ArticleExperimental and therapeutic medicine2022
Gelsolin impairs barrier function in pancreatic ductal epithelial cells by actin filament depolymerization in hypertriglyceridemia-induced pancreatitis
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Tricellulin regulates the tight junctions and cytoskeleton of pancreatic acinar cells through the NF-κB pathway in hypertriglyceridemic acute pancreatitis.Biomedical reports · 2026Article
- Drug-induced pancreatitis: a real-world analysis of the FDA Adverse Event Reporting System and network pharmacology.Frontiers in pharmacology · 2025Article
- 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
- X-Box binding protein 1 downregulates SIRT6 to promote injury in pancreatic ductal epithelial cells.Immunity, inflammation and disease · 2024Article
- Mitochondrial calcium uniporter promotes mitophagy by regulating the PINK1/Parkin pathway in caerulein‑treated pancreatic ductal epithelial cellsExperimental and therapeutic medicine · 2024Article
- NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development.Nature communications · 2023Article
- Cofilin activation in pancreatic acinar cells plays a pivotal convergent role for mediating CCK-stimulated enzyme secretion and growth.Frontiers in physiology · 2023Article
- Gelsolin inhibits autophagy by regulating actin depolymerization in pancreatic ductal epithelial cells in acute pancreatitis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gelsolin (GSN) is a calcium-regulated actin-binding protein that can sever actin filaments. Notably, actin dynamics affect the structure and function of epithelial barriers. The present study investigated the role of GSN in the barrier function of pancreatic ductal epithelial cells (PDECs) in hypertriglyceridemia-induced pancreatitis (HTGP). The human PDEC cell line HPDE6-C7 underwent GSN knockdown and was treated with caerulein (CAE) + triglycerides (TG). Intracellular calcium levels and the actin filament network were analyzed under a fluorescence microscope. The expression levels of GSN, E-cadherin, nectin-2, ZO-1 and occludin were evaluated by reverse transcription-quantitative polymerase chain reaction and western blotting. Ultrastructural changes in tight junctions were observed by transmission electron microscopy. Furthermore, the permeability of PDECs was analyzed by fluorescein isothiocyanate-dextran fluorescence. The results revealed that CAE + TG increased intracellular calcium levels, actin filament depolymerization and GSN expression, and increased PDEC permeability by decreasing the expression levels of E-cadherin, nectin-2, ZO-1 and occludin compared with the control. Moreover, changes in these markers, with the exception of intracellular calcium levels, were reversed by silencing GSN. In conclusion, GSN may disrupt barrier function in PDECs by causing actin filament depolymerization in HTGP
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