Notably, the Pearson coefficient demonstrated that the levels of the RAS components were positively correlated with the expression of VEGF and MMP-13 in OA and RA.
This review aims to provide a summary of relevant relationships between impaired angiogenesis, OA and cartilage regeneration highlighting how VEGF might play a paramount role in the pathophysiology of cartilage aging or degeneration as well as in cartilage repair.
Significant associations of SF biomarkers meeting FDR < 0.05 included soluble (s)VCAM-1 and MMP-3 with synovial inflammation (FDR-adjusted p = 0.025 and 1.06 × 10<sup>-7</sup>); sVCAM-1, sICAM-1, TIMP-1, and VEGF with radiographic OA severity (p = 1.85 × 10<sup>-5</sup> to 3.97 × 10<sup>-4</sup>); and VEGF, MMP-3, TIMP-1, sICAM-1, sVCAM-1, and MCP-1 with OA symptoms (p = 2.72 × 10<sup>-5</sup> to 0.050).
The aim of the study was to monitor VEGF levels after the administration of allogenic cellular material (SVF) in the course of treatment of dogs suffering from degenerative joint disease in the spinal region.
TGF<i>β</i>-mediated regulation of <i>VEGF</i> expression and VEGF protein production in the SYT of OA patients occurs through both the canonical and noncanonical pathway.
Moreover, miR-210 levels are positively correlated with VEGF levels, suggesting that miR-210 might contribute to OA development through promoting VEGF expression and angiogenesis.
Thus, the results of the present study demonstrated that intraperitoneal administration of thalidomide may alleviate the development of early OA by suppressing VEGF expression in mice and may have potential as a novel therapy for the treatment of OA.
Our data indicated that VEGF expression was increased in cartilage tissue from OA rats, while the chondrocytes were disorganized, and cartilage degeneration was increasing in OA rats.
Furthermore, treatment with the TNF-α inhibitor also decreased matrix metalloproteinase (MMP)-3, MMP-9, vascular endothelial growth factor and ADAMTS4 expression in synovial fibroblasts isolated from rats with osteoarthritis.
In the normal saline (NS) and VEGF groups, animals received bilateral anterior cruciate ligament (ACL) transection to establish the OA model; at 4 weeks post‑surgery, the rats received local intra‑articular injections of 100 µl NS or VEGF solution, respectively, every week for 4 weeks.
Among these, CSN1S1, COL10A1, WIF1, and SPARCL1 were the most prominent transcripts elevated in OA meniscus, POSTN and VEGFA were most highly repressed in OA meniscus.
In vivo, KGN-NPPs demonstrate higher bioactivity than a KGN solution in a murine mechanistic OA model based on histological assessment (Osteoarthritis Research Society International score), epiphyseal thickness (microcomputed tomography), OA biomarkers (e.g., vascular endothelial growth factor, Adamts5), and prolonged intra-articular persistence (fluorescence analysis).
Patients with OA had significantly higher baseline VEGF (10.5 ± 1.2 pg/mL vs 4.8 ± 0.2 pg/mL, P < .001), MCP-1 (130.6 ± 7.7 pg/mL vs 88.6 ± 3.9 pg/mL, P < .0001), and IL-8 (4.0 ± 0.5 pg/mL vs 2.6 ± 0.1 pg/mL, P < .05).
In surgically induced knee OA in mice, a model of post-traumatic OA in humans, increased expression of VEGF is associated with catabolic processes in chondrocytes and synovial cells.
In collagenase-mediated OA pathogenesis, miR-29a-overexpressing transgenic mice showed minor responses to hyperplasia, macrophage infiltration, fibrosis, hyperangiogenesis, and VEGF expression in synovial lesions.
Furthermore, using a surgically induced OA rat model, we showed that VEGF inhibition delayed OA progression in animals given intra-articular injection of LV-VEGF shRNA.
Arthritic synovial tissues from patients with rheumatoid arthritis (RA) or osteoarthritis (OA) were immunostained with antibodies to endocan and vascular endothelial growth factor (VEGF).
Both VEGF and syndecan-4 are expressed by chondrocytes and both are involved in the regulation of matrix metalloproteinase-3, resulting in the activation of aggrecanase II (ADAMTS-5), which is essential in the pathogenesis of OA.