Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.16 (calcineurin)
 17,112 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to examine the impact of insulin-like growth factor-1 (IGF-1) deficiency on abdominal aortic constriction (AAC)-induced cardiac geometric and functional changes with a focus on microRNA-1, 133a and 208, which are specially expressed in hearts and govern cardiac hypertrophy and stress-dependent cardiac growth. Liver-specific IGF-1-deficient (LID) and C57/BL6 mice were subject to AAC. Echocardiographic and cardiomyocyte function were assessed 4 wks later. Haematoxylin and eosin staining was used to monitor myocardial morphology. Western blot and real-time PCR were used to detect protein and miR expression, respectively. Neonatal rat cardiomyocytes (NRCMs) were transfected with miRs prior to IGF-1 exposure to initiate cell proliferation. Immunohistochemistry and [(3)H] Leucine incorporation were used to detect cell surface area and protein abundance. C57 mice subject to AAC displayed increased ventricular wall thickness, decreased left ventricular end diastolic and end systolic dimensions and elevated cardiomyocyte shortening capacity, all of which were attenuated in LID mice. In addition, IGF-1 deficiency mitigated AAC-induced increase in atrial natriuretic factor, GATA binding protein 4, glucose transporter 4 (GLUT4) and Akt phosphorylation. In contrast, neither AAC treatment nor IGF-1 deficiency affected glycogen synthase kinase 3b, mammalian target of rapamycin, the Glut-4 translocation mediator Akt substrate of 160 kD (AS160) and protein phosphatase. Levels of miR-1 and -133a (but not miR-208) were significantly attenuated by AAC in C57 but not LID mice. Transfection of miR-1 and -133a obliterated IGF-1-induced hypertrophic responses in NRCMs. Our data suggest that IGF-1 deficiency retards AAC-induced cardiac hypertrophic and contractile changes via alleviating down-regulation of miR-1 and miR-133a in response to left ventricular pressure overload.
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PMID:IGF-1 deficiency resists cardiac hypertrophy and myocardial contractile dysfunction: role of microRNA-1 and microRNA-133a. 2141 19

Hypercholesterol diets are the major causes of cardiac hypertrophy and various cardiac disorders. The purpose of this study is to evaluate the effects of garlic oil on cardiac hypertrophy induced by hypercholesterol diets. Golden Syrian hamsters were fed with 2% cholesterol or 2% cholesterol plus 1% garlic oil for 2 months. Heart architecture changes were measured by hematoxylin-eosin staining and the molecular mechanism was determined by western blotting. Garlic oil reduced whole-heart weight to bone weight ratio, and left ventricle weight to bone weight ratio in the cholesterol-fed group. Moreover, the garlic oil group showed significantly reduced interleukin-6, phosphorylated (p)-extracellular signal-regulated kinase-5, p-mitogen-activated protein kinase-5, calcineurin, nuclear transcription factor of nuclear factor of activated T-cells-3 and p-GATA binding protein 4 when compared with the cholesterol group. However, no changes were observed in gp-130, signal transducer and activator of transcription-3, p-P38 and p-Jun N-terminal kinases protein levels in all groups. The results show that garlic oil may be useful in the treatment of hypertrophy-associated cardiovascular diseases.
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PMID:Effects of garlic oil on interleukin-6 mediated cardiac hypertrophy in hypercholesterol-fed hamsters. 2879 59