Gene expression profiles of CLC chloride channels in animal models with different cardiovascular diseases

Cell Physiol Biochem. 2001;11(6):321-30. doi: 10.1159/000047818.

Abstract

Here for the first time we investigated the potential involvement of the CLC chloride channel family at the transcriptional level in different cardiovascular diseases. Northern blot and semiquantitative RT-PCR analyses were used to study the gene expression profiles of all CLC genes present in the heart and kidney; namely, CLC-2, CLC-3, CLC-4, CLC-5, CLC-6, CLC-7, CLC-K1, and CLC-K2. Rat models with distinctive cardiovascular diseases were studied: These included spontaneously hypertensive rats, nutritionally- and surgically-induced hypertensive rats with cardiac hypertrophy, as well as rats suffering from chronic heart failure due to myocardial infarction. The present data show that it was not possible to detect apparent differences in the CLC mRNA expression between the hearts and kidneys of diseased and control animals. Our data strongly suggest that altered transcript regulation of CLC chloride channels does not contribute to the cardiac and renal pathology in the examined cardiovascular diseases.

MeSH terms

  • Animals
  • Anion Transport Proteins*
  • CLC-2 Chloride Channels
  • Cardiovascular Diseases / genetics*
  • Chloride Channels / genetics*
  • Disease Models, Animal*
  • Gene Expression Profiling*
  • Male
  • Membrane Proteins*
  • Rats
  • Rats, Inbred Dahl / genetics
  • Rats, Inbred SHR / genetics
  • Rats, Sprague-Dawley
  • Rats, Wistar

Substances

  • Anion Transport Proteins
  • CLC-2 Chloride Channels
  • CLC-5 chloride channel
  • CLCNKA protein, human
  • Chloride Channels
  • ClC-3 channel
  • Clcn6 protein, rat
  • Clcn7 protein, rat
  • Clcnka protein, rat
  • Clcnkb protein, rat
  • Membrane Proteins