About: Arg(972) Insulin receptor substrate-1 is associated with decreased serum angiotensin-converting enzyme 2 levels in acute myocardial infarction patients: in vivo and in vitro evidence

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About: Arg(972) Insulin receptor substrate-1 is associated with decreased serum angiotensin-converting enzyme 2 levels in acute myocardial infarction patients: in vivo and in vitro evidence Goto Sponge NotDistinct Permalink

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Arg(972) Insulin receptor substrate-1 is associated with decreased serum angiotensin-converting enzyme 2 levels in acute myocardial infarction patients: in vivo and in vitro evidence
Creator	Liu, Wei Hu, Jianguo Hu, Wen Yu, Fenglei Zhou, Xinmin
Source	Medline; PMC
abstract	BACKGROUND: Activation of the renin-angiotensin system (RAS) plays a critical role in the pathophysiology of myocardial infarction (MI) and the development of heart failure. Both angiotensin-converting enzyme 2 (ACE2) and insulin/insulin receptor substrate-1 (IRS-1) show cardioprotective effects after acute MI. The Arg(972) IRS-1 polymorphism is associated with diminished activity of insulin. In the present study, we explored the association among Arg(972) IRS-1, acute MI, and serum levels of ACE2. METHODS: A total of 711 subjects, including 351 subjects with first-time acute MI and 360 subjects without a history of MI were genotyped for Arg(972) IRS-1 polymorphism. Serum levels of ACE2 and MI severity scores were determined. Primary human cardiomyocytes with overexpression of wild type IRS-1 or Arg(972) IRS-1 or knockdown of endogenous IRS-1 were exposed to normoxia and hypoxia, and the expression levels of ACE2 were determined. RESULTS: The serum ACE2 level was significantly increased in acute MI patients compared with that of non-MI controls. Compared with wild type IRS-1 carriers, Arg(972) IRS-1 carriers exhibited decreased serum ACE2 levels and increased MI severity scores after MI. Our in vitro data demonstrate that impairment of insulin/IRS-1/PI3K signaling by overexpression of Arg(972)-IRS-1, knockdown of endogenous IRS-1, or PI3K inhibitor can abolish hypoxia-induced IRS-1-associated PI3K activity and ACE2 expression in human cardiomyocytes, which suggests a causal relationship between Arg(972)-IRS-1 and decreased serum ACE2 levels in acute MI patients. Our in vitro data also indicate that insulin/IRS-1/PI3K signaling is required for ACE2 expression in cardiomyocytes, and that hypoxia can enhance the induction effect of insulin/IRS-1/PI3K signaling on ACE2 expression in cardiomyocytes. CONCLUSIONS: This study provides the first evidence of crosstalk between insulin/IRS-1/PI3K signaling and RAS after acute MI, thereby adding fresh insights into the pathophysiology and treatment of acute MI.
has issue date	2013-10-17(xsd:dateTime)
bibo:doi	10.1186/1475-2840-12-151
bibo:pmid	24134599
has license	cc-by
sha1sum (hex)	84aa85f8690419badcdb6d6777763e6fc3235af1
schema:url	https://doi.org/10.1186/1475-2840-12-151
resource representing a document's title	Arg(972) Insulin receptor substrate-1 is associated with decreased serum angiotensin-converting enzyme 2 levels in acute myocardial infarction patients: in vivo and in vitro evidence
has PubMed Central identifier	PMC4015180
has PubMed identifier	24134599
schema:publication	Cardiovasc Diabetol
resource representing a document's body	covid:84aa85f8690419badcdb6d6777763e6fc3235af1#body_text
is schema:about of	named entity 'INSULIN RECEPTOR SUBSTRATE-1' named entity 'IN VIVO' named entity 'cardiomyocytes' named entity 'acute' named entity 'signaling' named entity 'total' named entity 'fresh' named entity 'adding' named entity 'subjects' named entity 'critical role' named entity 'Arg' named entity 'EVIDENCE' named entity 'ANGIOTENSIN-CONVERTING ENZYME 2' named entity 'WILD TYPE' named entity 'CARDIOMYOCYTES' named entity 'ACTIVATION' named entity 'EFFECTS' named entity 'DIMINISHED' named entity 'RESULTS' named entity 'EVIDENCE OF' named entity 'LEVELS' named entity 'ENHANCE' named entity 'EFFECT' named entity 'RAS' named entity 'IN VITRO' named entity 'CARDIOPROTECTIVE' named entity 'ACUTE MI' named entity 'ANGIOTENSIN-CONVERTING ENZYME 2' named entity 'COMPARED' named entity 'SERUM' named entity 'RELATIONSHIP' named entity 'CONCLUSIONS' named entity 'PLAYS' named entity 'METHODS' named entity 'PI3K' named entity 'INSULIN' named entity 'INSIGHTS' named entity 'RENIN-ANGIOTENSIN SYSTEM' named entity 'ENDOGENOUS' named entity 'INCLUDING' named entity '360' named entity 'NON-' named entity 'TREATMENT' named entity 'SUBSTRATE' named entity 'REQUIRED' named entity 'ASSOCIATION' named entity 'SEVERITY' named entity 'MYOCARDIAL INFARCTION' named entity 'DEVELOPMENT' named entity 'INCREASED' named entity 'PATIENTS' named entity 'LEVEL' named entity 'SCORES' covid:arg/84aa85f8690419badcdb6d6777763e6fc3235af1 named entity 'PI3K INHIBITOR' named entity '2 LEVELS' named entity 'DECREASED' named entity 'ASSOCIATED WITH' named entity 'IN VITRO' named entity 'PATIENTS' named entity 'ARG' named entity 'STUDY' named entity 'OVEREXPRESSION' named entity 'ACE2' named entity 'HEART FAILURE' named entity 'ROLE' named entity 'FRESH' named entity 'PRESENT' named entity 'HUMAN' named entity 'ADDING' named entity 'EXPOSED TO' named entity 'INDUCTION' named entity 'CRITICAL' named entity 'TOTAL' named entity 'SERUM' named entity 'ACUTE MYOCARDIAL INFARCTION' named entity 'HISTORY OF'

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