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10.1016/j.prostaglandins.2016.08.001

http://scihub22266oqcxt.onion/10.1016/j.prostaglandins.2016.08.001
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suck abstract from ncbi


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pmid27554058
      Prostaglandins+Other+Lipid+Mediat 2016 ; 126 (ä): 1-8
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  • Cytosolic phospholipase A(2)? increases proliferation and de-differentiation of human renal tubular epithelial cells #MMPMID27554058
  • Montford JR ; Lehman AM ; Scobey MS ; Weiser-Evans MC ; Nemenoff RA ; Furgeson SB
  • Prostaglandins Other Lipid Mediat 2016[Nov]; 126 (ä): 1-8 PMID27554058 show ga
  • The group IVA calcium-dependent cytosolic phospholipase A(2) (cPLA(2)?) enzyme controls the release of arachidonic acid from membrane bound phospholipids and is the rate-limiting step in production of eicosanoids. A variety of different kidney injuries activate cPLA(2)?, therefore we hypothesized that cPLA(2)? activity would regulate pathologic processes in HK-2 cells, a human renal tubular epithelial cell line, by regulating cell phenotype and proliferation. In two lentiviral cPLA(2)?-silenced knockdowns, we observed decreased proliferation and increased apoptosis compared to control HK-2 cells. cPLA(2)?-silenced cells also demonstrated an altered morphology, had increased expression E-cadherin, and decreased expression of Ncadherin. Increased levels of E-cadherin were associated with increased promoter activity and decreased levels of SNAIL1, SNAIL2, and ZEB1, transcriptional repressors of E-cadherin expression. Addition of exogenous arachidonic acid, but not PGE2, reversed the phenotypic changes in cPLA(2)?-silenced cells. These data suggest that cPLA(2)? may play a key role in renal repair after injury through a PGE(2)-independent mechanism.
  • |*Cell Dedifferentiation/drug effects [MESH]
  • |Arachidonic Acid/pharmacology [MESH]
  • |Cadherins/genetics [MESH]
  • |Cell Line [MESH]
  • |Cell Proliferation/drug effects [MESH]
  • |Dinoprostone/metabolism [MESH]
  • |Epithelial Cells/*cytology/drug effects/metabolism [MESH]
  • |Gene Silencing [MESH]
  • |Group IV Phospholipases A2/deficiency/genetics/*metabolism [MESH]
  • |Humans [MESH]
  • |Kidney Tubules/*cytology [MESH]
  • |Phenotype [MESH]


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