RGD Reference Report - Effect of silencing VDR gene in kidney on renal epithelial calcium transporter proteins and urinary calcium excretion in genetic hypercalciuric stone-forming rats.

General

Effect of silencing VDR gene in kidney on renal epithelial calcium transporter proteins and urinary calcium excretion in genetic hypercalciuric stone-forming rats.
Authors:	Xi, QL Wang, SG Ye, ZQ Zhu, ZW Li, C Bai, J Yu, X Liu, JH
Citation:	Xi QL, etal., Urology. 2011 Dec;78(6):1442.e1-7. doi: 10.1016/j.urology.2011.08.051.
RGD ID:	7205675
Pubmed:	PMID:22137721 (View Abstract at PubMed)
DOI:	DOI:10.1016/j.urology.2011.08.051 (Journal Full-text)
OBJECTIVE: To address the molecular mechanisms that the vitamin D receptor (VDR) in the kidney might contribute to decreased renal calcium reabsorption in idiopathic hypercalciuria using genetic hypercalciuric stone-forming (GHS) rats. METHODS: We silenced the VDR gene in the GHS and normal control (NC) rat kidney in vivo using adenovirus vector-delivered microRNA targeting VDR through renal venous transduction. On days 3-21 after injection with adenovirus, the expression levels of the VDR, calcium-sensing receptor, and epithelial calcium transporters in the kidney were detected. The urine calcium and serum calcium, phosphorus, 1,25(OH)(2)D(3), and parathyroid hormone levels were measured. RESULTS: The basal expression levels in the kidney tissues of VDR, calbindin-D(28k), and calcium-sensing receptor were significantly greater in the GHS rats than in the NC rats, and the basal expression levels of transient receptor potential vanilloid receptor subtype 5, transient receptor potential vanilloid receptor subtype 6, calbindin-D(9k), and plasma membrane calcium-adenosine triphosphatase were significantly lower in the GHS rats than in the NC rats. VDR knockdown in the kidney caused significant increase in renal transient receptor potential vanilloid receptor subtype 5, sodium/calcium exchanger, and calbindin-D(9k) expression levels in the GHS rats. The GHS rats excreted significantly more urine calcium after VDR knockdown. The serum calcium, phosphorus, parathyroid hormone, and 1,25(OH)(2)D(3) levels were not altered during the study period in the GHS and NC rats. CONCLUSION: Our findings suggest that VDR knockdown in the kidney can upregulate the expression of transient receptor potential vanilloid receptor subtype 5 in GHS rats. However, VDR depletion results in an increase in urine calcium excretion. The role of VDR in the hypercalciuric formation needs to be elucidated further.

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
Hypercalciuria		ISO	Casr (Rattus norvegicus)	7205675; 7205675	mRNA and protein:increased expression:kidney (rat)	RGD
Hypercalciuria		IEP		7205675	mRNA and protein:increased expression:kidney (rat)	RGD

Objects Annotated

Genes (Rattus norvegicus)

Casr (calcium-sensing receptor)

Genes (Mus musculus)

Casr (calcium-sensing receptor)

Genes (Homo sapiens)

CASR (calcium sensing receptor)

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Effect of silencing VDR gene in kidney on renal epithelial calcium transporter proteins and urinary calcium excretion in genetic hypercalciuric stone-forming rats.