Dr. Jones is an professor in the Department of Surgery and a Research Health Scientist in the VA Research Service. Dr. Jones received his BA in Microbiology from the University of California San Diego, and his PhD in Biochemistry and Molecular Biology from the Medical University of South Carolina. He completed his graduate and post-doctoral training under Dr. Yusuf Hannun, studying protein-lipid interactions and sphingolipid signaling. Dr. Jones accepted a faculty appointment in the Division of Cardiothoracic Surgery in 2005. His research focuses on pathogenic mechanisms that drive extracellular matrix remodeling in the development of cardiovascular disease, with particular interest in thoracic aortic aneurysms.
Specifically he investigates mechanisms of thoracic aortic aneurysm (TAA) development related to aberrant TGF-b signaling and fibroblast transdifferentiation. Evidence from this laboratory and others, has implicated altered TGF-b signaling in TAA development. Examination of the TGF-β signaling pathway in an established murine model of TAA revealed alterations in TGF-β receptor abundance, shifting the signaling from a TGF-βRI to an ALK-1-mediated response that was coincident with TAA expansion. Importantly, recent data have suggested that this shift in TGF-b signaling through the ALK-1 pathway may result in the increased production of specific matrix metalloproteinases (MMPs) that contribute to the aberrant vascular remodeling occurring during TAA development.
His current focus will extend these results and will determine how increased MMP production mediates the release of TGF-b that is sequestered in the extracellular matrix. Using specific reagents designed to inhibit MMP activity and TGF-b signaling, as well as a conditional fibroblast-specific tamoxifen-inducible Cre-recombinase mouse, he will determine the cause-effect relationships between MMP activity, TGF-b signaling, myofibroblast transdifferentiation, and TAA formation and progression. The outcomes will provide exceptional insight into the development of TAA and may identify a cell-type and a significant signaling pathway through which TAA formation and progression can be attenuated.