Evaluation of genetic association and expression reduction of TRPC1 in the development of diabetic nephropathy

Am J Nephrol. 2009;29(3):244-51. doi: 10.1159/000157627. Epub 2008 Sep 19.

Abstract

Background/aims: The TRPC1 gene on chromosome 3q22-24 resides within the linkage region for diabetic nephropathy (DN) in type 1 (T1D) and type 2 diabetes mellitus (T2D). A recent study has demonstrated that TRPC1 expression is reduced in the kidney of diabetic ZDF- and STZ-treated rats. The present study aimed to evaluate the genetic and functional role of TRPC1 in the development of DN.

Methods: Genetic association study was performed with two independent cohorts, including 1,177 T1D European Americans with or without DN from GoKinD population and 850 African-American subjects with T2D-associated end-stage renal disease (ESRD), or with hypertensive (non-diabetic) ESRD, and nondiabetic controls. Seven tag SNP markers derived from HapMap data (phase II) were genotyped. TRPC1 gene expression was examined using real time RT-PCR.

Results: No significant association of TRPC1 DNA polymorphisms with DN or ERSD was found in GoKinD and African-American populations. TRPC1 gene mRNA expression in kidney was found to be trendily reduced in 12-week and significantly in 26-week-old db/db mice.

Conclusions: TRPC1 genetic polymorphism may not fundamentally contribute to the development of DN, while reduction of the gene expression in kidney may be a late phenomenon of DN as seen in diabetic animal models.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Animals
  • Black or African American / genetics
  • Case-Control Studies
  • Cohort Studies
  • Diabetes Mellitus, Type 1 / complications*
  • Diabetes Mellitus, Type 2 / complications*
  • Diabetic Nephropathies / ethnology
  • Diabetic Nephropathies / etiology
  • Diabetic Nephropathies / genetics*
  • Female
  • Gene Expression
  • Genotype
  • Humans
  • Hypertension / complications*
  • Kidney Failure, Chronic / etiology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Middle Aged
  • Polymorphism, Single Nucleotide
  • Sequence Analysis, DNA
  • TRPC Cation Channels / genetics*
  • White People / genetics

Substances

  • TRPC Cation Channels
  • transient receptor potential cation channel, subfamily C, member 1