Study summary · research use only
Pretreatment with mechano growth factor E peptide attenuates osteoarthritis through improving cell proliferation and extracellular matrix synthesis in chondrocytes under severe hypoxia
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This laboratory study examined severe hypoxia and pretreatment with mechano growth factor (MGF) E peptide in chondrocytes (species not specified) and in a monosodium iodoacetate (MIA)-induced osteoarthritis rat model. In chondrocytes, cobalt chloride-simulated severe hypoxia was associated with inhibited cell viability, proliferation, and type II collagen expression, and increased apoptosis and expression of hypoxia inducible factor 1 alpha, type I collagen, and matrix metalloproteinases 1/13; MGF E peptide pretreatment reduced these changes and increased proliferation via the PI3K-Akt and MEK-ERK1/2 pathways. In the rat model, MIA treatment was associated with tissue necrosis, cartilage degeneration, reduced histological score, and reduced type II collagen and aggrecan after 4 or 6 weeks; MGF E peptide was associated with reduced MIA-induced cartilage degeneration and increased type II collagen synthesis after 4 or 6 weeks.
Abstract
Osteoarthritis (OA) is characterized by pain and declining gait function associated with degeneration of cartilage. A severe hypoxic environment occurs due to tissue injury in the joint cavity and may aggravate the development of OA. In this study, the effects of severe hypoxia and treatment with mechano growth factor (MGF) E peptide on metabolism of the extracellular matrix (ECM) during the progression of OA were determined. The results showed that cell viability, cell proliferation, and type II collagen expression in chondrocytes were significantly inhibited by cobalt chloride (CoCl2)-simulated severe hypoxia, whereas cell apoptosis and expression levels of hypoxia inducible factor 1 alpha, type I collagen, and matrix metalloproteinases 1/13 were clearly induced. Pretreatment with MGF E peptide reduced the abovementioned adverse effects induced by CoCl2-simulated severe hypoxia in chondrocytes. Pretreatment also upregulated the proliferation of chondrocytes under severe hypoxia through the PI3K-Akt and MEK-ERK1/2 signaling pathways. In a rat model of monosodium iodoacetate (MIA)-induced OA. MIA treatment induced tissue necrosis and cartilage degeneration, and histological score was significantly decreased. The levels of type II collagen and aggrecan were reduced after MIA treatment for 4 or 6 weeks, and abnormal distribution of ECM occurred in the inner epicondyle after 6 weeks. MGF E peptide also reduced the progression of MIA-induced OA by retarding cartilage degeneration, upregulating type II collagen synthesis, and improving ECM distribution after 4 or 6 weeks. Our findings suggest that MGF attenuates the progression of OA, and thus may be applied for the treatment of OA in the clinic.
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