Effects of high glucose plus high insulin on proliferation and apoptosis of mouse endothelial progenitor cells

Zhang, W; Wang, X; Jin, Hongyue; Ran, Qian; Zhang, G; Chen, SF; Hu, Renming

doi:10.1007/s00011-008-8125-3

Cited by 12 publications

(13 citation statements)

References 19 publications

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“…6, A and B), which is regulated by intracellular ATP. Recently, there is increasing evidence that proliferation and invasion of EPCs are controlled by the increase of extracellular glucose level (5,44,52). Finally, we evaluated the expression of hERG1, known as Kv11.1, which can pass inwardly rectifying currents.…”

Section: Discussionmentioning

confidence: 99%

Endothelial progenitor cells functionally express inward rectifier potassium channels

Jang

Park

Hur

et al. 2011

American Journal of Physiology-Cell Physiology

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Since the first isolation of endothelial progenitor cells (EPCs) from human peripheral blood in 1997, many researchers have conducted studies to understand the characteristics and therapeutic effects of EPCs in vascular disease models. Nevertheless, the electrophysiological properties of EPCs have yet to be clearly elucidated. The inward rectifier potassium channel (Kir) performs a major role in controlling the membrane potential and cellular events. Here, via the whole cell patch-clamp technique, we found inwardly rectifying currents in EPCs and that these currents were inhibited by Ba(2+) (100 μM) and Cs(+) (1 mM), known as Kir blockers, in a dose-dependent manner (Ba(2+), 91.2 ± 1.4% at -140 mV and Cs(+), 76.1 ± 6.9% at -140 mV, respectively). Next, using DiBAC(3), a fluorescence indicator of membrane potential, we verified that Ba(2+) induced an increase of fluorescence in EPCs (10 μM, 123 ± 2.8%), implying the depolarization of EPCs. At the mRNA and protein levels, we confirmed the existence of several Kir subtypes, including Kir2.x, 3.x, 4.x, and 6.x. In a functional experiment, we observed that, in the presence of Ba(2+), the number of tubes on Matrigel formed by EPCs was dose-dependently reduced (10 μM, 62.3 ± 6.5%). In addition, the proliferation of EPCs was increased in a dose-dependent fashion (10 μM, 157.9 ± 17.4%), and specific inhibition of Kir2.1 by small interfering RNA also increased the proliferation of EPCs (116.2 ± 2.5%). Our results demonstrate that EPCs express several types of Kir which may modulate the endothelial function and proliferation of EPCs.

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Section: Discussionmentioning

confidence: 99%

Endothelial progenitor cells functionally express inward rectifier potassium channels

Jang

Park

Hur

et al. 2011

American Journal of Physiology-Cell Physiology

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“…These effects were found to be mediated by the action of the p38 MAPK pathway [55] and the Akt/p53/p21 pathway [56]. Furthermore, high glucose conditions were found to decrease EPC proliferation, by downregulation of cell cycle-regulating genes cyclin E, cyclin dependent kinase 2 (CDK2) and proliferating cell nuclear antigen (PCNA) leading to cell cycle arrest, and to upregulate caspase-3 expression, inducing EPC apoptosis [57]. This apoptotis-prone state of EPCs was additionally confirmed in a clinical study comparing diabetic with non-diabetic arterial disease patients [58].…”

Section: Diabetesmentioning

confidence: 93%

Current perspective of pathophysiological and interventional effects on endothelial progenitor cell biology: Focus on Pi3K/AKT/eNOS pathway

Everaert¹,

Craenenbroeck²,

Hoymans³

et al. 2010

International Journal of Cardiology

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“…Zhang et al showed high glucose induced apoptosis and growth arrest of mouse EPCs but high insulin concentration failed to reverse this effects [107]. Moreover, in another study high insulin dosage induced a rapid and powerful differentiation of EPCs into endothelial cells, which, however, showed reduced proliferation and low survival [108].…”

Section: Epcs and Insulinmentioning

confidence: 98%

Pharmacologic Targeting of Endothelial Progenitor Cells

Albiero¹,

Menegazzo²,

Avogaro³

et al. 2010

CHDDT

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The endothelium entered the field of regenerative medicine with the discovery of endothelial progenitor cells (EPCs). These cells participate in endothelial homeostasis and are actively involved in physiological and pathological neovascularization. Despite the unresolved discussion about the very phenotype of these cells, great efforts have been devoted to study the role of EPCs in cardiovascular diseases. EPCs are very rare in peripheral circulation and are further reduced in association with cardiovascular diseases. Therefore, finding therapies to improve EPCs could unleash the way to promising cell-based therapies. Ex-vivo expansion of EPCs is a critical step to augment EPCs number, but it still needs several improvements. An alternative strategy to partially overcome these limitations is to target EPCs with available drugs. In this review we will discuss how disparate pharmacological compounds have been used to improve EPCs number and functions.

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Effects of high glucose plus high insulin on proliferation and apoptosis of mouse endothelial progenitor cells

Abstract: The result indicated that GI-induced apoptosis and growth inhibition might be one of mechanisms of EPC reduction and dysfunction in diabetes.

Cited by 12 publications

References 19 publications

Endothelial progenitor cells functionally express inward rectifier potassium channels

Endothelial progenitor cells functionally express inward rectifier potassium channels

Current perspective of pathophysiological and interventional effects on endothelial progenitor cell biology: Focus on Pi3K/AKT/eNOS pathway

Pharmacologic Targeting of Endothelial Progenitor Cells

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