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Expression of Somatostatin and Somatostatin Receptor Subtypes 1–5 in Human Normal and Diseased Kidney

Sunil Bhandari, Neil Watson, Ervine Long, Steve Sharpe, Wenwen Zhong, Shang-Zhong Xu and Stephen L. Atkin

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 and Hull York Medical School, University of Hull, Kingston-upon Hull, United Kingdom (NW,WZ,S-ZX,SLA)

Correspondence to: Sunil Bhandari, Consultant Nephrologist/Honorary Clinical Reader in the Department of Renal Medicine, Hull Royal Infirmary, Hull and East Yorkshire Hospitals NHS Trust, Kingston-upon Hull HU3 2JZ, UK. E-mail: sunil.bhandari{at}hey.nhs.uk

Somatostatin mediates inhibitory functions through five G protein–coupled somatostatin receptors (sst_1–5). We used immunohistochemistry, immunofluorescence, and RT-PCR to determine the presence of somatostatin receptors sst₁, sst_2A, sst_2B, 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 was more condensed in the cytoplasm of tubular epithelial cells. In normal kidney tissue sections, podocytes and mesangial cells in the glomeruli stained for sst₁, sst_2B, 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, sst_2B, sst₄, and sst₅ within glomeruli. In the epithelial cells, the staining for sst_2B and sst₄ in proximal tubules and sst₁, sst_2B, and sst₅ in distal tubules was increased. The mRNA expression of sst_1–5 was also detected by RT-PCR. Somatostatin and all five receptor subtypes were ubiquitously 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. (J Histochem Cytochem 56:733–743, 2008)

Key Words: human kidney • IgA nephropathy • somatostatin • somatostatin receptors • tubule • podocytes • mesangial cells

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