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Lack or downregulation of the dopamine D 2  receptor (D 2 R) results in increased renal expression of injury markers and proinflammatory factors that is independent of a blood pressure increase. This study aimed to determine the mechanisms involved in the regulation of renal inflammation by D 2 Rs. Silencing D 2 Rs in mouse renal proximal tubule cells increased the expression of the proinflammatory TNF-α, monocyte chemoattractant protein-1 (MCP-1), and IL-6. D 2 R downregulation also increased Akt phosphorylation and activity, and glycogen synthase kinase-3β (GSK3β) phosphorylation and cyclin D1 expression, downstream targets of Akt; however. phosphatidylinositol 3-kinase (PI3K) activity was not affected. Conversely, D 2 R stimulation decreased Akt and GSK3β phosphorylation and cyclin D1 expression. Increased phospho-Akt, in the absence of increased PI3K activity, may result from decreased Akt dephosphorylation. Inhibition of protein phosphatase 2A (PP2A) with okadaic acid reproduced the effects of D 2 R downregulation on Akt, GSK3β, and cyclin D1. The PP2A catalytic subunit and regulatory subunit PPP2R2C coimmunoprecipitated with the D 2 R. Basal phosphatase activity and the expression of PPP2R2C were decreased by D 2 R silencing that also blunted the increase in phosphatase activity induced by D 2 R stimulation. Similarly, silencing PPP2R2C also increased the phosphorylation of Akt and GSK3β. Moreover, downregulation of PPP2R2C resulted in increased expression of TNF-α, MCP-1, and IL-6, indicating that decreased phosphatase activity may be responsible for the D 2 R effect on inflammatory factors. Indeed, the increase in NF-κB reporter activity induced by D 2 R silencing was blunted by increasing PP2A activity with protamine. Our results show that D 2 R controls renal inflammation, at least in part, by modulation of the Akt pathway through effects on PP2A activity/expression.

Dopamine D2receptors' effects on renal inflammation are mediated by regulation of PP2A function

Dopamine D₂receptors' effects on renal inflammation are mediated by regulation of PP2A function