Effects of chronic renal failure on caveolin-1, guanylate cyclase and AKT protein expression.

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  • Author(s): Sindhu RK;Sindhu RK; Ehdaie A; Vaziri ND; Roberts CK
  • Source:
    Biochimica et biophysica acta [Biochim Biophys Acta] 2004 Nov 05; Vol. 1690 (3), pp. 231-7.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Elsevier Pub. Co Country of Publication: Netherlands NLM ID: 0217513 Publication Model: Print Cited Medium: Print ISSN: 0006-3002 (Print) Linking ISSN: 00063002 NLM ISO Abbreviation: Biochim Biophys Acta Subsets: MEDLINE
    • Publication Information:
      Original Publication: Amsterdam : Elsevier Pub. Co.
    • Subject Terms:
      Gene Expression Regulation*; Caveolins/*metabolism ; Guanylate Cyclase/*metabolism ; Kidney Failure, Chronic/*metabolism ; Protein Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/*metabolism; Animals ; Caveolin 1 ; Cyclic GMP/metabolism ; Kidney Failure, Chronic/enzymology ; Male ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Sprague-Dawley
    • Abstract:
      Chronic renal failure (CRF) has been documented to cause oxidative stress and alter nitric oxide (NO) metabolism. However, the effect of CRF on proteins related to NO bioactivity has not been investigated. The present study was designed to test the hypothesis that CRF would induce changes in caveolin-1 (Cav-1), soluble guanylate cyclase (sGC) and Akt, three proteins important in regulating NO synthase (NOS) functionality. Male Sprague-Dawley rats were randomized to CRF via 5/6 nephrectomy or sham-operated control groups. After 6 weeks, body weight, blood pressure, creatinine clearance, plasma creatinine, urinary cyclic guanosine monophosphate (cGMP) and immunodetectable levels of Cav-1, sGC and Akt were determined in the renal, aorta, heart and liver tissues from both groups. CRF resulted in marked decreases in body weight and creatinine clearance, and elevation of blood pressure and plasma creatinine. An apparent upregulation of sGC protein abundance in renal tissue was noted, with no change in aorta, heart and liver. This was accompanied by a reduction in urinary cGMP levels, indicative of sGC dysfunction. Cav-1 protein abundance was increased in aortic, liver and renal tissues. In contrast, CRF depressed Akt abundance in aorta, heart and liver tissues. These data document that CRF is characterized by alteration in the abundance of proteins regulating NO function in hepatic, vascular, cardiac and renal tissues, and a decrease in cGMP, which contributes to hypertension and changes in NO bioactivity previously noted in this model.
    • Grant Information:
      F32 HL68406-01 United States HL NHLBI NIH HHS
    • Accession Number:
      0 (Cav1 protein, rat)
      0 (Caveolin 1)
      0 (Caveolins)
      0 (Proto-Oncogene Proteins)
      EC 2.7.11.1 (Akt1 protein, rat)
      EC 2.7.11.1 (Protein Serine-Threonine Kinases)
      EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
      EC 4.6.1.2 (Guanylate Cyclase)
      H2D2X058MU (Cyclic GMP)
    • Publication Date:
      Date Created: 20041030 Date Completed: 20041209 Latest Revision: 20211203
    • Publication Date:
      20240829
    • Accession Number:
      10.1016/j.bbadis.2004.06.013
    • Accession Number:
      15511630