Mechano Growth Factor (MGF)

MGF promotes PDLSC proliferation and fibrogenic differentiation by inducing Fyn-YAP Y357 phosphorylation.; Fyn activates YAP indirectly through RhoA in response to MGF stimulation.; The Fyn-RhoA-p-YAP Y357 pathway is significant for MGF-mediated PDLSC proliferation and differentiation.

MGF produced under occlusion force strongly enhances PDL remodeling in vivo.; MGF promotes PDLSC differentiation toward fibroblasts, confirmed by in vitro experiments and mathematical modeling.; The mechanochemical coupling effect is modulated by Fyn-FAK kinases signaling and subsequent MAPK pathway, including ERK1/2 and p38 phosphorylation.; MGF-centered adjuvant treatment could optimize PDL remodeling, especially for patients with weakened bite force or destroyed periodontium.

MGF is highly expressed in chondrocytes of damaged cartilage from trauma or osteoarthritis.; MGF regulates chondrocyte behaviors including proliferation, migration, differentiation, inflammation, and apoptosis.; MGF senses mechanical stimuli and helps maintain cartilage homeostasis under normal joint conditions.; The role of MGF in cartilage development and disease is still controversial and its mechanisms are elusive.

Aligned collagen topology induces BMSC elongation and facilitates osteogenic differentiation.; Aligned collagen-grown BMSCs show transcriptome correlation with periosteum-derived stromal cells and elevated PDSC marker expression.; Cell-extracellular matrix interaction is the major pathway initiating the osteo-friendly microenvironment.; Aligned collagen induces mechano-growth factor expression through Igf1 alternative splicing, guiding progenitor cell behavior.

At 4.5 mg/kg/day, the S/E and S/A peptides produced opposing effects on cardiac systolic and diastolic function, with no significant change in cardiac geometry.; Microarray analysis identified 21 genes differentially expressed in line with the opposing contractile effects, including Nr4a2, and E-domain peptides modulated Nr4a gene expression after KCl depolarization in vitro.; The S/A peptide destabilized 14-3-3 protein folding and inhibited its interaction with MYPC3 and PLN, while the S/E peptide only inhibited MYPC3 interaction; pSer18 increased 14-3-3 stability.

Injurious mechanical stretch reduced ACL fibroblast cell area, roundness, migration, and adhesion, which were improved by MGF (10, 100 ng/mL) treatment.; MGF improved expression of cell mobility-relevant molecules (PAK1/2, Cdc42, Rac1, RhoA, ROCK1), especially ROCK1, after injurious stretch.; In a rabbit partial ACLT model, MGF accelerated ACL regeneration and restored mechanical loading capacity after four weeks.

CoCl2-simulated severe hypoxia inhibited chondrocyte viability, proliferation, and type II collagen expression while inducing apoptosis and expression of HIF-1 alpha, type I collagen, and MMP-1/13.; MGF E peptide pretreatment reduced these adverse effects and upregulated chondrocyte proliferation under severe hypoxia via the PI3K-Akt and MEK-ERK1/2 signaling pathways.; In MIA-induced OA rats, MGF E peptide retarded cartilage degeneration, upregulated type II collagen synthesis, and improved ECM distribution after 4 or 6 weeks.; The findings suggest MGF attenuates OA progression and may have clinical application for OA treatment.

What is Mechano Growth Factor (MGF)?

Mechano Growth Factor (MGF), also known as IGF-1Ec, is a splice variant of insulin-like growth factor-1 (IGF-1) that is upregulated in response to mechanical stress or muscle damage. Its mechanism of action involves binding to the IGF-1 receptor, which activates downstream signaling pathways such as PI3K/Akt, leading t

How does Mechano Growth Factor (MGF) work?

Mechanically activated IGF-1 splice variant that activates muscle satellite cells for repair and hypertrophy.

What is the research status of Mechano Growth Factor (MGF)?

Mechano Growth Factor (MGF) is currently classified as preclinical, with 194 research references on record. This is for research purposes only and is not medical advice.