Title of article :
Calcium-dependent expression of transient receptor potential canonical type 3 channels in patients with chronic kidney disease
Author/Authors :
Liu، نويسنده , , Ying and Krueger، نويسنده , , Katharina and Hovsepian، نويسنده , , Anahit and Tepel، نويسنده , , Martin and Thilo، نويسنده , , Florian، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2011
Pages :
6
From page :
44
To page :
49
Abstract :
It is unknown whether extracellular calcium may regulate the expression of transient receptor potential canonical type 3 (TRPC3) channels in patients with chronic kidney disease. quantitative in-cell Western assay we compared the expression of TRPC3 channel protein in monocytes from 20 patients with chronic kidney disease and 19 age- and sex-matched healthy control subjects. TRPC3 channels were identified by immunoblotting using specific antibodies and TRPC3 protein was further confirmed by mass spectrometry. erved a significant increase of TRPC3 channel protein expression in patients with chronic kidney disease compared to healthy control subjects (normalized expression, 0.42 ± 0.06 vs. 0.19 ± 0.03; p < 0.01). Expression of TRPC3 was significantly inversely correlated with estimated glomerular filtration rates (Spearman r = −0.41) or serum calcium concentration (Spearman r = −0.34). During a hemodialysis session serum calcium concentrations significantly increased, whereas the expression of TRPC3 channels and calcium influx significantly decreased. In vitro studies confirmed that higher calcium concentrations but not magnesium, barium nor sodium concentrations significantly decreased TRPC3 expression in human monocytes. tudy indicates that reduced extracellular calcium concentrations up-regulate TRPC3 channel protein expression in patients with chronic kidney disease.
Keywords :
Calcium , Transient receptor potential channel , Chronic kidney disease
Journal title :
Archives of Biochemistry and Biophysics
Serial Year :
2011
Journal title :
Archives of Biochemistry and Biophysics
Record number :
1603422
Link To Document :
بازگشت