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Cell adhesion molecule-1 shedding induces apoptosis of renal epithelial cells and exacerbates human nephropathies

Takashi Kato1,2, Man Hagiyama1, Yasutoshi Takashima1

  • 1Department of Pathology, Faculty of Medicine, Kindai University , Osaka , Japan.

American Journal of Physiology. Renal Physiology
|October 27, 2017
PubMed

Insights

Reduced cell adhesion molecule-1 (CADM1) levels in chronic kidney disease (CKD) promote renal tubular cell apoptosis and worsen kidney injuries. This finding highlights CADM1 as a potential therapeutic target for CKD.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Chronic kidney disease (CKD) is a global health issue characterized by elevated blood urea nitrogen (BUN) and serum creatinine (sCre), alongside renal tubular damage.
  • Understanding the molecular mechanisms of renal injury is vital for developing novel therapeutics and early diagnostic tools.
  • Cell adhesion molecule-1 (CADM1), particularly its isoform SP4, is expressed in renal distal tubules and plays a role in cell-cell adhesion.

Purpose of the Study:

  • To investigate the occurrence and role of CADM1 α-shedding in human nephropathies, specifically arterionephrosclerosis (AS) and diabetic nephropathy (DN).
  • To determine the correlation between reduced full-length CADM1 (FL-CADM1) levels and renal injury markers and apoptosis in CKD.

Main Methods:

  • Western blotting and immunohistochemical analysis of kidney specimens from autopsied patients with AS and DN.
  • Assessment of FL-CADM1 levels, its cleaved fragment (α-CTF), and correlation with renal injury markers (BUN, sCre, tubular damage).
  • In vitro studies involving small interfering RNA (siRNA) knockdown of FL-CADM1 in cultured renal tubular epithelial cells (TECs) to assess apoptosis and Bcl-2 expression.

Main Results:

  • CADM1 α-shedding was observed in AS and DN kidneys, indicated by decreased FL-CADM1 and increased α-CTF.
  • Reduced FL-CADM1 levels correlated significantly with tubular and tubulointerstitial injuries, as well as elevated BUN and sCre.
  • Apoptosis of renal TECs was promoted in both nephropathies and strongly correlated with decreased FL-CADM1. FL-CADM1 knockdown in vitro reduced anti-apoptotic Bcl-2 and increased TEC apoptosis.

Conclusions:

  • The reduction of FL-CADM1 contributes to renal TEC apoptosis, exacerbating renal tubular and tubulointerstitial injuries in CKD.
  • CADM1 α-shedding and subsequent FL-CADM1 reduction are implicated in the pathogenesis of CKD.
  • Targeting FL-CADM1 may offer a novel therapeutic strategy for managing CKD and its associated renal injuries.
Keywords:
CADM1DM nephropathyapoptosisarterionephrosclerotic nephropathyshedding

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