Abstract
C1q/TNF-related protein 9 (CTRP9), the closest paralog of adiponectin, has been reported to protect against inflammation-related diseases. However, its role in regulating osteoarthritis (OA) has not been fully elucidated. First, a rat model of OA was generated. Furthermore, rats with OA were injected with different doses of recombinant CTRP9 protein (rCTRP9), and the knee cartilage damage was evaluated. Finally, the phosphorylation of p38 and the secretion of matrix metalloproteinases (MMPs) were detected by Western blotting and enzyme-linked immunosorbent assay. Results revealed that CTRP9 was highly expressed in adipose tissue, followed by skeletal muscle and cartilage tissue, and less expressed in liver, kidney and lung. Moreover, the expression of CTRP9 significantly decreased in the monosodium iodoacetate (MIA) group in the knee cartilage and knee synovial fluid, and the contents of interleukin-1β (IL-1β) and IL-6 significantly increased in knee synovial fluid. In addition, rCTRP9 alleviated MIA-induced inflammation, oxidative stress and knee cartilage damage in a dose-dependent way. In addition, rCTRP9 could attenuate the expression of p38MAPK and p-p38 and suppress the expression of nuclear factor-kappa B (NF-κB), p65 and MMPs. Collectively, the results of the present study suggested that CTRP9 alleviates the inflammation of MIA-induced OA through deactivating p38MAPK and NF-κB signaling pathways in rats.
Highlights
Adiponectin is a well-known adipokine and is considered to be a regulator of insulin signaling and inflammation
We investigated the expression of C1q/TNF-related protein 9 (CTRP9) in several tissues including heart, subcutaneous fat, inguinal fat, kidney, lung, liver, brain, skeletal muscle, bone marrow and knee cartilage
In order to verify the role of CTRP9 in OA, different doses of CTRP9 recombinant protein were injected into MIAinduced osteoarthritic rats and the indicators were detected on 14 and 28 days
Summary
Adiponectin is a well-known adipokine and is considered to be a regulator of insulin signaling and inflammation. C1q/TNF-related protein 9 (CTRP9) is the closest paralog of adiponectin. Its biochemical function is comparable to that of adiponectin due to their structural similarity [1]. CTRP9 is a member of the CTRP family, which is secreted mainly by adipose tissue [2]. CTRP9 plays an important role in the communication between skeletal muscle, liver and adipose tissue [3,4]. A recent study reported that CTRP9 regulates the growth, differentiation and apoptosis of keratinocytes via the transforming growth factor-β1-p38-dependent pathway [5]. Mice with CTRP9 overexpression showed improvement in blood glucose and insulin levels, significant weight loss and improvement in fatty liver. CTRP9 knockout mice showed significant weight gain, insulin resistance and hepatic steatosis [6]
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