- Research conducted by MCRI investigators on the ways in which hormones like estrogen act directly on the blood vessels and heart have altered how scientists and clinicians think about and design hormone replacement therapies and has led to new approaches in the pharmaceutical industry to develop more effective and safer approaches to medicines for women's health.
- Investigators within the MCRI recently identified a protein called striatin that plays a key role in allowing the estrogen receptor to interact with and bind to other proteins that mediate the effects of estrogen in cells in the blood vessel and other tissues.
- MCRI investigators have been studying how blood vessels relax and contract for nearly 20 years. MCRI investigators have discovered several important mechanisms of vascular smooth muscle relaxation in response to nitrovasodilators. These mechanisms involve, in many cases, a critical molecule that regulates vessel tone, called cyclic GMP-dependent protein Kinase I (PKGI). New drugs will likely be developed using information about PKGI in blood vessels.
- MCRI researchers discovered a new regulatory molecule for blood vessel relaxation, called Myosin Phosphatase-rho Interacting Protein (M-RIP) which has at least two important targeting functions. It localizes the myosin phosphatase complex to the actinomyosin contractile complex to dephosphorylate myosin, and it links the RhoA/ROCK pathway with myosin phosphatase, allowing RhoA/ROCK to inhibit myosin phosphatase activity in response to vasoconstrictors.
- Researchers within the MCRI have discovered that a specific class of protein hormones, named BMPs, prevents smooth muscle cells from growing too much and losing their ability to regulate blood pressure. This work continues with study of the requirement of BMPs for maintenance of vascular smooth cell function and the molecular mechanism by which BMPs act.
- Recent studies have implicated a potential role of Toll-like receptors (TLRs), receptors that are expressed by immune cells and activated by microbial products, in the pathogenesis of atherosclerosis. MCRI researchers have shown that vascular smooth muscle cells also express several TLRs, and that activation of these receptors upon exposure to microbial products elicits dramatic changes in smooth muscle cell phenotype, including cell proliferation and synthesis of chemokines, phenotypic changes similar to those that contribute to vascular disease.