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Growth abnormalities in cultured mesangial cells from rats with spontaneous glomerulosclerosis

F Pugliese1, R G Ferrario, A Ciavolella

  • 1Department of Medicine, University of Rome La Sapienza, Italy.

Kidney International
|January 1, 1995
PubMed

Insights

Mesangial cell (MC) proliferation and matrix synthesis differ between aging normotensive (MNS) and hypertensive (MHS) rats. MNS rats show increased MC proliferation and matrix production with age, unlike MHS rats, suggesting a protective mechanism against glomerulosclerosis in MHS.

Area of Science:

  • Nephrology
  • Cell Biology
  • Genetics

Background:

  • Age-related glomerulosclerosis (GS) is a kidney scarring process affecting mesangial cells (MC).
  • Milan normotensive (MNS) rats develop GS with age, while genetically similar Milan hypertensive (MHS) rats do not.
  • Understanding MC behavior in aging is crucial for explaining these differences.

Purpose of the Study:

  • To investigate age-related changes in MC proliferation and matrix protein synthesis.
  • To compare these changes between MNS and MHS rats.
  • To elucidate potential mechanisms underlying the absence of GS in MHS rats.

Main Methods:

  • Cultured MCs from 1-month-old (young) and 8-month-old (old) MNS and MHS rats.
  • Assessed DNA synthesis ([3H]-thymidine incorporation) and cell counts.
  • Measured cytosolic calcium ([Ca2+]i) using fura-2.
  • Quantified collagen production and collagen IV/laminin B1 mRNA expression.

Main Results:

  • In MNS rats, MC proliferation, DNA synthesis, [Ca2+]i response, collagen production, and related mRNA expression increased with age.
  • In MHS rats, MC DNA synthesis and proliferation declined with age.
  • No significant age-related changes in [Ca2+]i or collagen production were observed in MHS MCs.

Conclusions:

  • Aging MNS rats exhibit increased MC proliferative activity and matrix synthesis, correlating with GS development.
  • Aging MHS rats show a decline in MC proliferative capacity, potentially a protective mechanism against GS.
  • Differential regulation of MC aging processes may explain the absence of GS in MHS rats.

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