Abstract

Abstract A positive correlation between serum prolactin (PRL) and lupus disease activity such as IgG anti-DNA antibody deposition in the kidney has previously been shown. While the presence of immune complex deposition is required for the initiation of lupus nephritis (LN), renal MCP-1 expression and the subsequent infiltration and activation of macrophages ultimately results in inflammation and full-blown LN. The influence of PRL on the inflammatory component of LN has not been reported. Mice were 6-8 month-old males and were either C57Bl/6 wild-type (WT), C57Bl/6 PRL KO, or BcN (lupus strain). Renal proximal tubule cells were isolated and the PRL receptor expression was determined by RT-PCR and immunofluorescence microscopy. Renal proximal tubule cells from C57Bl/6 WT mice were stimulated with PRL and the amount of MCP-1 in the media was determined by ELISA. Cell surface expression and the mRNA expression of all 4 isoforms of the PRL receptor were comparable in the 3 genotypes. Proximal tubule cells produced significantly more MCP-1 when stimulated with 1000 ng/ml of PRL compared to 0 ng/ml (p<0.01). Our results indicate that PRL has the potential to directly stimulate proximal tubule cell MCP-1 production/release. Whether lower doses of PRL would have a greater impact in the presence of immune complexes is unknown. Because the renal tubule cell isolation technique most likely removes immune complexes, an in vivo model of SLE to ascertain whether PRL .....

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