Effect of Curcumin on Proliferation of Human Retinal Endothelial Cells under In Vitro Conditions

Premanand, C.; Rema, M.; Sameer, Mahmood Z.; Sujatha, Mohan; Balasubramanyam, M

doi:10.1167/iovs.05-0580

Cited by 74 publications

(46 citation statements)

References 30 publications

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“…However, the effect of high glucose on the proliferation of HRECs found in these studies has varied. Yuan et al demonstrated that treatment of HRECs with 30 mM glucose for 48 h increased the proliferation of HRECs compared with 5 mM glucose treatment (18), while two other studies indicated that treatment with 30 mM glucose for 24 and 72 h failed to increase the proliferation of HRECs (20,22). Differences in cell lines and culture times have been suggested as a cause of the discrepancy.…”

Section: Discussionmentioning

confidence: 99%

Kaempferol targets estrogen‑related receptor α and suppresses the angiogenesis of human retinal endothelial cells under high glucose conditions

Zhang

2017

Exp Ther Med

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Abstract. Diabetic retinopathy (DR) is the most common complication of diabetes and a major cause of new-onset blindness in the developed world. The present study aimed to examine the effect of kaempferol on high glucose-induced human retinal endothelial cells (HRECs) in vitro. The expression levels of various mRNAs and proteins were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting, respectively. The target of kaempferol was determined using a luciferase reporter assay. In addition, HREC proliferation, migration and cell sprouting were determined using Cell Counting kit-8, wound scratch and tube formation assays, respectively. RT-qPCR and western blotting results showed that treatment with 30 mM glucose for 12, 24 and 48 h increased the expression level of estrogen-related receptor α (ERRα) mRNA and protein.The luciferase reporter assay demonstrated that kaempferol inhibited ERRα activity in HRECs. Compared with 5 mM normal glucose treatment, high (30 mM) glucose significantly promoted the proliferation, migration and tube formation of HRECs, which was antagonized by 10 and 30 µM kaempferol in a dose-dependent manner. Treatment with 30 mM glucose also increased the expression of vascular endothelial growth factor (VEGF) mRNA and protein, and the expression levels of VEGF mRNA and protein were suppressed by kaempferol (10 and 30 µM). Kaempferol (30 µM) treatment also increased the expression levels of thrombospondin 1 (TSP-1) and a disintegrin and metalloproteinase with thrombospondin motifs 1 (ADAMTS-1) mRNA; however, TSP-1 and ADAMTS-1 levels did not differ between high glucose and normal (5 mM) glucose conditions. The results of this study suggest that kaempferol targets ERRα and suppresses the angiogenesis of HRECs under high glucose conditions. Kaempferol may be a potential drug for use in controlling the progression of DR; however, in vivo studies are required to evaluate its efficacy and safety.

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Section: Discussionmentioning

confidence: 99%

Kaempferol targets estrogen‑related receptor α and suppresses the angiogenesis of human retinal endothelial cells under high glucose conditions

Zhang

2017

Exp Ther Med

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“…15 Sameermahmood et al 16 demonstrated that human retinal endothelial cell (HREC) treated with 30 lM of curcumin inhibited SDF-1a-induced cell migration through blockage of Ca 2þ influx and reduction of PI3K/AKT signaling. Premanand et al 17 also indicated 10 lM of curcumin induced the HRECs apoptosis partly by the control of iROS production. Bian et al 18 reported that 20 lM of curcumin effectively reduced glycated human serum albumin-induced IL-8 and MCP-1 secretion in human RPE cells.…”

Section: Discussionmentioning

confidence: 94%

Curcumin Protects Trabecular Meshwork Cells From Oxidative Stress

Lin

2016

Invest. Ophthalmol. Vis. Sci.

