Rabbit Anti-Human FSTL1 (a.a. 751-847) Polyclonal antibody

Follistatin-like protein 1 (FSTL1) showed overexpression in the inflammatory synovial pannus, serum, and synovial tissues of osteoarthritis (OA) patients. However, FSTL1 knock out (KO) embryos exhibited reduced vertebral cartilage cellularity, extensive skeleton defects and reduced MSCs proliferation. Thus, the role of FSTL1 in chondrocyte proliferation is not completely understood. In vitro studies revealed that Human recombinant FSTL1 (hFSTL1) promoted chondrogenic signals in the MSCs and cell viability only at low concentrations. Recent reports suggest that high levels of FSTL-1 are proposed to enhance inflammatory signals which suppress chondrogenesis leading to cartilage destruction. Altogether, FSTL1 has the potential to promote MSC proliferation and chondrogenic differentiation in a low concentration-dependent manner. However, the mechanism by which FSTL-1 affects MSCs chondrogenic differentiation and chondrogenesis remains unknown. Therefore, this review introduces a deep discussion of FSTL1's molecular functions in the OA pathophysiology, which will contribute to the deep understanding of FSTL1 molecular activity in the OA pathogenesis.

BackgroundMulti-walled carbon nanotube (MWCNT)-induced lung fibrosis leads to health concerns in human. However, the mechanisms underlying fibrosis pathogenesis remains unclear. The adenosine (ADO) is produced in response to injury and serves a detrimental role in lung fibrosis. In this study, we aimed to explore the ADO signaling in the progression of lung fibrosis induced by MWCNT.ResultsMWCNT exposure markedly increased A(2B) adenosine receptor (A(2B)AR) expression in the lungs and ADO level in bronchoalveolar lavage fluid, combined with elevation of blood neutrophils, collagen fiber deposition, and activation of myeloperoxidase (MPO) activity in the lungs. Furthermore, MWCNT exposure elicited an activation of transforming growth factor (TGF)-1 and follistatin-like 1 (Fstl1), leading to fibroblasts recruitment and differentiation into myofibroblasts in the lungs in an A(2B)AR-dependent manner. Conversely, treatment of the selective A(2B)AR antagonist CVT-6883 exhibited a significant reduction in levels of fibrosis mediators and efficiently decreased cytotoxicity and inflammatory in MWCNT treated mice.ConclusionOur results reveal that accumulation of extracellular ADO promotes the process of the fibroblast-to-myofibroblast transition via A(2B)AR/TGF-1/Fstl1 signaling in MWCNT-induced lung fibrosis.