Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension

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Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension. / Jobs, Alexander; Schmidt, Kjestine; Schmidt, Volker J; Lübkemeier, Indra; van Veen, Toon A B; Kurtz, Armin; Willecke, Klaus; de Wit, Cor.

I: Hypertension (Dallas, Tex. : 1979), Bind 60, Nr. 6, 12.2012, s. 1422-9.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Jobs, A, Schmidt, K, Schmidt, VJ, Lübkemeier, I, van Veen, TAB, Kurtz, A, Willecke, K & de Wit, C 2012, 'Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension', Hypertension (Dallas, Tex. : 1979), bind 60, nr. 6, s. 1422-9. https://doi.org/10.1161/HYPERTENSIONAHA.112.201194

APA

Jobs, A., Schmidt, K., Schmidt, V. J., Lübkemeier, I., van Veen, T. A. B., Kurtz, A., Willecke, K., & de Wit, C. (2012). Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension. Hypertension (Dallas, Tex. : 1979), 60(6), 1422-9. https://doi.org/10.1161/HYPERTENSIONAHA.112.201194

Vancouver

Jobs A, Schmidt K, Schmidt VJ, Lübkemeier I, van Veen TAB, Kurtz A o.a. Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension. Hypertension (Dallas, Tex. : 1979). 2012 dec.;60(6):1422-9. https://doi.org/10.1161/HYPERTENSIONAHA.112.201194

Author

Jobs, Alexander ; Schmidt, Kjestine ; Schmidt, Volker J ; Lübkemeier, Indra ; van Veen, Toon A B ; Kurtz, Armin ; Willecke, Klaus ; de Wit, Cor. / Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension. I: Hypertension (Dallas, Tex. : 1979). 2012 ; Bind 60, Nr. 6. s. 1422-9.

Bibtex

@article{6c8574dba6154b43aa20bcc161a3c709,
title = "Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension",
abstract = "The gap junction channel protein connexin40 (Cx40) is crucial in vascular and renal physiology, because Cx40-deficient mice exhibit impaired conduction of endothelium-dependent dilations and pronounced hypertension. The latter precludes mechanistic insights into the role of endothelial Cx40, because long-lasting hypertension itself may affect conduction and Cx expression. We aimed to identify endothelial Cx40 functions, their dependency on the conductive capability, and to separate these from hypertension-related alterations. We assessed conduction and Cx expression in mice with cell type-specific deletion of Cx40 and in mice expressing a defective Cx40 (Cx40A96S) identified in humans, which forms nonconducting gap junction channels. Confined arteriolar stimulation with acetylcholine or bradykinin elicited local dilations that conducted upstream without attenuation of the amplitude for distances up to 1.2-mm in controls with a floxed Cx40 gene (Cx40(fl/fl)). Conducted responses in hypertensive animals devoid of Cx40 in renin-producing cells were unaltered but remote dilations were reduced in normotensive animals deficient for Cx40 in endothelial cells (Cx40(fl/fl):Tie2-Cre). Surprisingly, Cx37 expression was undetectable by immunostaining in arteriolar endothelium only in Cx40(fl/fl):Tie2-Cre; however, transcriptional activity of Cx37 in the cremaster was comparable with Cx40(fl/fl) controls. Cx40A96S mice were hypertensive with preserved expression of Cx40 and Cx37. Nevertheless, conducted responses were blunted. We conclude that endothelial Cx40 is necessary to support conducted dilations initiated by endothelial agonists and to locate Cx37 into the plasma membrane. These functions are unaltered by long-lasting hypertension. In the presence of a nonconducting Cx40, Cx37 is present but cannot support the conduction highlighting the importance of endothelial Cx40.",
keywords = "Acetylcholine/pharmacology, Animals, Blood Pressure/physiology, Connexins/genetics, Endothelial Cells/drug effects, Endothelium, Vascular/drug effects, Gap Junctions/drug effects, Heart Rate/physiology, Hypertension/genetics, Mice, Mice, Transgenic, Vasodilation/drug effects",
author = "Alexander Jobs and Kjestine Schmidt and Schmidt, {Volker J} and Indra L{\"u}bkemeier and {van Veen}, {Toon A B} and Armin Kurtz and Klaus Willecke and {de Wit}, Cor",
year = "2012",
month = dec,
doi = "10.1161/HYPERTENSIONAHA.112.201194",
language = "English",
volume = "60",
pages = "1422--9",
journal = "Hypertension",
issn = "0194-911X",
publisher = "Lippincott Williams & Wilkins",
number = "6",

