PDGF-D contributes to neointimal hyperplasia in rat model of vessel injury

Expression of platelet‐derived growth factors C and D in the synovial membrane of patients with rheumatoid arthritis and osteoarthritis

“…Indeed, in the present study, stimulation with PDGF-D increased the expression of MMP-1 mRNA in RA synovial fibroblasts. Similar results for PDGF-D have been reported in the case of MMP-2 in vascular smooth muscle cells (31), for MMP-9 in renal carcinoma cells (33), as well as for PDGF-C with respect to MMP-1 expression in dermal fibroblasts (32). Taken together, these findings indicate the relevance of the protease-activated PDGF isoforms in tissue remodeling, a process of major importance during the progression of arthritic diseases.…”

“…Because both PDGFRs are expressed in the rheumatoid synovium (14), it is conceivable that binding of PDGF-D, and possibly also PDGF-C, to their receptors contributes to the proliferation and semitransformation of cells that is observed during pannus formation in RA (11). This hypothesis is further supported by the finding that the PDGF-D core protein stimulated the proliferation of synovial fibroblasts, as was previously shown for vascular fibroblasts transfected with the PDGF-D gene (31).…”

Cytochrome P450 1B1 Contributes to the Development of Angiotensin II–Induced Aortic Aneurysm in Male Apoe−/− Mice

“…29,30 It stimulates VSMC migration and proliferation, monocytes/macrophage recruitment, and increased secretion of MMPs in various cell types. 46,47 Although we did not assess the involvement of VSMCs specifically in this study, we did observe enhanced macrophage and T-cell infiltration and MMP expression at the site of aortic lesion. PDGF also activates Itga2, 48 which is crucial for platelet aggregation/adhesion.…”

Interleukin-1β modulates smooth muscle cell phenotype to a distinct inflammatory state relative to PDGF-DD via NF-κB-dependent mechanisms

“…In addition, in vivo blockade of PDGF-BB or PDGFR-␤ reduces SMC migration into neointimal lesions after vascular injury and decreases SMC accumulation and fibrous cap formation within developing atherosclerotic plaques in mice (25,37,54,66,69). Recent studies have demonstrated that PDGF-DD, a newly discovered PDGF isoform that is a more selective agonist of the PDGFR-␤, also promotes SMC phenotypic modulation through repressing SMC differentiation marker gene expression and increasing SMC proliferation and migration (5,13,38,73). Genetic deletion of the PDGFR-␤ in cultured SMCs abrogated PDGF-DD-and PDGF-BB-induced repression of SMC differentiation marker genes, suggesting that these effects of PDGF on SMC phenotype are mediated via PDGFR-␤ activation (73).…”