Growth Of Synovial Fibroblasts Research Articles

Pure Platelet and Leukocyte-Platelet-Rich Plasma for Regenerative Medicine in Orthopedics-Time- and Preparation-Dependent Release of Growth Factors and Effects on Synovial Fibroblasts: A Comparative Analysis.

Intra-articular injections of autologous platelet concentrates are considered capable to enhance the healing of cartilage lesions, alleviate joint inflammation, and relieve other musculoskeletal pathological conditions. The aim of this study was to analyze the soluble fractions obtained from platelet-rich plasma (pure- and leukocyte-PRP) to compare time- and preparation-dependent modifications of growth factor concentrations and the supporting activity of the two preparations on synovial fibroblast growth and hyaluronic acid (HA) production in vitro. The release kinetics of FGF-2, SDF-1, VEGF, HGF, EGF, PD GF-AB/BB, IGF-1, VCAM-1, and TGF-β isoforms were followed up to 168 h after PRP activation, and their amounts were determined by multiplex-beads immunoassay. Synovial cell growth and supernatant HA production were respectively analyzed by Alamar Blue assay and ELISA. Time-dependent modifications grouped molecules in three peculiar patterns: one reaching the highest concentrations within 18 h and decreasing afterwards, another progressively increasing up to 168 h, and the last peaking at the central time points. Synovial fibroblast growth in response to L-PRP and P-PRP revealed differences over time and among added concentrations. Both preparations displayed a preserved supporting capacity of HA synthesis.

Downregulation of lymphocyte activity and human synovial fibroblast growth in rheumatoid arthritis by triptolide

Downregulation of lymphocyte activity and human synovial fibroblast growth in rheumatoid arthritis by triptolide

The Mechanism of Glucocorticoid Effects in Fibroblasts

In vivo, the glucocorticoid steroids inhibit fibroblast growth and the production of specific cell products such as collagen and mucopolysaccharide. Depending on the source of the fibroblasts and their growth conditions, several responses can be observed in cultured cells; the proliferation of L cells is inhibited, the growth of synovial fibroblasts is usually stimulated, and some cultured fibroblasts do not respond. The inhibition of L cell growth is preceded by alterations in the rates of hexose and amino acid transport. As in other cell types, there is evidence that the effects of glucocorticoids in fibroblasts are mediated via the induction of new protein synthesis. The specific induced proteins responsible for inhibiting the growth of mouse L929 fibroblasts (or any other cell type) have not been identified. It is possible that glucocorticoids induce the synthesis of a few proteins that, by virtue of their ability to modify (either during or after translation) other proteins involved in several key cellular events, are able to compromise multiple systems and produce growth inhibition. Glucocorticoid-mediated alteration of protein phosphorylation could account for the pleiotropic nature of the hormone effect. To cause a glucocorticoid-specific response in the cell, these hormones must first bind to a cellular receptor. A significant amount of evidence suggests (a) that glucocorticoid receptors may undergo an energy-dependent cycling in the cell and (b) that a single receptor may be able to participate several times in the process of steroid binding and gene activation. Maximal physiological response to, and consequently the clinical response achieved with, a glucocorticoid is usually a function of the extent to which the hormone can be bound in a specific manner. Investigators have proposed that the specific glucocorticoid-binding capacity of a cell is determined by a phosphorylation-dephosphorylation mechanism.