Enhanced atherosclerosis in mice with endothelial-specific deletion of connexin40

Chadjichristos, Christos; Wit, Cor de; Roth, Isabelle; Hoepfl, Bernd; Deutsch, Urban; Kempen, Marjan J. A. van; Veen, Toon A.B. van; Kwak, BR

doi:10.1016/j.vph.2006.08.255

Cited by 3 publications

(5 citation statements)

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“…To avoid this deleterious effect, we have made atherosclerosissusceptible ApoE −/− mice with specific Cx40 deletion in ECs. Indeed, these mice are not hypertensive and have a normal heart rate [43]. Preliminary data indicate that the EC-specific deletion of Cx40 induced increased atherosclerotic plaque development compared to control mice [43].…”

Section: Connexin40mentioning

confidence: 89%

“…Cx are differentially expressed in different vascular cell types (see below), and cell-specific Cx deletion may be used to study the implication of the Cx in a particular cell type. For example, the Cre-loxP system under the control of the Tie2 promoter has been used to create mice in which Cx40 or Cx43 has been deleted from the endothelium only [42][43][44].…”

Section: Transgenic Micementioning

confidence: 99%

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Connexins participate in the initiation and progression of atherosclerosis

2009

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Connexins are members of a large family of transmembrane proteins that form hemichannels or gap junctions. These channels allow the exchange of ions and small metabolites between the cytosol and extracellular space or between neighboring cells. Connexins are important in vascular physiology; they support radial and longitudinal cell-to-cell communication in the vascular wall. Four connexins are expressed in the vascular wall: Cx37, Cx40, Cx43, and Cx45. Their expression is not uniform in all blood vessels and varies with vascular territory and species. Significant changes in the expression pattern of vascular connexins have been described during the development of atherosclerosis, a progressive inflammatory disease. In this review, we provide an overview of (1) the tools used to study the involvement of connexins in atherosclerosis, (2) the participation of connexins in atherogenesis, (3) the increasing interest of a polymorphism in the human connexin37 gene as marker of cardiovascular disease, and (4) the possible therapeutic implications of connexins.

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Section: Connexin40mentioning

confidence: 89%

Section: Transgenic Micementioning

confidence: 99%

Connexins participate in the initiation and progression of atherosclerosis

2009

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“…Finally, the Cx-1019T polymorphism appears in a prospective study of death after acute coronary syndrome (68). The association of the polymorphism with CAD or MI has not been found in an Irish study group (52 high-cholesterol diet (18). Altogether, all these results underline the importance of GJ communication for and during leukocytes infiltration in atherosclerosis.…”

Section: Connexins As Cardiovascular Risk Markers and Therapeutic Tarmentioning

confidence: 92%

Intercellular Communication in Atherosclerosis

et al. 2009

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“…Therefore, we have recently established a mouse model with selective deletion of Cx40 in endothelium using the Cre-LoxP system under the control of the Tie2 promotor. Indeed, the endothelial-specific deletion of Cx40 did not affect mean arterial pressure or heart rate in mice (14). Preliminary data also indicates that the surface of atherosclerotic lesions in ApoE -/- mice lacking endothelial Cx40 is larger as compared to control animal fed a high-cholesterol die, suggesting that Cx40 has atheroprotective potential (14).…”

Section: Gap Junctions In Atherosclerosismentioning

confidence: 99%

“…Indeed, the endothelial-specific deletion of Cx40 did not affect mean arterial pressure or heart rate in mice (14). Preliminary data also indicates that the surface of atherosclerotic lesions in ApoE -/- mice lacking endothelial Cx40 is larger as compared to control animal fed a high-cholesterol die, suggesting that Cx40 has atheroprotective potential (14). The loss of Cx40 in the endothelium covering early atherosclerotic lesions might thus further facilitate the development of atherosclerosis.…”

Section: Gap Junctions In Atherosclerosismentioning

confidence: 99%

Connexins in Vascular Physiology and Pathology

Brisset

Isakson

Kwak

2009

Antioxidants & Redox Signaling

166

145

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Cellular interaction in blood vessels is maintained by multiple communication pathways, including gap junctions. They consist of intercellular channels ensuring direct interaction between endothelial and smooth muscle cells and the synchronization of their behavior along the vascular wall. Gap junction channels arise from the docking of two hemichannels or connexons, formed by the assembly of six connexins, and achieve direct cellular communication by allowing the transport of small metabolites, second messengers and ions between two adjacent cells. Physiological variations in connexin expression are observed along the vascular tree, with most common connexins being Cx37, Cx40 and Cx43. Changes in the level of expression of connexins have been correlated to the development of vascular disease, such as hypertension, atherosclerosis or restenosis. Recent studies on connexin-deficient mice highlighted key roles of these communication pathways in the development of these pathologies, and urged the need for targeted pharmacological approaches for their prevention and treatment. The aim of this issue is to review the current knowledge on the implication of gap junctions in vascular function and most common cardiovascular diseases.

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Enhanced atherosclerosis in mice with endothelial-specific deletion of connexin40

Cited by 3 publications

References 0 publications

Connexins participate in the initiation and progression of atherosclerosis

Connexins participate in the initiation and progression of atherosclerosis

Intercellular Communication in Atherosclerosis

Connexins in Vascular Physiology and Pathology

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