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Expression of adhesion molecules in rat renal cortex during experimental hydronephrosis
S D Ricardo1, M E Levinson, M R DeJoseph
1Department of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA.
Kidney International
|December 1, 1996
Summary
Unilateral ureteral obstruction (UUO) increases intercellular adhesion molecule (ICAM)-1 expression in kidneys, driving macrophage infiltration. Angiotensin II, released due to tubular injury, plays a key role in ICAM-1 release.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Unilateral ureteral obstruction (UUO) causes macrophage infiltration into the renal cortex.
- Adhesion molecules like ICAM-1 and VCAM-1 are implicated in macrophage recruitment during UUO.
- Understanding the temporal expression of these molecules is crucial for renal injury insights.
Purpose of the Study:
- To investigate the time course of ICAM-1 and VCAM-1 mRNA and protein expression in UUO.
- To explore the role of angiotensin II in ICAM-1 regulation in proximal tubules.
- To elucidate the mechanisms of macrophage recruitment in obstructed kidneys.
Main Methods:
- UUO model in rodents to assess renal ICAM-1 and VCAM-1 expression.
- Quantitative real-time PCR for mRNA analysis.
- Immunohistochemistry and in situ hybridization for protein and mRNA localization.
- In vitro studies using isolated proximal tubules exposed to angiotensin II and losartan.
Main Results:
- ICAM-1 mRNA significantly increased at 12, 24, 48, and 96 hours post-UUO, with sustained levels post-obstruction relief.
- VCAM-1 mRNA showed no significant difference between obstructed and contralateral kidneys.
- ICAM-1 protein localized to renal tubules, interstitium, and vessels by 12 hours post-UUO.
- Angiotensin II exposure elevated ICAM-1 mRNA in proximal tubules, an effect blocked by losartan.
Conclusions:
- ICAM-1 plays a critical role in initiating macrophage recruitment to the renal cortex during UUO.
- Angiotensin II, produced secondary to tubular injury in UUO, is a key mediator of ICAM-1 release from proximal tubule cells.
- These findings highlight a novel pathway involving angiotensin II and ICAM-1 in UUO-induced renal inflammation.