Author(s): Katsuyama K, Fujinaka H, Yamamoto K, Nameta M, Yaoita E,
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Abstract BACKGROUND/AIMS: A chemokine fractalkine (FKN/CX3CL1) is induced primarily by endothelial cells and accumulates inflammatory cells via its receptor CX3CR1. Since glomerular preferential expression of FKN/CX3CL1 gene was reported in normal human kidney, we presumed FKN/CX3CL1 might play some roles in glomerular physiology. The purpose of this study is to examine the expression and localization of FKN/CX3CL1 in normal and proteinuric glomeruli. METHODS: Normal and proteinuric rat kidneys were studied. The gene and protein expressions of FKN/CX3CL1 and CX3CR1 were examined by real-time RT-PCR, in situ hybridization and immunohistochemistry, Western blotting. RESULTS: By real-time RT-PCR, glomerular preferential expression of FKN/CX3CL1 was confirmed, whereas CX3CR1 was detected in glomeruli and cortices. The localization of FKN/CX3CL1 gene and protein were demonstrated in glomerular cells including podocytes. In nephrotic puromycin aminonucleoside (PAN) nephrosis glomeruli, increased expression of FKN/CX3CL1 in podocyte was shown by immunohistochemistry. Western blotting showed that in nephrotic glomeruli, the membrane-anchored form of FKN/CX3CL1 was increased while the soluble form was decreased. CONCLUSION: The expression of FKN/CX3CL1 in normal podocytes and the increased expression of the membrane-anchored form in nephrotic glomeruli strongly suggest that FKN/CX3CL1 may play roles in glomerular physiology such as maintaining glomerular filtration barrier. Copyright 2009 S. Karger AG, Basel.
This article was published in Nephron Exp Nephrol
and referenced in Journal of Nanomedicine & Nanotechnology