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APOL1 promotes endothelial cell activation beyond the glomerulus.

Miguel Carracedo1, Elke Ericson2, Rasmus Ågren3

  • 1Bioscience Renal, Research and Early Development, Cardiovascular , Renal and Metabolism (CVRM), BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Iscience
|May 30, 2023
PubMed
Summary

High-risk Apolipoprotein L1 (APOL1) gene variants may drive chronic kidney disease (CKD) by activating kidney endothelial cells (ECs). This activation increases monocyte adhesion, suggesting a novel mechanism in CKD pathogenesis.

Keywords:
Nephrology

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Area of Science:

  • Nephrology
  • Vascular Biology
  • Genetics

Background:

  • Apolipoprotein L1 (APOL1) high-risk genotypes are linked to chronic kidney disease (CKD) in individuals of West African ancestry.
  • Endothelial cells (ECs) play a critical role in CKD pathogenesis.
  • The specific mechanisms by which APOL1 influences ECs in CKD remain incompletely understood.

Purpose of the Study:

  • To investigate whether APOL1 high-risk genotypes contribute to CKD through intrinsic activation and dysfunction of kidney ECs.
  • To identify molecular pathways and cellular changes associated with APOL1 expression in renal ECs.

Main Methods:

  • Single cell RNA sequencing (scRNA-seq) analysis of kidney tissue from the Kidney Precision Medicine Project.
  • Transcriptomic analysis of public datasets from African Americans with CKD and APOL1-expressing transgenic mice.
  • In vitro studies using human induced pluripotent stem cell-derived ECs and glomerular ECs with APOL1 expression.

Main Results:

  • APOL1 expression was detected in ECs across various renal vascular compartments.
  • An EC activation signature was identified, characterized by increased intercellular adhesion molecule 1 (ICAM-1) and enrichment in leukocyte migration pathways.
  • APOL1 expression in vitro increased ICAM-1 and PECAM-1 expression, leading to enhanced monocyte attachment to ECs.

Conclusions:

  • APOL1 appears to induce EC activation in multiple renal vascular beds.
  • This EC activation, involving increased ICAM-1 and monocyte adhesion, may be a key mechanism contributing to CKD.
  • The effects of APOL1 on ECs may extend beyond the glomerular vasculature, impacting overall kidney health.