Expression of the chemokine fractalkine (FKN/CX3CL1) by podocytes in normal and proteinuric rat kidney glomerulus

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.