Constant or fluctuating hyperglycemias increases cytomembrane stiffness of human umbilical vein endothelial cells in culture: roles of cytoskeletal rearrangement and nitric oxide synthesis

Chen, Xianxian; Feng, Lin; Jin, Hua

doi:10.1186/1471-2121-14-22

Cited by 24 publications

(17 citation statements)

References 38 publications

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“…These processes exacerbate the oxidative stress [ 33 – 35 ] which damages cells and induces apoptosis [ 36 , 37 ]. Apoptosis may be promoted also by DNA damage [ 11 , 38 ] and irreversible changes in cytoskeletal organization at high glucose concentration [ 39 , 40 ]. IL-6 secreted during the acute phase of inflammation has varied effects on cells in diabetes [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Low-level laser irradiation effect on endothelial cells under conditions of hyperglycemia

et al. 2016

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Diabetes mellitus is considered to be a very serious lifestyle disease leading to cardiovascular complications and impaired wound healing observed in the diabetic foot syndrome. Chronic hyperglycemia is the source of the endothelial activation. The inflammatory process in diabetes is associated with the secretion of inflammatory cytokines by endothelial cells, e.g., tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6). The method of phototherapy using laser beam of low power (LLLT—low-level laser therapy) effectively supports the conventional treatment of diabetic vascular complications such as diabetic foot syndrome. The aim of our study was to evaluate the effect of low-power laser irradiation at two wavelengths (635 and 830 nm) on the secretion of inflammatory factors (TNF-α and IL-6) by the endothelial cell culture—HUVEC line (human umbilical vein endothelial cell)—under conditions of hyperglycemia. It is considered that adverse effects of hyperglycemia on vascular endothelial cells may be corrected by the action of LLLT, especially with the wavelength of 830 nm. It leads to the reduction of TNF-α concentration in the supernatant and enhancement of cell proliferation. Endothelial cells play an important role in the pathogenesis of diabetes; however, a small number of studies evaluate an impact of LLLT on these cells under conditions of hyperglycemia. Further work on this subject is warranted.

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Section: Discussionmentioning

confidence: 99%

Low-level laser irradiation effect on endothelial cells under conditions of hyperglycemia

et al. 2016

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“…Hyperglycemia, particularly the fluctuation of glucose levels, causes a significant oxidative stress, decreasing the expression of endothelial nitric oxide synthase and impairing NO metabolism [ 34 ]. Fluctuating hyperglycemia induces an increased production of collagen.…”

Section: Discussionmentioning

confidence: 99%

High glucose induces and activates Toll-like receptor 4 in endothelial cells of diabetic retinopathy

Wang

Jia

et al. 2015

Diabetol Metab Syndr

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BackgroundHyperglycemia-induced inflammation causes the dysfunction of blood vessels, and Toll-like receptor 4 (TLR4) plays a key role in inflammation-induced angiogenesis. However, the impact of TLR4 on the pathogenesis of diabetic retinopathy (DR) is poorly understood. In this study, we examined the expression of TLR4 in retinal vascular endothelial cells of patients with DR and diabetic mice, and explored the role of TLR4 in mediating inflammatory responses by human microvascular endothelial cells (HMEC-1) under high-glucose condition.MethodsThe expression of TLR4 in retinal vascular endothelial cells of patients with proliferative diabetic retinopathy and diabetic mice induced by streptozotocin was examined using immunofluorescence. HMEC-1 cells were cultured and the expression of TLR4, MyD88 and Interleukin-1β (IL-1β) was examined under high-glucose condition. Endothelial cells with TLR4 silencing and antagonist of TLR4 as well as endothelial cells from TLR4 deficient mice were used to study the effect of activated TLR4 on inflammation induced by high-glucose treatment.ResultsWe observed that TLR4 was detected in CD31-labled human retinal vascular endothelia and its expression was markedly increased in fibrovascular membranes from DR patients and in retinal vascular endothelial cells of diabetic mice. The expression of TLR4, MyD88 and IL-1β was enhanced by high glucose in cultured HMEC-1 and the expression of TLR4 and IL-1β was inhibited by TLR4 siRNA knock-down and TLR4 antagonist. The expression of IL-1β by endothelial cells from TLR4 deficient mice under high glucose condition was decreased.ConclusionsOur results revealed that hyperglycemia induced overexpression and activation of TLR4 in endothelial cells. This effect may lead to inflammatory responses contribute to the pathogenesis of diabetic retinopathy.Electronic supplementary materialThe online version of this article (doi:10.1186/s13098-015-0086-4) contains supplementary material, which is available to authorized users.

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“…Another possible explanation is that variability in glycaemic control is more deleterious to endothelial cells than persistent hyperglycaemia. For example, some previous studies reported that fluctuating or intermittent high glucose increased expression of adhesion molecules ICAM-1, VCAM-1, and E-selectin [ 42 ], augmented apoptosis [ 43 ], and downregulated NO production [ 44 ]. No studies have investigated hyperglycaemia per se on human SV-EC angiogenesis but the failure of intensive glycaemic control to normalise macrovascular complications in T2DM in the medium term (ACCORD, ADVANCE, and VADT clinical trials [ 5 , 6 ]) suggests involvement of other factors.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Phenotype in Human Endothelial Cells of Diabetic Origin: Implications for Saphenous Vein Graft Failure?

Roberts

Gohil

Hudson

et al. 2015

Journal of Diabetes Research

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Type 2 diabetes (T2DM) confers increased risk of endothelial dysfunction, coronary heart disease, and vulnerability to vein graft failure after bypass grafting, despite glycaemic control. This study explored the concept that endothelial cells (EC) cultured from T2DM and nondiabetic (ND) patients are phenotypically and functionally distinct. Cultured human saphenous vein- (SV-) EC were compared between T2DM and ND patients in parallel. Proliferation, migration, and in vitro angiogenesis assays were performed; western blotting was used to quantify phosphorylation of Akt, ERK, and eNOS. The ability of diabetic stimuli (hyperglycaemia, TNF-α, and palmitate) to modulate angiogenic potential of ND-EC was also explored. T2DM-EC displayed reduced migration (~30%) and angiogenesis (~40%) compared with ND-EC and a modest, nonsignificant trend to reduced proliferation. Significant inhibition of Akt and eNOS, but not ERK phosphorylation, was observed in T2DM cells. Hyperglycaemia did not modify ND-EC function, but TNF-α and palmitate significantly reduced angiogenic capacity (by 27% and 43%, resp.), effects mimicked by Akt inhibition. Aberrancies of EC function may help to explain the increased risk of SV graft failure in T2DM patients. This study highlights the importance of other potentially contributing factors in addition to hyperglycaemia that may inflict injury and long-term dysfunction to the homeostatic capacity of the endothelium.

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Constant or fluctuating hyperglycemias increases cytomembrane stiffness of human umbilical vein endothelial cells in culture: roles of cytoskeletal rearrangement and nitric oxide synthesis

Cited by 24 publications

References 38 publications

Low-level laser irradiation effect on endothelial cells under conditions of hyperglycemia

Low-level laser irradiation effect on endothelial cells under conditions of hyperglycemia

High glucose induces and activates Toll-like receptor 4 in endothelial cells of diabetic retinopathy

Aberrant Phenotype in Human Endothelial Cells of Diabetic Origin: Implications for Saphenous Vein Graft Failure?

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