FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2103181489> ?p ?o ?g. }

• W2103181489 endingPage "1358" @default.
• W2103181489 startingPage "1348" @default.
• W2103181489 abstract "New Findings What is the central question of this study? Cardiac dysfunction in sepsis is associated with apoptosis of cardiomyocytes. Is endoplasmic reticulum (ER) stress induced in lipopolysaccharide (LPS)‐treated cardiomyocytes? Does ER stress‐induced autophagy protect against LPS‐induced apoptosis of cardiomyocytes? What is the mechanism in detail? What is the main finding and its importance? Our results indicate that ER stress is activated and mediates autophagy in LPS‐treated murine atrium‐derived cardiac HL‐1 cells. Protein kinase regulated by RNA‐like ER‐associated kinase (PERK), one arm of ER stress, is involved in protecting against LPS‐induced apoptosis of HL‐1 cells by promotion of autophagy. Apoptosis of cardiomyocytes limits the contractile efficiency of the heart during sepsis. Prosurvival autophagy has been proposed as a novel mechanism to maintain normal heart function. Here, we demonstrated that autophagy was activated in lipopolysaccharide (LPS)‐treated HL‐1 cells, and it counteracted the LPS‐induced apoptosis. We investigated further the mechanism by which LPS triggered autophagy in HL‐1 cells. We discovered that endoplasmic reticulum (ER) stress played an important role in LPS‐triggered autophagy. The ER activated a survival pathway through the ER‐localized transmembrane protein PERK, which was essential for LPS‐induced autophagy. Lipopolysaccharide increased expression of GRP78, phosphorylated PERK and phosphorylated eukaryotic initiation factor 2 α . Similar results were observed after administration of tunicamycin, a well‐known ER stressor. Most importantly, we found that 4‐phenylbutyrate, an inhibitor of ER stress, suppressed LPS‐activated autophagy in the presence of LPS in HL‐1 cells. The same results were observed after small interfering RNA‐mediated silencing of PERK protein. We also noticed that LPS‐induced apoptosis appeared early, at 4 h. Our findings revealed that PERK, one arm of ER stress, facilitated survival of LPS‐treated HL‐1 cells by promoting autophagy, and could serve as a potential therapeutic strategy to alleviate septic myocardial dysfunction." @default.
• W2103181489 created "2016-06-24" @default.
• W2103181489 creator A5003409121 @default.
• W2103181489 creator A5037371879 @default.
• W2103181489 creator A5041057625 @default.
• W2103181489 creator A5052883326 @default.
• W2103181489 creator A5059927836 @default.
• W2103181489 creator A5081920875 @default.
• W2103181489 date "2014-07-14" @default.
• W2103181489 modified "2023-09-30" @default.
• W2103181489 title "Endoplasmic reticulum stress-mediated autophagy protects against lipopolysaccharide-induced apoptosis in HL-1 cardiomyocytes" @default.
• W2103181489 cites W1546139069 @default.
• W2103181489 cites W1906849814 @default.
• W2103181489 cites W1963521777 @default.
• W2103181489 cites W1965323386 @default.
• W2103181489 cites W1965514223 @default.
• W2103181489 cites W1968543843 @default.
• W2103181489 cites W1969072747 @default.
• W2103181489 cites W1969698093 @default.
• W2103181489 cites W1970090817 @default.
• W2103181489 cites W1973472942 @default.
• W2103181489 cites W1976531450 @default.
• W2103181489 cites W1977767269 @default.
• W2103181489 cites W1980942517 @default.
• W2103181489 cites W1982417846 @default.
• W2103181489 cites W1990771260 @default.
• W2103181489 cites W1994823455 @default.
• W2103181489 cites W1996335775 @default.
• W2103181489 cites W1998895168 @default.
• W2103181489 cites W2004547943 @default.
• W2103181489 cites W2007598683 @default.
• W2103181489 cites W2010568558 @default.
• W2103181489 cites W2010611237 @default.
• W2103181489 cites W2019447372 @default.
• W2103181489 cites W2023465240 @default.
• W2103181489 cites W2025665129 @default.
• W2103181489 cites W2036903182 @default.
• W2103181489 cites W2038291983 @default.
• W2103181489 cites W2039975172 @default.
• W2103181489 cites W2040595737 @default.
• W2103181489 cites W2044241702 @default.
• W2103181489 cites W2049789360 @default.
• W2103181489 cites W2054357322 @default.
• W2103181489 cites W2057688774 @default.
• W2103181489 cites W2057764483 @default.
• W2103181489 cites W2060342342 @default.
• W2103181489 cites W2061216487 @default.
• W2103181489 cites W2069917288 @default.
• W2103181489 cites W2070224555 @default.
• W2103181489 cites W2078042237 @default.
• W2103181489 cites W2088971374 @default.
• W2103181489 cites W2101748704 @default.
• W2103181489 cites W2104850613 @default.
• W2103181489 cites W2113425981 @default.
• W2103181489 cites W2118337893 @default.
• W2103181489 cites W2120054003 @default.
• W2103181489 cites W2127916470 @default.
• W2103181489 cites W2132688471 @default.
• W2103181489 cites W2136703555 @default.
• W2103181489 cites W2137288609 @default.
• W2103181489 cites W2137392137 @default.
• W2103181489 cites W2140487984 @default.
• W2103181489 cites W2142931701 @default.
• W2103181489 cites W2156759984 @default.
• W2103181489 cites W2157096314 @default.
• W2103181489 cites W2157101465 @default.
• W2103181489 cites W2157515789 @default.
• W2103181489 cites W2164990391 @default.
• W2103181489 doi "https://doi.org/10.1113/expphysiol.2014.079012" @default.
• W2103181489 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24951501" @default.
• W2103181489 hasPublicationYear "2014" @default.
• W2103181489 type Work @default.
• W2103181489 sameAs 2103181489 @default.
• W2103181489 citedByCount "34" @default.
• W2103181489 countsByYear W21031814892014 @default.
• W2103181489 countsByYear W21031814892015 @default.
• W2103181489 countsByYear W21031814892016 @default.
• W2103181489 countsByYear W21031814892017 @default.
• W2103181489 countsByYear W21031814892018 @default.
• W2103181489 countsByYear W21031814892019 @default.
• W2103181489 countsByYear W21031814892020 @default.
• W2103181489 countsByYear W21031814892021 @default.
• W2103181489 countsByYear W21031814892022 @default.
• W2103181489 countsByYear W21031814892023 @default.
• W2103181489 crossrefType "journal-article" @default.
• W2103181489 hasAuthorship W2103181489A5003409121 @default.
• W2103181489 hasAuthorship W2103181489A5037371879 @default.
• W2103181489 hasAuthorship W2103181489A5041057625 @default.
• W2103181489 hasAuthorship W2103181489A5052883326 @default.
• W2103181489 hasAuthorship W2103181489A5059927836 @default.
• W2103181489 hasAuthorship W2103181489A5081920875 @default.
• W2103181489 hasConcept C134018914 @default.
• W2103181489 hasConcept C139447449 @default.
• W2103181489 hasConcept C158617107 @default.
• W2103181489 hasConcept C184235292 @default.
• W2103181489 hasConcept C185592680 @default.
• W2103181489 hasConcept C190283241 @default.
• W2103181489 hasConcept C203522944 @default.

• next