Gap junction permeability is diminished  in proliferating vascular smooth muscle cells

Kurjiaka, David T.; Steele, Timothy Doak; Olsen, Mary V.; Burt, Janis M.

doi:10.1152/ajpcell.1998.275.6.c1674

Cited by 33 publications

(29 citation statements)

References 34 publications

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“…9). In view of the importance of Cx43 gap junctions in smooth muscle cell proliferation and migration, as well as in vascular morphogenesis (55,112,124,151,214), the effect of high glucose on Cx43 gapjunction activity may contribute to the development of the diabetes-associated angiopathy. In addition, the permeability properties of the Cx43-derived gap-junction channel were reported to be altered in corporeal vascular smooth muscle cells isolated from streptozotocin-induced diabetic rats (14) (Fig.…”

Section: Diabetesmentioning

confidence: 99%

Gap Junctions in the Control of Vascular Function

Figueroa

Duling

2009

Antioxidants & Redox Signaling

249

265

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Direct intercellular communication via gap junctions is critical in the control and coordination of vascular function. In the cardiovascular system, gap junctions are made up of one or more of four connexin proteins: Cx37, Cx40, Cx43, and Cx45. The expression of more than one gap-junction protein in the vasculature is not redundant. Rather, vascular connexins work in concert, first during the development of the cardiovascular system, and then in integrating smooth muscle and endothelial cell function, and in coordinating cell function along the length of the vessel wall. In addition, connexin-based channels have emerged as an important signaling pathway in the astrocyte-mediated neurovascular coupling. Direct electrical communication between endothelial cells and vascular smooth muscle cells via gap junctions is thought to play a relevant role in the control of vasomotor tone, providing the signaling pathway known as endothelium-derived hyperpolarizing factor (EDHF). Consistent with the importance of gap junctions in the regulation of vasomotor tone and arterial blood pressure, the expression of connexins is altered in diseases associated with vascular complications. In this review, we discuss the participation of connexin-based channels in the control of vascular function in physiologic and pathologic conditions, with a special emphasis on hypertension and diabetes. Antioxid. Redox Signal. 11, 251-266. 251

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Section: Diabetesmentioning

confidence: 99%

Gap Junctions in the Control of Vascular Function

Figueroa

Duling

2009

Antioxidants & Redox Signaling

249

265

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“…In conduit vessels, gap junctions have been implicated in a role in regulating vascular tone (Christ et al, 1996;Chaytor et al, 1998). Junctional communication may also be important in the control of vascular cell proliferation and migration (Larson and Haudenschild, 1988;Pepper et al, 1989;Kurjiaka et al, 1998). In this regard, gap junctions could have important roles in the development of the vasculature and in responses to blood vessel wounding.…”

Section: Introductionmentioning

confidence: 99%

Decreased intercellular dye-transfer and downregulation of non-ablated connexins in aortic endothelium deficient in connexin37 or connexin40

Simon

McWhorter

2003

Journal of Cell Science

127

145

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Vascular endothelial cells are coupled by gap junctions that permit cell-to-cell transfer of small molecules, including signals that may be important for vasomotor responses. Connexin37 (Cx37) and connexin40 (Cx40) are the predominant gap-junction proteins present in mouse endothelium. We examined the effect of eliminating Cx37, Cx40, or both, on interendothelial communication in mouse aorta. Intercellular transfer of biocytin and[2-(4-nitro-2,1,3-benzoxadiazol-7-yl)aminoethyl]trimethylammonium (NBD-TMA)was used to assess gap-junction-mediated coupling. Ablation of Cx40 generally had a greater effect on dye-transfer than ablation of Cx37. The effect of Cx40 ablation on dye-transfer was age dependent. There was a 27-fold reduction in biocytin transfer in embryonic Cx40–/– aortic endothelium, a much larger change than in aortas of 6-7-week-old Cx40–/– animals, which showed a 3.5-fold reduction. By contrast, there was no reduction in biocytin transfer in embryonic Cx37–/– endothelium. Embryonic aortas lacking both Cx37 and Cx40 showed a complete loss of endothelial dye-transfer. Surprisingly,elimination of Cx40 resulted in up to a 17-fold drop in endothelial Cx37 on western blots, whereas deletion of Cx37 reduced endothelial Cx40 up to 4.2-fold. By contrast, in the medial layer, both Cx37 and Cx43 increased∼fourfold in Cx40–/– aortas. Declines in non-ablated endothelial connexins were not mediated by changes in connexin mRNA levels, suggesting a post-transcriptional effect. Our results indicate that Cx37 and Cx40 are the only functional connexins expressed in mouse aortic endothelium and are collectively crucial for endothelial communication. Furthermore, Cx37 and Cx40 are codependent on each other for optimal expression in vascular endothelium.

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“…[1][2][3][4] Gap junctions are formed from combinations of 1 or more of the 4 connexin protein isomers that are known to be expressed in the vasculature: Cx37, 40, 43, and 45, [5][6][7][8][9][10] and there is accumulating evidence indicating that the connexins may play a role in a variety of vascular pathologies including: hypertension, [11][12][13][14] ischemia/reperfusion injury, 15 and atherosclerosis. 16 -22 Moreover, gap junctional communication is reduced in proliferating vascular smooth muscle (VSM) cells, 23 suggesting that the connexins might play a role in the modulation of the vascular response to injury or experimental atherogenesis. 24 Our studies tested the hypothesis that selective deletion of a particular connexin in VSM would modify the response to vascular injury.…”

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confidence: 99%

Smooth Muscle–Targeted Knockout of Connexin43 Enhances Neointimal Formation in Response to Vascular Injury

Liao

Regan

Manabe

et al. 2007

ATVB

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Objective-Vascular disease alters and reduces connexin expression and a reduction in connexin 43 (Cx43) expression diminishes the extent of atherosclerosis observed in a high-cholesterol diet murine model. We hypothesized that connexins might play a role in the smooth muscle cell response to vascular injury. Methods and Results-We therefore studied a line of smooth muscle cell-specific, Cx43 gene knockout mice (SM Cx43 KO) in which the carotid arteries were injured, either by vascular occlusion or by a wire injury. In the SM Cx43 KO mice both types of injury manifested accelerated growth of the neointima and of the adventitia. Isolated vascular smooth muscle cells from the SM Cx43 KO mice grew at a slightly faster rate in culture, and to marginally higher saturation densities than those of control mice, but these changes were not adequate to explain the large changes in the injured vessels. Conclusions-These observations provide direct evidence that smooth muscle Cx43 gap junctions play a multi-faceted role in modulating the in vivo growth response of vascular smooth muscle cells to vascular injury. (Arterioscler Thromb Vasc Biol.

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Gap junction permeability is diminished in proliferating vascular smooth muscle cells

Cited by 33 publications

References 34 publications

Gap Junctions in the Control of Vascular Function

Gap Junctions in the Control of Vascular Function

Decreased intercellular dye-transfer and downregulation of non-ablated connexins in aortic endothelium deficient in connexin37 or connexin40

Smooth Muscle–Targeted Knockout of Connexin43 Enhances Neointimal Formation in Response to Vascular Injury

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