A mouse renin distal enhancer is essential for blood pressure homeostasis in BAC-rescued renin-null mutant mice

Keiji Tanimoto, Sumiyo Kanafusa, Aki Ushiki, Hitomi Matsuzaki, Junji Ishida, Fumihiro Sugiyama, Akiyoshi Fukamizu

研究成果: Contribution to journalArticle査読

4 被引用数 (Scopus)

抄録

Renin is predominantly expressed in juxtaglomerular cells in the kidney and regulates blood pressure homeostasis. To examine possible in vivo functions of a mouse distal enhancer (mdE), we generated transgenic mice (TgM) carrying either wild-type or mdE-deficient renin BACs (bacterial artificial chromosome), integrated at the identical chromosomal site. In the kidneys of the TgM, the mdE contributed 80% to basal renin promoter activity. To test for possible physiological roles for the mdE, renin BAC transgenes were used to rescue the hypotensive renin-null mice. Interestingly, renal renin expression in the TgBAC:renin-null compound mice was indistinguishable between the wild-type and mutant BAC carriers. Surprisingly, however, the plasma renin activity and angiotensin I concentration in the mdE compound mutant mice were significantly lower than the same parameters in the control mice, and the mutants were consistently hypotensive, demonstrating that blood pressure homeostasis is regulated through transcriptional cis elements controlling renin activity.

本文言語英語
ページ(範囲)401-409
ページ数9
ジャーナルJournal of Receptors and Signal Transduction
34
5
DOI
出版ステータス出版済み - 7 21 2014
外部発表はい

All Science Journal Classification (ASJC) codes

  • 生化学
  • 分子生物学
  • 細胞生物学

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