ArticleDiabetologia2003
Effects of protein kinase C inhibition and activation on proliferation and apoptosis of bovine retinal pericytes.
Article in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Reciprocal Inhibitions of HRP and REC in a Coculture System.Archives of ophthalmology and optometry · 2025Article
- Sodium-glucose co-transporter 2 inhibitor add-on therapy for metformin delays diabetic retinopathy progression in diabetes patients: a population-based cohort study.Scientific reports · 2023Article
- Dimethyl-2-oxoglutarate improves redox balance and mitochondrial function in muscle pericytes of individuals with diabetes mellitus.Diabetologia · 2020Article
- Evolving mechanisms of vascular smooth muscle contraction highlight key targets in vascular disease.Biochemical pharmacology · 2018Review
- Article
- Activated microglia induce the production of reactive oxygen species and promote apoptosis of co-cultured retinal microvascular pericytes.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017Article
- Protein Kinase C as Regulator of Vascular Smooth Muscle Function and Potential Target in Vascular Disorders.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Presence of retinal pericyte-reactive autoantibodies in diabetic retinopathy patients.Scientific reports · 2016Article
- Vasoregression: A Shared Vascular Pathology Underlying Macrovascular And Microvascular Pathologies?Omics : a journal of integrative biology · 2015Review
- PKCδ impaired vessel formation and angiogenic factor expression in diabetic ischemic limbs.Diabetes · 2013Article
- Cellular and physiological mechanisms underlying blood flow regulation in the retina and choroid in health and disease.Progress in retinal and eye research · 2012Review
- Antibody-mediated retinal pericyte injury: implications for diabetic retinopathy.Investigative ophthalmology & visual science · 2012Article
- Factors associated with changes in endothelin-1 gene expression in patients with diabetic retinopathy in type 2 diabetes mellitus.Molecular vision · 2010Article
- NADPH Oxidase versus Mitochondria-Derived ROS in Glucose-Induced Apoptosis of Pericytes in Early Diabetic Retinopathy.Journal of ophthalmology · 2010Article
- Glucose and TGFbeta2 modulate the viability of cultured human retinal pericytes and their VEGF release.Current eye research · 2008Article
- Cellular signaling and potential new treatment targets in diabetic retinopathy.Experimental diabetes research · 2007Review
- Protein kinase C inhibition and diabetic retinopathy: a shot in the dark at translational research.The British journal of ophthalmology · 2004Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisDrop-out of capillary pericytes occurs early and selectively in diabetic retinopathy. High glucose concentrations decrease replication and increase apoptosis of cultured pericytes. Since glucose activates protein kinase C, we investigated the effects of modulating this intracellular mediator on replication, cell cycle and apoptosis of cultured bovine retinal pericytes.
methodsPericytes cultured in 5.6 or 28 mmol/l glucose were exposed to a protein kinase C activator (phorbol 12-myristate 13-acetate) and/or a selective inhibitor of its beta2 isoform (LY379196). Cells were counted after 7 days. Proliferation by the tetrazolium to formazan assay and DNA synthesis by 5-bromo-2'-deoxyuridine incorporation were measured at day 4. Cell cycle by flow cytometry and apoptosis by ELISA were assessed at day 2.
resultsHigh glucose reduced pericyte replication and increased apoptosis. Protein kinase C activation increased proliferation, while inhibition of its beta2 isoform decreased it. Cell cycle was accelerated by protein kinase C activation and delayed by inhibition. Apoptosis was enhanced by protein kinase C inhibition and reduced by activation. CONCLUSIONS/
interpretationProtein kinase C inhibition amplifies the anti-proliferative and pro-apoptotic effects of high glucose on cultured pericytes, whereas stimulation reduces apoptosis and promotes proliferation both in physiological glucose and high glucose. Protein kinase C inhibition, proposed for the treatment of diabetic macular edema and proliferative retinopathy, might accelerate pericyte dropout in earlier stages when these cells are still present in retinal capillaries.
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