Influence of periostin-positive cell-specific Klf5 deletion on aortic thickening in DOCA-salt hypertensive mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-11

AUTHORS

Hirofumi Zempo, Jun-ichi Suzuki, Masahito Ogawa, Ryo Watanabe, Katsuhito Fujiu, Ichiro Manabe, Simon J Conway, Yoshiaki Taniyama, Ryuichi Morishita, Yasunobu Hirata, Mitsuaki Isobe, Ryozo Nagai

ABSTRACT

Chronic hypertension causes vascular remodeling that is associated with an increase in periostin- (postn) positive cells, including fibroblasts and smooth muscle cells. Krüppel-like factor (KLF) 5, a transcription factor, is also observed in vascular remodeling; however, it is unknown what role KLF5 plays in postn-positive cells during vascular remodeling induced by deoxycorticosterone-acetate (DOCA) salt. We used postn-positive cell-specific Klf5-deficient mice (Klf5PostnKO: Klf5flox/flox; PostnCre/-) and wild-type mice (WT: Klf5flox/flox; Postn-/-). We implanted a DOCA pellet and provided drinking water containing 0.9% NaCl for 8 weeks. The DOCA-salt treatment induced hypertension in both genotypes, as observed by increases in systolic blood pressure. In WT animals, DOCA-salt treatment increased the aortic medial area compared with the non-treated controls. Similarly, Tgfb1 was overexpressed in the aortas of the DOCA-salt treated WT mice compared with the controls. Immunofluorescence staining revealed that fibroblast-specific protein 1 (FSP1)+-α smooth muscle actin (αSMA)+ myofibroblasts exist in the medial area of the WT aortas after DOCA-salt intervention. Importantly, these changes were not observed in the Klf5PostnKO animals. In conclusion, the results of this study suggest that the presence of KLF5 in postn-positive cells contributes to the pathogenesis of aortic thickening induced by DOCA-salt hypertension. More... »

PAGES

764

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/hr.2016.65

DOI

http://dx.doi.org/10.1038/hr.2016.65

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001309271

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27334059


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