Characterization of plasma fibronectin for migration, proliferation, and differentiation on human articular chondrocytes

Abstract

Plasma fibronectin (pFN) plays a crucial role in wound healing by binding to integrins and inducing cell migration. It is known to induce the migration and proliferation of mesenchymal progenitor cells in vitro, which play a key role during microfracture in cartilage repair. Endogenous chondrocytes from the native cartilage of the defect rim might aid in cartilage repair. In this study, the effect of pFN on proliferation, migration, and differentiation was tested on human articular chondrocytes. Results showed that treatment with pFN increased the migration of chondrocytes in a range of 1-30 μg/ml as tested with no effect on proliferation. TGFβ3-induced chondrogenesis was not affected by pFN. Especially, gene expression of matrix metalloproteinases was not increased by pFN. Plasma FN fragmentation due to storage conditions could be excluded by SDS-PAGE. Moreover, bioactivity of pFN did not alter during storage at 4°C and 40°C for up to 14 days. Taken together, pFN induces the migration but not proliferation of human articular chondrocytes with no inhibitory effect on chondrogenic differentiation. Additionally, no loss of activity or fragmentation of pFN was observed after lyophilization and storage, making pFN an interesting bioactive factor for chondrocyte recruitment.

Single-cell RNA sequencing reveals hub genes of myocardial infarction-associated endothelial cells

“…Consistent with the findings of previous literature, Timp1 knockdown was revealed to promote the migration and tube formation of HUVECs, but its specific mechanism is still unclear. Fibronectin 1 (Fn1), as a member of the glycoprotein family [ 31 ], is essential for cell growth, differentiation, and plays an important part in wound healing [ 32 ]. As reported, VEGF regulated Fn1 to affect the proliferation, migration and angiogenesis of HUVECs [ 33 ].…”