scholarly journals Distribution of Gap Junction Protein Connexin 37 in Smooth Muscle Cells of the Rat Trachea and Pulmonary Artery.

1999 ◽  
Vol 62 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Kyoko NAKAMURA ◽  
Tetsuichiro INAI ◽  
Keiichiro NAKAMURA ◽  
Yosaburo SHIBATA
2011 ◽  
Vol 300 (3) ◽  
pp. F743-F748 ◽  
Author(s):  
Birguel Kurt ◽  
Lisa Kurtz ◽  
Maria L. Sequeira-Lopez ◽  
R. Ariel Gomez ◽  
Klaus Willecke ◽  
...  

Gap junctional coupling of renin-producing cells is of major functional importance for the control of renin synthesis and release. This study was designed to determine the relevance of the vascular gap junction protein connexin 45 (Cx45) for the control of renin expression and secretion. By crossbreeding mice which drive Cre recombinase under the control of the endogenous renin promoter with mice harboring floxed Cx45 gene alleles, we generated viable mice with a deletion of Cx45 in the renin cell lineage. These mice were normotensive, and renin cells in their kidneys were normal with regard to localization and number. Sodium deficiency induced typical recruitment of renin-producing cells along afferent arterioles, whereas sodium overload resulted in a decrease in the number of cells expressing renin. Regulation of renin secretion by perfusion pressure, catecholamines, and angiotensin II from isolated kidneys of mice with renin cell-specific deletion of Cx45 was normal. Analyzing Cx45 promoter activity in cells of the preglomerular arteriolar tree by using mice driving the reporter gene LacZ under the control of the Cx45 promoter revealed strong staining in smooth muscle cells of the media, whereas renin-expressing cells were almost devoid of LacZ staining. Conversely, renin-producing cells, but not vascular smooth muscle cells expressed the gap junction protein Cx40. These findings suggest that Cx45 plays no major functional role in renin-producing cells, probably because the expression of Cx45 is downregulated in these cells. Since renin-producing cells in the adult kidney can reversibly transform into vascular smooth muscle cells and vice versa, our findings on connexin expression indicate that these phenotype switches are paralleled by characteristic reciprocal changes in the transcriptional activity of Cx40 and Cx45 genes.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Sandrine Morel ◽  
Esther Sutter ◽  
Isabelle Roth ◽  
Bernard Foglia ◽  
Urban Deutsch ◽  
...  

Decreasing the expression of the gap junction protein connexin43 (Cx43) in mice provides beneficial effects on both the progression and composition of the atherosclerotic lesions. During atherosclerotic lesion development, Cx43 expression is temporarily up-regulated in intimal smooth muscle cells, induced in macrophages close to the lipid core and triggered in a subset of endothelial cells covering the shoulder of atherosclerotic lesions. The purpose of this study was to examine the role of endothelial Cx43 in the development of atherosclerosis in vivo. For this purpose, we have used the Cre-loxP system to create an atherosclerosis-susceptible mouse line in which Cx43 is deleted from the endothelium only. The natural progression of atherosclerosis and the composition of the atherosclerotic lesions were studied in 18 month-old male TIE2Cre+ Cx43fl/fl ApoE−/− mice and TIE2Cre- Cx43fl/fl ApoE−/− littermate controls. Body weights were not different between both groups. Interestingly, the progression of atherosclerosis (measured as % of surface stained with Sudan IV) was significantly reduced in the thoracic-abdominal aorta of TIE2Cre+ Cx43fl/fl ApoE−/− mice (21.53±7.14%; N=4) compared with TIE2Cre- Cx43/fl/fl ApoE−/− controls (46.84±11.60%, N=6, P<0.05). In addition, advanced atheroma in TIE2Cre+ Cx43fl/fl ApoE−/− mice contained less lipids and showed decreased calcium deposition compared with lesions in TIE2Cre- Cx43fl/fl ApoE−/− controls. Thus, endothelial-specific deletion of Cx43 in mice provides beneficial effects on both the natural progression and composition of the atherosclerotic lesions. Future studies are aimed at obtaining insight into the participation of Cx43 in macrophages and smooth muscle cells in atherosclerosis.


2003 ◽  
Vol 2 (1) ◽  
pp. 123
Author(s):  
B TANTINI ◽  
M FATTORI ◽  
E FIUMANA ◽  
A MANES ◽  
N GALIE ◽  
...  

CHEST Journal ◽  
1998 ◽  
Vol 114 (1) ◽  
pp. 29S-30S ◽  
Author(s):  
Edward C. Dempsey ◽  
Mita Das ◽  
Maria G. Frid ◽  
Yongjian Xu ◽  
Kurt R. Stenmark

CHEST Journal ◽  
2005 ◽  
Vol 128 (6) ◽  
pp. 582S-583S
Author(s):  
Vijaya Karoor ◽  
Sandra J. Walchak ◽  
York E. Miller ◽  
Edward C. Dempsey

2006 ◽  
Vol 44 (5) ◽  
pp. 275-282 ◽  
Author(s):  
Yan-Ping Dai ◽  
Shaner Bongalon ◽  
Honglin Tian ◽  
Samuel D. Parks ◽  
Violeta N. Mutafova-Yambolieva ◽  
...  

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