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Title:

Tissue expression of TRPC3 and TRPC6 in hypertensive Munich Wistar Frömter rats showing proteinuria.

Document type:
Journal Article
Author(s):
Liu, Y; Thilo, F; Kreutz, R; Schulz, A; Wendt, N; Loddenkemper, C; Jankowski, V; Tepel, M
Abstract:
BACKGROUND: We investigated whether alterations of transient receptor potential canonical (TRPC) channel expression may be observed in tissues from Munich Wistar Frömter (MWF) rats showing proteinuria compared to control Wistar rats. METHODS: TRPC expression was investigated in tissue from MWF and Wistar rats using quantitative real time PCR, immunoblotting, and immunohistochemistry. RESULTS: Compared to Wistar rats MWF rats showed significantly increased systolic blood pressure and significantly higher left ventricle weight (each p < 0.01). Quantitative real time PCR revealed that TRPC3 transcripts were significantly higher in kidney cortex from MWF rats compared to Wistar rats (p < 0.01). TRPC3 transcripts were not significantly different in kidney medulla nor in aorta from both groups (p = n.s.). Furthermore, TRPC6 transcripts were significantly lower in kidney cortex from MWF rats compared to Wistar rats (p < 0.001). Immunoblotting showed that TRPC3 channel protein expression was also significantly higher in kidney cortex from MWF rats compared to Wistar rats (p < 0.01). There was a significant correlation of TRPC3 mRNA and a specific marker for endothelium, von Willebrand factor (vWF; Spearman r = 0.564; p < 0.01). We observed a significant correlation between the TRPC3 transcripts to TRPC6 transcripts ratio in kidney cortex and urinary albumin excretion (Spearman r = 0.785, p < 0.001). CONCLUSION: Altered TRPC expression pattern in kidney cortex is associated with kidney damage in MWF rats showing hypertension and albuminuria.
Journal title abbreviation:
Am J Nephrol
Year:
2010
Journal volume:
31
Journal issue:
1
Pages contribution:
36-44
Language:
eng
Fulltext / DOI:
doi:10.1159/000254060
Pubmed ID:
http://view.ncbi.nlm.nih.gov/pubmed/19887786
Print-ISSN:
0250-8095
TUM Institution:
Institut für Allgemeine Pathologie und Pathologische Anatomie
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