ArticleMolecular and cellular biochemistry2004
Defective sarcolemmal phospholipase C signaling in diabetic cardiomyopathy.
Article in Molecular and cellular biochemistry, 2004. 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, 29 citations in OpenAlex.
- Immunomodulatory, Antioxidant, and Potential Anticancer Activity of the Polysaccharides of the FungusMolecules (Basel, Switzerland) · 2024Article
- Emerging Roles of Phospholipase C Beta Isozymes as Potential Biomarkers in Cardiac Disorders.International journal of molecular sciences · 2023Review
- Mechanisms of subcellular remodeling in heart failure due to diabetes.Heart failure reviews · 2014Review
- Endoplasmic reticulum stress and diabetic cardiomyopathy.Experimental diabetes research · 2012Review
- Effects of amino acid supplementation on myocardial cell damage and cardiac function in diabetes.Experimental and clinical cardiology · 2011Article
- Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes.Journal of molecular and cellular cardiology · 2008Review
- Involvement of endoplasmic reticulum stress in myocardial apoptosis of streptozocin-induced diabetic rats.Journal of clinical biochemistry and nutrition · 2007Article
- Upregulation of the alpha1-adrenoceptor-induced phosphoinositide and inotropic response in hypothyroid rat heart.Molecular and cellular biochemistry · 2006Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phospholipase C (PLC) activity is known to influence cardiac function. This study was undertaken to examine the status of PLC beta3 in the cardiac cell plasma membrane (sarcolemma, SL) in an experimental model of chronic diabetes. SL membrane was isolated from diabetic rat hearts at 8 weeks after a single i.v. injection of streptozotocin (65 mg/kg body weight). The total SL PLC was decreased in diabetes and was associated with a decrease in SL PLC beta3 activity, which immunofluorescence in frozen diabetic left ventricular tissue sections revealed to be due to a decrease in PLC beta3 protein abundance. In contrast, the SL abundance of Gqalpha was significantly increased during diabetes. These changes were associated with a loss of contractile function (+/- dP/dt). A 2-week insulin treatment of 6-week diabetic animals partially normalized all of these parameters. These findings suggest a defect in PLC beta3-mediated signaling processes may contribute to the cardiac dysfunction seen during diabetes.
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