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Rat mesangial alpha-endosulfine.

Jerry Yee1, Pedro Cortes, Jeffrey L Barnes

  • 1Department of Medicine, Division of Nephrology and Hypertension, Henry Ford Hospital, Detroit, Michigan 48202, USA. Jyee1@hfhs.org

Kidney International
|April 17, 2004
PubMed
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Alpha-endosulfine (ENSA) is present in rat kidneys and mesangial cells. High glucose levels increase ENSA expression, suggesting a role in regulating cell metabolism and contractility.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Endocrinology

Background:

  • Sulfonylurea agents modulate adenosine triphosphate-sensitive potassium (K(ATP)) channels.
  • Mesangial cells express K(ATP) channels and respond to sulfonylureas.
  • Alpha-endosulfine (ENSA) is an endogenous sulfonylurea-like phosphoprotein.

Purpose of the Study:

  • Investigate mesangial cell expression of the ENSA gene.
  • Determine the regulation of ENSA by glucose in mesangial cells.

Main Methods:

  • Reverse transcription-polymerase chain reaction (RT-PCR) and Northern analysis for ENSA transcripts.
  • In situ hybridization to localize ENSA in the kidney.
  • Immunoblotting, immunofluorescence, and confocal microscopy for alpha-endosulfine protein.

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Main Results:

  • Abundant ENSA transcripts (2.4 kb and 1.2 kb) found in rat kidney and mesangial cells.
  • ENSA expression localized to glomeruli within the kidney cortex.
  • High glucose concentrations significantly increased both ENSA gene and alpha-endosulfine protein expression.

Conclusions:

  • ENSA and alpha-endosulfine are expressed in rat glomeruli and mesangial cells.
  • High glucose environments up-regulate ENSA gene and protein expression.
  • Alpha-endosulfine may regulate mesangial cell metabolism and contractility via K(ATP) channels.