Anti-C1QTNF6 (C-terminal) polyclonal antibody

C1qTNF-Related proteins (CTRPs), a new highly conserved family of adiponectin paralogs, were recently identified as being involved in diverse processes including metabolism, host defense, apoptosis, cell differentiation, and organogenesis. However, the functional role of CTRP6 remains poorly identified. Here we provide evidence that CTRP6 induces the expression of interleukin-10 (IL-10) in macrophages. Conditioned medium from CTRP6-expressing HEK293 cells increased IL-10 expression in Raw264.7 cells. The globular domain of CTRP6 (gCTRP6) also dose-dependently increased both IL-10 mRNA and protein expression levels, with transcript levels increasing within 2 h. Furthermore, the globular domain of CTRP6 rapidly induced phosphorylation of ERK1/2 in Raw264.7 cells. Treatment with U0126, a selective inhibitor, abolished CTRP6-stimulated IL-10 induction. Taken together, there results demonstrate that CTRP6 induces expression of IL-10 via ERK1/2 activation. Considering that IL-10 is a potent anti-inflammatory cytokine that modulates inflammatory signaling pathways, CTRP6 may be a novel target for pharmacological drugs in inflammatory diseases.

C1q/TNF-related protein 6 (CTRP6) is a member of the CTRP family that has been reported to exhibit a nephroprotective effect. However, the role of CTRP6 in renal ischaemia/reperfusion (I/R) injury (IRI) remains unclear. In the present study, we aimed to explore the protective effect of CTRP6 in renal IRI and the potential mechanism. We found that CTRP6 expression was markedly decreased in the kidneys of mice subjected to I/R and HK-2 cells in response to hypoxia/reoxygenation (H/R) stimulation. Recombinant CTRP6 protein protected against renal I/R injury by the reduction of blood urea nitrogen (BUN) and creatinine levels. The increased production of ROS and malondialdehyde (MDA), as well the decreased activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) caused by H/R induction were mitigated by CTRP6 in HK-2 cells. The caspase-3 activity and apoptotic rate were both decreased in CTRP6-overexpressing HK-2 cells. In addition, we also found that knockdown of CTRP6 aggravated H/R-caused oxidative stress and cell apoptosis in HK-2 cells. Moreover, CTRP6 overexpression enhanced the H/R-stimulated activation of PI3K/Akt pathway in HK-2 cells. Inhibition of PI3K reversed the nephroprotective effects of CTRP6 in HK-2 cells. Taken together, CTRP6 exerted protective effects against H/R-caused oxidative injury in HK-2 cells via activating the PI3K/Akt pathway.