Abstract
Vasoactive intestinal peptide (VIP) plays important roles in many biological functions, such as, stimulation of contractility in the heart, vasodilation, promoting neuroendocrine-immune communication, lowering arterial blood pressure, and anti-inflammatory and immune-modulatory activity. Osteoarthritis (OA) is a chronic and degenerative bone disease, which is one of the most common causes of disability and most common in both sexes as people become older. Interestingly VIP can prevent chronic cartilage damage and joint remodeling. This review article provides update information on the association of VIP and OA and its treatment. Evidences suggest that VIP is down-regulated in synovial fluid of OA, and VIP down-regulation leads to increase in the production of pro-inflammatory cytokines that might contribute to the pathogenesis of OA; however contradictory reports also exist suggesting that accumulation of VIP in joints can also contribute OA. A number of studies indicated that up-regulation of VIP can counteract the action of pro-inflammatory stimuli and alleviate the pain in OA. More clinical investigations are necessary to determine the biology of VIP and its therapeutic potential in OA that might represent the future standards of care for OA.
Highlights
The vasoactive intestinal peptide (VIP) known as the vasoactive intestinal polypeptide is a neuropeptide that belongs to a glucagon/secretin superfamily, the ligand of class II G protein-coupled receptors [1, 2]
The inflammatory neuropeptides substance P, calcitonin gene-related peptide, as well as VIP, have all been reported to be immunolocalized in joint tissues and their levels are increased in arthritis [14]
We have focused on the association of VIP in the development and progression of OA and the potential effects of VIP as a therapeutic agent for the treatment of OA
Summary
The vasoactive intestinal peptide (VIP) known as the vasoactive intestinal polypeptide is a neuropeptide that belongs to a glucagon/secretin superfamily, the ligand of class II G protein-coupled receptors [1, 2]. In focus on controlling joint inflammation, VIP plays dual role, as it functions as a macrophage deactivating factor which inhibits the production of the pro-inflammatory cytokines (IL-1, IL-6, IL-12) and tumor necrosis factor-α (TNF-α), while stimulates the production of anti-inflammatory cytokines such as IL-4, IL-10, IL-13 and insulin-like growth factor 1 (IGF-1) [4, 22].
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