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Updated: Jun 5, 2026
09:12
Isolation of Glomeruli and In Vivo Labeling of Glomerular Cell Surface Proteins
Published on: January 18, 2019
Intercellular adhesion molecule-1 plays a critical role in glomerulosclerosis after subtotal nephrectomy
Yuichi Kido1, Daisuke Ogawa, Kenichi Shikata
1Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama 700-8558, Japan.
Clinical and Experimental Nephrology
|December 25, 2010
Summary
Glomerular hyperfiltration causes glomerulosclerosis, a condition worsened by intercellular adhesion molecule (ICAM)-1. Depleting ICAM-1 in mice reduced kidney injury, suggesting ICAM-1 plays a key role in this disease progression.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Glomerular hyperfiltration is a known cause of kidney injury.
- The role of intercellular adhesion molecule (ICAM)-1 in glomerulosclerosis is unclear.
Purpose of the Study:
- To investigate the impact of ICAM-1 deficiency on hyperfiltration-induced glomerular damage.
- To determine if ICAM-1 influences macrophage infiltration and matrix expansion in glomerulosclerosis.
Main Methods:
- Utilized subtotally nephrectomized ICAM-1(+/+) and ICAM-1(-/-) mice.
- Assessed macrophage infiltration, mesangial matrix expansion, and accumulation of TGF-β and type IV collagen in glomeruli.
Main Results:
- ICAM-1(-/-) mice showed reduced macrophage infiltration and mesangial matrix expansion.
- Depletion of ICAM-1 ameliorated glomerular hyperfiltration-induced injury and TGF-β/collagen accumulation.
Conclusions:
- Glomerular hyperfiltration is a primary driver of glomerulosclerosis.
- ICAM-1 expression and subsequent macrophage infiltration are crucial mediators in this process.
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