Expression of Somatostatin and Somatostatin Receptor Subtypes 1–5 in Human Normal and Diseased Kidney
Sunil Bhandari 1*, Neil Watson 1, Ervine Long 1, Steve Sharpe 1, Wenwen Zhong 1, Shang-Zhong Xu 1 and Stephen L. Atkin 1
1 Department of Renal Medicine and Hull York Medical School (SB) and Department of Histopathology (EL,SS), Hull Royal Infirmary, Hull and East Yorkshire Hospitals NHS Trust, Kingston-upon Hull, United Kingdom, and Diabetes, Endocrinology and Metabolism, Postgraduate Medical Institute & Hull York Medical School, University of Hull, Hull, United Kingdom (NW,WZ,S-ZX,SLA)
* To whom correspondence should be addressed. E-mail: sunil.bhandari{at}hey.nhs.uk.
Submitted on January 26, 2008
Accepted on 9 April 2008
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Abstract |
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Somatostatin mediates inhibitory functions through five G-protein coupled somatostatin receptors (sst1-5). We have used immunohistochemistry, immunofluorescence and RT-PCR to determine the presence of somatostatin receptors sst1, sst2A, sst2B, sst3, sst4 and sst5 in normal and IgA nephropathy human kidney. All somatostatin receptors were detected in the thin tubules (distal convoluted tubules and loops of Henle) and thick tubules (proximal convoluted tubules) in the tissue sections from nephrectomy and biopsy samples. Immunopositive sst1 and sst4 staining were more condensed in the cytoplasm of tubular epithelial cells. In normal kidney tissue sections, podocytes and mesangial cells in the glomeruli stained for sst1, sst2B, sst4 and sst5, and stained weakly for sst3. In IgA kidney tissue the expression of somatostatin receptors was significantly increased with particular immmunopositive staining for sst1, sst2B, sst4 and sst5 within glomeruli. In the epithelial cells, the staining for sst2B and sst4 in proximal tubules and sst1, sst2B and sst5 in distal tubules was increased. The mRNA expression of sst1-5 was also detected by RT-PCR. Somatostatin and all five receptor subtypes were ubiquitous distributed in normal kidney and IgA nephropathy. The increased expression of somatostatin receptors in IgA nephropathy kidney might be the potential pathogenesis of inflammatory renal disease.
Key Words:
human kidney, IgA nephropathy, somatostatin, somatostatin receptors, tubule, podocytes, mesangial cells