About: Dual roles of calpain in facilitating Coxsackievirus B3 replication and prompting inflammation in acute myocarditis

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About: Dual roles of calpain in facilitating Coxsackievirus B3 replication and prompting inflammation in acute myocarditis Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Dual roles of calpain in facilitating Coxsackievirus B3 replication and prompting inflammation in acute myocarditis
Creator	Yu, Ying Chen, Ruizhen Ge, Junbo Li, Minghui Su, Yangang Wang, Xinggang Yu, Yong Zou, Yunzeng
Source	Elsevier; Medline; PMC
abstract	Abstract Background Viral myocarditis (VMC) treatment has long been lacking of effective methods. Our former studies indicated roles of calpain in VMC pathogenesis. This study aimed at verifying the potential of calpain in Coxsackievirus B3 (CVB3)-induced myocarditis treatment. Methods A transgenic mouse overexpressing the endogenous calpain inhibitor, calpastatin, was introduced in the study. VMC mouse model was established via intraperitoneal injection of CVB3 in transgenic and wild mouse respectively. Myocardial injury was assayed histologically (HE staining and pathology grading) and serologically (myocardial damage markers of CK-MB and cTnI). CVB3 replication was observed in vivo and in vitro via the capsid protein VP1 detection or virus titration. Inflammation/fibrotic factors of MPO, perforin, IFNγ, IL17, Smad3 and MMP2 were evaluated using western blot or immunohistology stain. Role of calpain in regulating fibroblast migration was studied in scratch assays. Results Calpastatin overexpression ameliorated myocardial injury induced by CVB3 infection significantly in transgenic mouse indicated by reduced peripheral CK-MB and cTnI levels and improved histology injury. Comparing with CVB3-infected wild type mouse, the transgenic mouse heart tissue carried lower virus load. The inflammation factors of MPO, perforin, IFNγ and IL17 were down-regulated accompanied with fibrotic agents of Smad3 and MMP2 inhibition. And calpain participated in the migration of fibroblasts in vitro, which further proves its role in regulating fibrosis. Conclusion Calpain plays dual roles of facilitating CVB3 replication and inflammation promotion. Calpain inhibition in CVB3-induced myocarditis showed significant treatment effect. Calpain might be a novel target for VMC treatment in clinical practices.
has issue date	2016-10-15(xsd:dateTime)
bibo:doi	10.1016/j.ijcard.2016.07.121
bibo:pmid	27472894
has license	els-covid
sha1sum (hex)	311d140154026feab3f47bedda187565a9b1641f
schema:url	https://doi.org/10.1016/j.ijcard.2016.07.121
resource representing a document's title	Dual roles of calpain in facilitating Coxsackievirus B3 replication and prompting inflammation in acute myocarditis
has PubMed Central identifier	PMC7114300
has PubMed identifier	27472894
schema:publication	International Journal of Cardiology
resource representing a document's body	covid:311d140154026feab3f47bedda187565a9b1641f#body_text
is schema:about of	named entity 'DUAL' named entity 'facilitating' named entity 'VMC' named entity 'stain' named entity 'myocarditis' named entity 'fibrotic' named entity 'capsid' named entity 'MMP2' named entity 'transgenic' named entity 'factors' named entity 'injury' named entity 'IFNγ' named entity 'inflammation' named entity 'PROMOTION' named entity 'PERFORIN' named entity 'STAIN' named entity 'MMP2' named entity 'EFFECTIVE' named entity 'ENDOGENOUS' named entity 'IMPROVED' named entity 'DOWN-REGULATED' named entity 'VERIFYING' named entity 'DUAL' named entity 'CALPAIN' named entity 'COMPARING' named entity 'PLAYS' named entity 'MOUSE MODEL' named entity 'FIBROTIC' named entity 'EVALUATED' named entity 'INFECTION' named entity 'LACKING' named entity 'DAMAGE' named entity 'PATHOGENESIS' named entity 'TITRATION' named entity 'INJURY' named entity 'COXSACKIEVIRUS B3' named entity 'TRANSGENIC MOUSE' named entity 'CALPASTATIN' named entity 'RESULTS' named entity 'METHODS' named entity 'BACKGROUND' named entity 'SMAD3' named entity 'ROLES' named entity 'INFLAMMATION' named entity 'VIRUS LOAD' named entity 'PROTEIN ' named entity 'ITS' named entity 'INDICATED' named entity 'POTENTIAL' named entity 'LONG' named entity 'FACILITATING' named entity 'CLINICAL' named entity 'LOWER' named entity 'ROLE' named entity 'DETECTION' named entity 'MARKERS' named entity 'IL17' named entity 'INHIBITION' named entity 'REGULATING' named entity 'SIGNIFICANT' named entity 'REPLICATION' named entity 'CALPAIN' named entity 'HISTOLOGICALLY' named entity 'HISTOLOGY' named entity 'CALPAIN INHIBITOR' named entity 'INTRODUCED' named entity 'IN VIVO' named entity 'WILD' named entity 'PRACTICES' named entity 'MOUSE HEART' named entity 'PERIPHERAL' named entity 'MIGRATION' named entity 'HEART TISSUE' named entity 'REPLICATION'

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