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Study of Cell Migration in Microfabricated Channels
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ET

Erika I Boesen1

  • 1Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska.

Physiological Reports
|September 11, 2018
PubMed
Summary

Blocking the endothelin ETA receptor reduced T cell infiltration into kidneys following ischemia-reperfusion (IR) injury. This suggests a role for endothelin-1 in the immune response to acute kidney injury (AKI).

Area of Science:

  • Nephrology
  • Immunology
  • Cardiovascular Research

Background:

  • Acute kidney injury (AKI) and renal ischemia-reperfusion (IR) injury are linked to hypertension development.
  • T cells are implicated in the mechanisms connecting AKI to hypertension.
  • Endothelin, primarily via the ETA receptor, is known to promote T cell infiltration in various diseases.

Purpose of the Study:

  • To investigate the role of ETA receptor activation in promoting T cell infiltration into the kidney following IR injury.
  • To determine if blocking the ETA receptor can mitigate T cell infiltration post-renal IR injury.

Main Methods:

  • Male C57BL/6 mice were treated with an ETA receptor antagonist (ABT-627) or vehicle.
  • Mice underwent unilateral renal IR injury.
Keywords:
ETA receptorsEndothelinsT lymphocyteischemiakidney

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  • Renal tissue was analyzed at 24 hours and 10 days post-IR for injury and T cell infiltration (CD3+ cells, RORγt expression).

    • Main Results:

    • Endothelin-1 (ET-1) was upregulated in injured kidneys post-IR in both groups.
    • ABT-627 treatment significantly reduced CD3+ T cell infiltration in the outer medulla (35%) and cortex (23%) at 10 days post-IR.
    • Outer medullary RORγt expression, a T helper 17 marker, was reduced by ABT-627 treatment.

    Conclusions:

    • Endothelin-1, acting through the ETA receptor, contributes to T cell infiltration in the kidney after IR injury.
    • Targeting the ETA receptor may be a strategy to manage immune-mediated long-term consequences of AKI.
    • Further research is needed to explore the specific T cell subsets involved and long-term implications.