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Decrease in Gs protein expression may impair adenylate cyclase activation in old kidneys

C T Liang1, J Barnes, H Hanai

  • 1Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore 21224.

The American Journal of Physiology
|May 1, 1993
PubMed
Summary
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Aging reduces stimulatory guanine nucleotide-binding protein (Gs) alpha mRNA levels in rat kidneys. This decrease in Gs expression is likely due to reduced transcription, contributing to impaired parathyroid hormone signaling in older rats.

Area of Science:

  • Molecular Biology
  • Gerontology
  • Renal Physiology

Background:

  • Aging is associated with diminished cellular responses to hormones.
  • Parathyroid hormone (PTH)-stimulated adenylate cyclase activity in the kidney is blunted in aged rats.
  • Alterations in stimulatory guanine nucleotide-binding protein (Gs) expression may underlie these age-related functional deficits.

Purpose of the Study:

  • To investigate whether changes in Gs expression contribute to the blunted renal PTH-stimulated adenylate cyclase activity in aged rats.
  • To determine the molecular mechanisms responsible for altered Gs expression with age.

Main Methods:

  • Quantification of Gs alpha mRNA levels using Northern blot analysis.
  • Assessment of Gs alpha mRNA transcription rates via nuclear runoff assays.

Related Experiment Videos

  • Measurement of beta-actin mRNA as a control.

    • Main Results:

    • Gs alpha mRNA levels decreased by 23% in aged rats compared to younger rats.
    • The transcription rate of Gs alpha mRNA was significantly reduced (89%) in aged rat kidneys.
    • mRNA levels of Gi alpha 2 increased with age, while beta-actin mRNA remained unchanged.

    Conclusions:

    • The reduction in steady-state Gs alpha mRNA levels in aged rats is specific and primarily due to decreased transcription.
    • Reduced Gs transcription contributes to impaired renal adenylate cyclase activation in aging.
    • These findings highlight a molecular mechanism for age-related decline in renal hormone signaling.