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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Prolactin blocks the expression of receptor activator of nuclear factor κB ligand and reduces osteoclastogenesis and bone loss in murine inflammatory arthritis

Fig. 5

TNFα, IL-1β, and IFNγ (Cyt) induce the expression of the long prolactin (PRL) receptor (Prlr) in synovial membrane and synovial fibroblasts and PRL blocks Cyt-induced Tnfrsf11 expression in synovial fibroblasts by a STAT3-dependent pathway. a Quantification by quantitative real-time PCR (qRT-PCR) of PRL receptor long isoform mRNA levels in synovial membrane from mouse knees injected with or without Cyt. b qRT-PCR and western blot evaluation of PRL receptor long isoform mRNA and protein in primary cultures of synovial fibroblasts incubated with or without Cyt. Bars show the quantification of PRLR Long/β-Tubulin by densitometry. c qRT-PCR quantification of Tnfa, Il1b, Il6, Tnfrsf11, and Tnfrsf11b mRNA levels in primary cultures of synovial fibroblasts incubated or not with Cyt in the absence or presence of 100 nM PRL. d qRT-PCR and e western blot evaluation of Stat3 mRNA levels and phosphorylated STAT3 (p-STAT3), respectively, in primary cultures of synovial fibroblasts incubated with or without Cyt and with or without 100 nM PRL. Bars show the quantification of pSTAT3/β-Tubulin by densitometry. f qRT-PCR quantification of Tnfrsf11 mRNA levels in primary cultures of synovial fibroblasts incubated with or without Cyt and with or without 100 nM PRL in the absence or presence of 50 μM of the STAT3 inhibitor S31-201. Values are means ± SEM of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, n.s. non-significant

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