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Alteration of epidermal growth factor receptor expression following ischaemia of renal tissue
A Ertuğrul1, L N Türkeri, M Ozyürek
1Department of Urology, Marmara University School of Medicine, Istanbul, Turkey.
Abstract:
This study was aimed to investigate Epidermal Growth Factor Receptor (EGF-R) expression after ischaemic injury in renal tissue and the effects of calcium channel blockers in the prevention of damage due to ischaemic insult. Simple nephrectomy was performed in a group of Sprague-Dawley rats, and kidneys were grouped according to cold ischaemia time (1, 6, 12, 24 and 48 hours, respectively) and to the type of calcium channel blockers (diltiazem and verapamil) used. EGF-R expression status was investigated in each group by immunohistochemistry on paraffin sections. Overall expression of EGF-receptor was detected in 8 (22.8%) kidneys. In terms of localization of EGF-receptor expression cortical tubular staining was detected in 8 (100%) kidneys, medullar tubular staining in (62.5%) kidneys and glomerular mesangial staining in 5 (62.5%) kidneys. There was no difference between various ischaemia times and different calcium channel blockers used. It has been concluded that hypoxia and cold ischaemia causes widespread down-regulation of EGF-receptor expression in renal tissue regardless of treatment with calcium channel blockers.
Insights
Cold ischemia and hypoxia down-regulate Epidermal Growth Factor Receptor (EGF-R) expression in renal tissue. Calcium channel blockers did not prevent this widespread down-regulation in rats.
Area of Science:
- Nephrology
- Renal Physiology
- Molecular Biology
Background:
- Renal ischemia-reperfusion injury is a significant clinical challenge.
- Epidermal Growth Factor Receptor (EGF-R) plays a role in renal tissue repair.
- The impact of ischemia on EGF-R expression and the potential protective effects of calcium channel blockers require further investigation.
Purpose of the Study:
- To investigate Epidermal Growth Factor Receptor (EGF-R) expression in renal tissue following ischemic injury.
- To evaluate the effects of calcium channel blockers (diltiazem and verapamil) on preventing ischemia-induced renal damage.
Main Methods:
- Sprague-Dawley rats underwent simple nephrectomy.
- Kidneys were exposed to varying cold ischemia times (1-48 hours).
- Immunohistochemistry was used to assess EGF-R expression in renal tissues.
Main Results:
- EGF-R expression was detected in 22.8% of kidneys.
- Cortical tubular staining for EGF-R was observed in all positive samples (100%).
- No significant differences in EGF-R expression were found related to ischemia duration or calcium channel blocker treatment.
Conclusions:
- Hypoxia and cold ischemia lead to a broad down-regulation of EGF-R expression in renal tissue.
- Calcium channel blockers (diltiazem, verapamil) did not mitigate the down-regulation of EGF-R expression post-ischemia.
- EGF-R down-regulation appears to be an inherent response to renal ischemic insult, independent of tested calcium channel blocker interventions.