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Citation: Lin C, Wu X. Curcumin protects trabecular meshwork cells from oxidative stress. Invest Ophthalmol Vis Sci. 2016;57:4327-4332. DOI:10.1167/iovs.16-19883 PURPOSE. Glaucoma is closely linked with oxidative stress and inflammation, and difficult to treat. Its occurrence frequently is contributed by the failure of the trabecular meshwork (TM). Curcumin is known as an antioxidative and anti-inflammatory substance, possessing the potential to treat glaucoma. METHODS.Using TM cells as the in vitro model system, we investigated the effects of curcumin on oxidative stress-induced markers for TM impairments, including cell death, production of intracellular reactive oxygen species (iROS), induction of proinflammatory proteins, activation of senescence marker, accumulation of carbonylated proteins, and apoptotic cell numbers. RESULTS.Curcumin treatment protected TM cells against oxidative stress-induced cell death. Curcumin treatment at concentrations between 1 and 20 lM reduced the production of iROS in H 2 O 2 -exposed TM cells in a dose-dependent manner. Further studies demonstrated that curcumin treatment (20 lM) significantly inhibited proinflammatory factors, including IL-6, ELAM-1, IL-1a, and IL-8, whereas it decreased activities of senescence marker SA-b-gal, and lowered levels of carbonylated proteins and apoptotic cell numbers.CONCLUSIONS. Curcumin is capable of protecting TM cells against oxidative stress, shedding new light on potential treatment for glaucoma.

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“…Previous studies using HRECs, but not other endothelial cells, have obtained similar results to those of the present study. Premanand et al (19) failed to identify an increase in cell proliferation following high glucose (30 mM) exposure in HRECs, despite observing an increased expression of vascular endothelial growth factor (VEGF). This finding is consistent with the results of the present study indicating cell proliferation under high glucose …”

Section: Discussionmentioning

confidence: 99%

Translocation of protein kinase C δ contributes to the moderately high glucose-, but not hypoxia-induced proliferation in primary cultured human retinal endothelial cells

Liu

et al. 2014

Molecular Medicine Reports

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Diabetic retinopathy is one of the most common complications in patients with diabetes and affects ~75% of them within 15 years of the onset of the disease. Activation of protein kinase C (PKC) is a key feature of diabetes mellitus and may be involved in the pathogenesis of diabetic retinop-athy. The present study aimed to examine the translocation of protein kinase C (PKC) isoforms, which are triggered by high an moderately high glucose levels as well as hypoxic conditions. The underlying cell mechanisms of PKC translocation in primary cultured human retinal endothelial cells (HRECs) were also investigated. The expression levels of PKC isoforms were assessed using western blot analysis. Cell proliferation was determined using the MTT assay and DNA synthesis was assessed by bromodeoxyuridine incorporation. Translocation of PKC isoforms was examined by western blot analysis and immunofluorescence. The expression of PKC α, βI, βII, δ and ε was detected, while PKC ζ was not detected in HRECs. The results of the present study were consistent with the findings of a previous study by our group, reporting that moderately high glucose levels and hypoxia, but not high glucose levels, significantly increased cell proliferation. It was demonstrated that the PKC δ isoform was translocated from the cytosol to the membrane only under moderately high glucose conditions , while PKC α and ε isoforms were translocated from the cytosol to the membrane at high glucose conditions. In addition, PKC βI was translocated under all three conditions. Translocation of PKC βII was comparable among all groups. Furthermore, rottlerin, an inhibitor of PKC δ, blocked cell proliferation, which was induced by moderately high glucose levels, but not by hypoxia. Ro32-0432, an inhibitor of PKC α, βI and ε, did not significantly affect proliferation of HRECs in all treatment groups. In conclusion, the present study suggested that PKC α, βI, βII, δ and ε were expressed in primary cultured HRECs, whereas PKC ζ was not. Cell proliferation induced by moderately high glucose concentrations was associated with translocation of the PKC δ isoform; however, hypoxic conditions did not induce translocation.

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Effect of Curcumin on Proliferation of Human Retinal Endothelial Cells under In Vitro Conditions

Abstract: These data suggest an underlying mechanism whereby curcumin induces the apoptosis in HRECs by the regulation of intracellular ROS generation, VEGF expression and release, and VEGF-mediated PKC-betaII translocation.

Cited by 74 publications

References 30 publications

Kaempferol targets estrogen‑related receptor α and suppresses the angiogenesis of human retinal endothelial cells under high glucose conditions

Kaempferol targets estrogen‑related receptor α and suppresses the angiogenesis of human retinal endothelial cells under high glucose conditions

Curcumin Protects Trabecular Meshwork Cells From Oxidative Stress

Translocation of protein kinase C δ contributes to the moderately high glucose-, but not hypoxia-induced proliferation in primary cultured human retinal endothelial cells

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