ITGB3 (integrin β3) is regulated by the Polycomb protein CBX7 •β3 regulates senescence by activating TGF-β in a paracrine and autocrine fashion •β3 is highly expressed in OIS and induces senescence via ligand-independent pathway •There is a positive correlation between β3 levels and aging in different tissues
A protein has been found to have a previously unknown role in the aging of cells, according to an early study by Queen Mary University of London (QMUL). The researchers hope that the findings could one day lead to new treatments for aging and early cancer. A number of ‘abnormal’ cells have previously been found in tissues derived from old patients and at the initial stages of cancer. These cells suffer a growth arrest ie senescence, which is thought to affect how the tissue functions. Senescent cells fail to proliferate, but they manage to communicate with their neighbouring cells, mainly through the release of inflammatory proteins.
The study, published in Cell Reports, describes a new way that senescent cells communicate, which is via the expression of integrin membrane proteins, including a protein called integrin beta 3′ which is highly expressed during senescence. “This finding is particularly interesting, as there is actually a drug against integrin beta 3, called ‘cilengitide’, that averts one of the disadvantages of aging in our model – inflammation. It does this without increasing cell proliferation, which is an advantage, as an increase in cell proliferation imposes a risk for cancer.”
The study was performed using human primary fibroblasts and fibroblast cells derived from young and old human donors. The researchers discovered how integrin beta 3 was regulated and the signaling mechanism it uses to transmit senescence to surrounding cells. They could also see that integrin beta 3 was ‘upregulated’ in a subset of tissue from mice, confirming the importance of their results in two different species. http://www.qmul.ac.uk/media/news/items/smd/193510.html
Recent Comments