Key protein to speed up wound healing
Tuesday 21 November, 2017
Peer Reviewed

Key protein to speed up wound healing

Published On: Sun, Dec 7th, 2014 | Cell Biology | By BioNews

An Indian-origin doctor has discovered the key role a protein related to the immune system plays in healing, paving the path for manipulating the immune system to speed up the healing process.

The findings could also lead to novel treatment for infectious and autoimmune diseases.

The current study results revolve around proteinases which are enzymes that break down proteins as part of cellular life.

The team found that Matrix metalloproteinases (MMP) 2 has another signalling role related to the human immune system.

“Our results show that MMP-2 uses a multitude of mechanisms to modulate the immune system,” said lead investigator Nina Bhardwaj, director of immunotherapy at Tisch Cancer Center at Mount Sinai.

MMP-2 may shift a set of cells to become part of immune response that accelerates healing in some cases, but may worsen inflammatory disease in others.

Drug designers may be able to leverage the newfound MMP-2 mechanisms to prevent the contribution of inflammatory signals to tumour growth and autoimmune diseases, or to promote wound healing, the researchers noted.

“These data provides context to how this mechanism happens and could lead to novel treatments,” Bhardwaj added.

The study appeared in the journal Cell Reports.


Scientific Summary
Godefroy E, Gallois A, Idoyaga J, Merad M, Tung N, Monu N, Saenger Y, Fu Y,Ravindran R, Pulendran B, Jotereau F, Trombetta S, Bhardwaj N. Activation of Toll-like Receptor-2 by Endogenous Matrix Metalloproteinase-2 Modulates Dendritic-Cell-Mediated Inflammatory Responses. Cell Rep. 2014 Nov 26. pii: S2211-1247(14)00936-X.

Matrix metalloproteinase-2 (MMP-2) is involved in several physiological mechanisms, including wound healing and tumor progression. We show that MMP-2 directly stimulates dendritic cells (DCs) to both upregulate OX40L on the cell surface and secrete inflammatory cytokines. The mechanism underlying DC activation includes physical association with Toll-like receptor-2 (TLR2), leading to NF-?B activation, OX40L upregulation on DCs, and ensuing TH2 differentiation. Significantly, MMP-2 polarizes T cells toward type 2 responses in vivo, in a TLR2-dependent manner. MMP-2-dependent type 2 polarization may represent a key immune regulatory mechanism for protection against a broad array of disorders, such as inflammatory, infectious, and autoimmune diseases, which can be hijacked by tumors to evade immunity.

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