}

RIS

TY - JOUR

T1 - Defective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension

AU - Jobs, Alexander

AU - Schmidt, Kjestine

AU - Schmidt, Volker J

AU - Lübkemeier, Indra

AU - van Veen, Toon A B

AU - Kurtz, Armin

AU - Willecke, Klaus

AU - de Wit, Cor

PY - 2012/12

Y1 - 2012/12

N2 - The gap junction channel protein connexin40 (Cx40) is crucial in vascular and renal physiology, because Cx40-deficient mice exhibit impaired conduction of endothelium-dependent dilations and pronounced hypertension. The latter precludes mechanistic insights into the role of endothelial Cx40, because long-lasting hypertension itself may affect conduction and Cx expression. We aimed to identify endothelial Cx40 functions, their dependency on the conductive capability, and to separate these from hypertension-related alterations. We assessed conduction and Cx expression in mice with cell type-specific deletion of Cx40 and in mice expressing a defective Cx40 (Cx40A96S) identified in humans, which forms nonconducting gap junction channels. Confined arteriolar stimulation with acetylcholine or bradykinin elicited local dilations that conducted upstream without attenuation of the amplitude for distances up to 1.2-mm in controls with a floxed Cx40 gene (Cx40(fl/fl)). Conducted responses in hypertensive animals devoid of Cx40 in renin-producing cells were unaltered but remote dilations were reduced in normotensive animals deficient for Cx40 in endothelial cells (Cx40(fl/fl):Tie2-Cre). Surprisingly, Cx37 expression was undetectable by immunostaining in arteriolar endothelium only in Cx40(fl/fl):Tie2-Cre; however, transcriptional activity of Cx37 in the cremaster was comparable with Cx40(fl/fl) controls. Cx40A96S mice were hypertensive with preserved expression of Cx40 and Cx37. Nevertheless, conducted responses were blunted. We conclude that endothelial Cx40 is necessary to support conducted dilations initiated by endothelial agonists and to locate Cx37 into the plasma membrane. These functions are unaltered by long-lasting hypertension. In the presence of a nonconducting Cx40, Cx37 is present but cannot support the conduction highlighting the importance of endothelial Cx40.

AB - The gap junction channel protein connexin40 (Cx40) is crucial in vascular and renal physiology, because Cx40-deficient mice exhibit impaired conduction of endothelium-dependent dilations and pronounced hypertension. The latter precludes mechanistic insights into the role of endothelial Cx40, because long-lasting hypertension itself may affect conduction and Cx expression. We aimed to identify endothelial Cx40 functions, their dependency on the conductive capability, and to separate these from hypertension-related alterations. We assessed conduction and Cx expression in mice with cell type-specific deletion of Cx40 and in mice expressing a defective Cx40 (Cx40A96S) identified in humans, which forms nonconducting gap junction channels. Confined arteriolar stimulation with acetylcholine or bradykinin elicited local dilations that conducted upstream without attenuation of the amplitude for distances up to 1.2-mm in controls with a floxed Cx40 gene (Cx40(fl/fl)). Conducted responses in hypertensive animals devoid of Cx40 in renin-producing cells were unaltered but remote dilations were reduced in normotensive animals deficient for Cx40 in endothelial cells (Cx40(fl/fl):Tie2-Cre). Surprisingly, Cx37 expression was undetectable by immunostaining in arteriolar endothelium only in Cx40(fl/fl):Tie2-Cre; however, transcriptional activity of Cx37 in the cremaster was comparable with Cx40(fl/fl) controls. Cx40A96S mice were hypertensive with preserved expression of Cx40 and Cx37. Nevertheless, conducted responses were blunted. We conclude that endothelial Cx40 is necessary to support conducted dilations initiated by endothelial agonists and to locate Cx37 into the plasma membrane. These functions are unaltered by long-lasting hypertension. In the presence of a nonconducting Cx40, Cx37 is present but cannot support the conduction highlighting the importance of endothelial Cx40.

KW - Acetylcholine/pharmacology

KW - Animals

KW - Blood Pressure/physiology

KW - Connexins/genetics

KW - Endothelial Cells/drug effects

KW - Endothelium, Vascular/drug effects

KW - Gap Junctions/drug effects

KW - Heart Rate/physiology

KW - Hypertension/genetics

KW - Mice

KW - Mice, Transgenic

KW - Vasodilation/drug effects

U2 - 10.1161/HYPERTENSIONAHA.112.201194

DO - 10.1161/HYPERTENSIONAHA.112.201194

M3 - Journal article

C2 - 23090768

VL - 60

SP - 1422

EP - 1429

JO - Hypertension

JF - Hypertension

SN - 0194-911X

IS - 6

ER -

ID: 329568827