission electron microscopy after 24 h of CAE treatment. The expression of GSN and autophagy markers LC3, P62, and LAMP2 was evaluated in PDECs by immunohistochemistry and western blotting. Actin filaments were observed microscopically. Amylase levels were highest at 6 h of AP, and pancreatic tissue damage increased over time. Mitochondrial vacuolization and autophagy were observed in PDECs. CAE increased GSN expression in these cells over time, increased the LC3-II/LC3-I ratio and LAMP2 expression at 24 and 6 h of treatment, respectively, and decreased P62 expression at all time points. CB treatment for 24 h decreased the LC3-II/LC3-I ratio and LAMP2 expression, increased P62 levels, but had no impact on GSN expression in CAE-treated PDECs. CAE induced actin depolymerization, and CB potentiated this effect. GSN silencing increased the LC3-II/LC3-I ratio and LAMP2 expression and reduced actin depolymerization in CAE-treated PDECs. GSN may inhibit autophagosome biogenesis and autophagosome-lysosome fusion by increasing actin depolymerization in PDECs in AP.
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