Scientists then studied how injections of TGF-beta in lab rats accelerated fibrotic scarring at a wound site.
Mice that were bred without the gene for TGF-beta scarred less and soon died from severe inflammation.
InterMune's entry, Actimmune, suppresses production of TGF-beta by disrupting the signals inside the factorylike fibroblast cells that make it.
The latest work revolves around two culprit proteins, transforming growth factor beta (TGF-beta) and connective tissue growth factor (CTGF).
He found that once TGF-beta activated a cell, it triggered the CTGF gene to make its protein (see chart).
The best part: CTGF, concerned primarily with spreading collagen production to neighboring cells, had a much more limited role than TGF-beta.
TGF-beta was one of the first proteins to show up at the wound, leading a cascade of molecules that produce collagen.
An experimental new class of drugs is aimed at rendering TGF-beta and CTGF ineffective by blocking their ability to bind with cell receptors.
In the late 1970s several researchers made an important breakthrough when they stumbled onto TGF-beta while studying the relationship between cancer and tumor growth.
During this period Gary Grotendorst , then an assistant professor at the Medical University of South Carolina, was testing TGF-beta's relationship to other growth factors.
By 1992 Grotendorst, who had done work at the University of South Florida and is now at the University of Miami, concluded that it was CTGF, not TGF-beta, that triggers collagen production by binding to specific cell receptors.
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