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Related Experiment Videos

Chemokine expression in the obstructed kidney.

J M Crisman1, L L Richards, D P Valach

  • 1Pennsylvania State College of Medicine, Milton S. Hershey Medical Center, Hershey, Pa 17033-0850, USA. jmc35@psu.edu

Experimental Nephrology
|June 26, 2001
PubMed
Summary

Unilateral ureteral obstruction in mice increases kidney expression of chemokines like MCP-1, RANTES, and IP-10. Cortical tubules significantly contribute to RANTES, highlighting their role in hydronephrosis inflammation.

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Area of Science:

  • Immunology
  • Nephrology
  • Molecular Biology

Background:

  • Chemokines are crucial for immune cell movement.
  • Leukocyte extravasation and chemotaxis are key inflammatory processes mediated by chemokines.
  • Experimental hydronephrosis involves kidney inflammation.

Purpose of the Study:

  • To investigate chemokine expression in the obstructed kidney during unilateral ureteral obstruction (UUO).
  • To identify specific chemokines elevated in the obstructed kidney.
  • To determine the cellular sources of chemokine expression, particularly RANTES, in experimental hydronephrosis.

Main Methods:

  • Unilateral ureteral obstruction (UUO) model in mice.
  • Measurement of chemokine expression (MCP-1, RANTES, IP-10, MIP-2) in obstructed kidneys (OBK) and contralateral control kidneys (CLK).

Related Experiment Videos

  • In situ hybridization to localize RANTES expression within the OBK.

    • Main Results:

    • UUO induced expression of MCP-1, RANTES, and IP-10 by day 1 in the OBK.
    • MIP-2 expression was elevated by day 7 in the OBK.
    • RANTES was the most abundant chemokine detected in the OBK after 7 days.
    • In situ hybridization revealed substantial contribution of cortical tubules to elevated RANTES expression.

    Conclusions:

    • The obstructed kidney exhibits increased expression of multiple chemokines following UUO.
    • RANTES is a major chemokine upregulated in experimental hydronephrosis.
    • Cortical tubular epithelium plays a significant role in the inflammatory response during hydronephrosis.