Targeted vitamin D receptor expression in juxtaglomerular cells suppresses renin expression independent of parathyroid hormone and calcium

Juan Kong, Guilin Qiao, Zhongyi Zhang, Shu Qian Liu, Yan Chun Li

Research output: Contribution to journalArticle

82 Citations (Scopus)

Abstract

Previously, we showed that vitamin D receptor gene knockout leads to hyperreninemia independent of calcium metabolism; however, the contribution of parathyroid hormone to renin upregulation remained unclear. Here we separated the role of vitamin D and parathyroid hormone in the regulation of renin expression in vivo by generating transgenic mice that overexpressed the human vitamin D receptor in renin-producing cells using the 4.1 kb Ren-1c gene promoter. Targeting of human vitamin D receptor to the juxtaglomerular cells of the mice was confirmed by immunohistochemistry. Renal renin mRNA levels and plasma renin activity were decreased in these transgenic mice by about 50% and 30%, respectively, with no significant change in blood pressure, calcium, or parathyroid hormone levels. Moreover using vitamin D receptor knockout mice, we found that expression of the human receptor in their juxtaglomerular cells reduced renin expression in these mice without affecting calcium or parathyroid hormone status. Our study shows that suppression of renin expression by 1,25-dihydroxyvitamin D in vivo is independent of parathyroid hormone and calcium.

Original languageEnglish (US)
Pages (from-to)1577-1581
Number of pages5
JournalKidney international
Volume74
Issue number12
DOIs
StatePublished - Jan 1 2008

Fingerprint

Calcitriol Receptors
Parathyroid Hormone
Renin
Calcium
Transgenic Mice
Gene Knockout Techniques
Knockout Mice
Vitamin D
Up-Regulation
Immunohistochemistry
Blood Pressure
Kidney
Messenger RNA
Genes

Keywords

  • PTH
  • Renin
  • Transgenic mice
  • VDR
  • Vitamin D

ASJC Scopus subject areas

  • Nephrology

Cite this

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abstract = "Previously, we showed that vitamin D receptor gene knockout leads to hyperreninemia independent of calcium metabolism; however, the contribution of parathyroid hormone to renin upregulation remained unclear. Here we separated the role of vitamin D and parathyroid hormone in the regulation of renin expression in vivo by generating transgenic mice that overexpressed the human vitamin D receptor in renin-producing cells using the 4.1 kb Ren-1c gene promoter. Targeting of human vitamin D receptor to the juxtaglomerular cells of the mice was confirmed by immunohistochemistry. Renal renin mRNA levels and plasma renin activity were decreased in these transgenic mice by about 50{\%} and 30{\%}, respectively, with no significant change in blood pressure, calcium, or parathyroid hormone levels. Moreover using vitamin D receptor knockout mice, we found that expression of the human receptor in their juxtaglomerular cells reduced renin expression in these mice without affecting calcium or parathyroid hormone status. Our study shows that suppression of renin expression by 1,25-dihydroxyvitamin D in vivo is independent of parathyroid hormone and calcium.",
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Targeted vitamin D receptor expression in juxtaglomerular cells suppresses renin expression independent of parathyroid hormone and calcium. / Kong, Juan; Qiao, Guilin; Zhang, Zhongyi; Liu, Shu Qian; Li, Yan Chun.

In: Kidney international, Vol. 74, No. 12, 01.01.2008, p. 1577-1581.

Research output: Contribution to journalArticle

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AU - Kong, Juan

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