ArticleDiabetes2009
Selective inhibition of protein kinase C beta(2) attenuates inducible nitric oxide synthase-mediated cardiovascular abnormalities in streptozotocin-induced diabetic rats.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 49 citations in OpenAlex.
- Endothelial Dysfunction and Cardiovascular Disease: Hyperbaric Oxygen Therapy as an Emerging Therapeutic Modality?Journal of cardiovascular development and disease · 2024Review
- Signature precursor and mature microRNAs in cervical ripening during gestational diabetes mellitus lead to pre-term labor and other impediments in future.Journal of diabetes and metabolic disorders · 2023Review
- PKCβ/NF-κB pathway in diabetic atrial remodeling.Journal of physiology and biochemistry · 2020Article
- Curcumin, Alone or in Combination with Aminoguanidine, Increases Antioxidant Defenses and Glycation Product Detoxification in Streptozotocin-Diabetic Rats: A Therapeutic Strategy to Mitigate Glycoxidative Stress.Oxidative medicine and cellular longevity · 2020Article
- Endotoxin-induced cerebral pathophysiology: differences between fetus and newborn.Physiological reports · 2019Article
- Early Effects of Hyperbaric Oxygen on Inducible Nitric Oxide Synthase Activity/Expression in Lymphocytes of Type 1 Diabetes Patients: A Prospective Pilot Study.International journal of endocrinology · 2019Article
- Propofol induces excessive vasodilation of aortic rings by inhibiting protein kinase Cβ2 and θ in spontaneously hypertensive rats.British journal of pharmacology · 2017Article
- Protein Kinase C β: a New Target Therapy to Prevent the Long-Term Atypical Antipsychotic-Induced Weight Gain.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- RhoA/rock signaling mediates peroxynitrite-induced functional impairment of Rat coronary vessels.BMC cardiovascular disorders · 2016Article
- The Protective Effect of Antioxidants Consumption on Diabetes and Vascular Complications.Diseases (Basel, Switzerland) · 2016Review
- Uncoupling of Vascular Endothelial Growth Factor (VEGF) and Inducible Nitric Oxide Synthase (iNOS) in Gingival Tissue of Type 2 Diabetic Patients.Inflammation · 2016Article
- Low molecular weight fucoidan alleviates cardiac dysfunction in diabetic Goto-Kakizaki rats by reducing oxidative stress and cardiomyocyte apoptosis.Journal of diabetes research · 2014Article
- Article
- Acute Rho-kinase inhibition improves coronary dysfunction in vivo, in the early diabetic microcirculation.Cardiovascular diabetology · 2013Article
- Article
- Diabetes-induced increased oxidative stress in cardiomyocytes is sustained by a positive feedback loop involving Rho kinase and PKCβ2.American journal of physiology. Heart and circulatory physiology · 2012Article
- Disorder gene expression of extracellular matrix and adhesion molecules in saphenous vein conduits of diabetic patients.Interactive cardiovascular and thoracic surgery · 2012Article
- Specific PKC isoforms regulate LPS-stimulated iNOS induction in murine microglial cells.Journal of neuroinflammation · 2011Article
- Effect of lignin-derived lignophenols on vascular oxidative stress and inflammation in streptozotocin-induced diabetic rats.Molecular and cellular biochemistry · 2011Article
- Regulation of Inducible Nitric Oxide Synthase (iNOS) and its Potential Role in Insulin Resistance, Diabetes and Heart Failure.The open cardiovascular medicine journal · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveImpaired cardiovascular function in diabetes is partially attributed to pathological overexpression of inducible nitric oxide synthase (iNOS) in cardiovascular tissues. We examined whether the hyperglycemia-induced increased expression of iNOS is protein kinase C-beta(2) (PKCbeta(2)) dependent and whether selective inhibition of PKCbeta reduces iNOS expression and corrects abnormal hemodynamic function in streptozotocin (STZ)-induced diabetic rats. RESEARCH DESIGN AND
methodsCardiomyocytes and aortic vascular smooth muscle cells (VSMC) from nondiabetic rats were cultured in low (5.5 mmol/l) or high (25 mmol/l) glucose or mannitol (19.5 mmol/l mannitol + 5.5 mmol/l glucose) conditions in the presence of a selective PKCbeta inhibitor, LY333531 (20 nmol/l). Further, the in vivo effects of PKCbeta inhibition on iNOS-mediated cardiovascular abnormalities were tested in STZ-induced diabetic rats.
resultsExposure of cardiomyocytes to high glucose activated PKCbeta(2) and increased iNOS expression that was prevented by LY333531. Similarly, treatment of VSMC with LY333531 prevented high glucose-induced activation of nuclear factor kappaB, extracellular signal-related kinase, and iNOS overexpression. Suppression of PKCbeta(2) expression by small interference RNA decreased high-glucose-induced nuclear factor kappaB and extracellular signal-related kinase activation and iNOS expression in VSMC. Administration of LY333531 (1 mg/kg/day) decreased iNOS expression and formation of peroxynitrite in the heart and superior mesenteric arteries and corrected the cardiovascular abnormalities in STZ-induced diabetic rats, an action that was also observed with a selective iNOS inhibitor, L-NIL.
conclusionsCollectively, these results suggest that inhibition of PKCbeta(2) may be a useful approach for correcting abnormal hemodynamics in diabetes by preventing iNOS mediated nitrosative stress.
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