The Tufts Center for Innovations in Wound Healing Research

Recent work from the Tufts Center for Innovations in Wound Healing Research has revealed that two novel peptides combine to synergistically accelerate wound healing using an in vivo model of impaired healing.  This work was recently published in PLoS One ( http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0032146 ) and was recently covered globally ( https://www.google.com/search?q=novel+bioactive+wound+healing+peptide&ie=utf-8&oe=utf-8&aq=t&rls=org.mozilla:en-US:official&client=firefox-a )

Work ongoing at the Center for Innovations in Wound Healing Research was recently highlighted in Technology Review

Recent work reveals that wound healing dynamics are tightly and reciprocally regulated. In particular, cellular components within the epidermal and dermal wound microenvironments transduce signals that control extracellular matrix remodeling and wound healing dynamics. In turn, these cellular and extracellular signaling cascades control whether or to what extent wound repair progresses or is chronically impaired. In this recent report, we consider these key aspects of dynamic reciprocity.

Newly-created bioactive peptides promote wound healing through the growth of new blood vessels and epithelial tissue, such as skin. These wound-healing peptides, synthesized by researchers at the Tufts Center for Innovations in Wound Healing Research promote re-epithelialization and wound healing angiogenesis as reported online in Wound Repair and Regeneration

News Release

News Release

In a recent report that was published in Microvascular Research http://www.ncbi.nlm.nih.gov/pubmed/20709086 (ePub ahead of print), we have revealed a key relationship between the control of microvascular pericyte shape, contractility and mechanical stiffness. The work points to the pivotal role that the neutral cysteine protease family member, calpain I, is likely to be playing in modulating pericyte adhesion and signaling (to/through the basement membrane and onto the capillary endothelium). We postulate that these mechano-chemical signaling networks that originate within pericyte cytoplasm and the plasma membrane-cytoskeletal interface are likely to orchestrate capillary dynamics during physiologic or, possibly, pathologic angiogenesis.

Posted on: Tuesday, 15 June 2010, 09:35 CDT

Cell contractions may be key to initiating new blood-vessel growth near tumors.

Cancer researchers have been studying angiogenesis — the growth of new blood vessels — since the early 1970s, when Judah Folkman first theorized that tumors could be destroyed by cutting off their blood supply.

For most of that time, scientists have focused on the biochemical signals that promote angiogenesis, in hopes of finding drugs that can starve tumors by blocking their ability to release the proteins that promote vessel growth. More recently, a few scientists have taken a new approach: studying how contractions in nearby cells can stimulate angiogenesis.

Krystyn Van Vliet, associate professor of materials science and engineering at MIT, and researchers at Tufts University recently showed that cells called pericytes, which surround small blood vessels, generate contractions that could serve as a mechanical signal to initiate angiogenesis. “Up to now, people have assumed that the role of pericytes was biochemical in nature,” says Van Vliet.

Pinpointing the role of those mechanical signals could help researchers develop drugs that either promote angiogenesis to enhance wound healing or suppress the harmful angiogenesis that leads to tumor growth or vision loss (in age-related macular degeneration or diabetes-induced retinal damage), says Ira Herman, a professor of physiology at Tufts University School of Medicine and expert in pericyte cell biology who collaborated with Van Vliet on this study.

http://article.wn.com/view/2010/06/15/Researchers_seek_to_put_the_squeeze_on_cancer/

http://www.redorbit.com/news/health/1879653/putting_the_squeeze_on_cancer/

http://www.newswise.com/articles/cellular-mechanical-forces-may-initiate-angiogenesis