Dr. Thomas J. Jones is an Assistant Professor in the Department of Pharmaceutical Sciences at the Northeastern Ohio Universities College of Pharmacy. Dr. Jones earned his Ph.D. from the Medical College of Ohio in 2004, completed a post-doctorate at The University of Pittsburgh, School of Pharmacy in 2004 and The University of Pittsburgh, School of Medicine in 2006.
|
| 2004 | Ph.D. (Molecular and Cellular Biology), Medical College of Ohio |
| 1997 | MS. (Biology), The University of Akron, OH |
Professional Experience:
| 2008–present | Assistant Professor of Pharmaceutical Sciences, Northeastern Ohio Universities College of Pharmacy, Rootstown, OH |
| 2006–2008 | Visiting Assistant Professor, College of Pharmacy, Department of Pharmacology, The University of Toledo |
| 2004-2006 | Post-doctorate, The University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania |
| 2004 | Post-doctorate, The University of Pittsburgh, School of Pharmacy, Pittsburgh, Pennsylvania |
Honors:
Molecular Pahogenesis of Cancer Training Program
National Institutes of Health (2002-2003)
Department of Biochemistry and Molecular Biology
Research Interests:
The focus of my research involves the investigation of Cilia Biology in the Development of Hypertension and Cardiovascular Disease through the modulation and Molecular Signaling of Heat Shock Proteins and Steroid Receptor.
Our research goal is to understand the role of primary cilia as a stress signaling organelle and it potential role in vascular disease and remodeling. I am interested in understanding how changes in primary cilia, under various stress conditions affects the small hsp, hsp27, and shapes a cells adaptive response to stress. The comprehensive goal is to propose a role for cilia in the development and genesis of essential hypertension through changes in vascular cilia. Research will evaluate primary cilia in the development of multiple genetic models of essential hypertension through scanning electron microscopy (SEM), immunoblottin, and mRNA analysis. Initial projects revolve around the use of primary cell culture from normal and cilia knock out mouse endothelial cells (Tg737orpk/orpk and/or Pkd2null/null).
It is well understood that cells have devised a defense mechanism to respond to stressful events through the induction of heat shock proteins (hsps). The small hsp, hsp27, is one member of that family that functions to maintain, modulate, and stabilize the cytoskeleton along with the ability to modulate apoptotic pathways and actin myosin interactions. Heat shock proteins themselves are induced through the activation of heat shock factor 1 (HSF1), the major stress activated protein. Stressors such as mechanical stress, heat, oxidizing conditions, or toxic agents that are deleterious to a cells survival can activate HSF1 and induce hsps. The induction of the hsps is the cellular defense mechanism that provides the time necessary for cells to adapt to their changing environment and the stress.
Primary cilia are once thought vestigial organelles that function like antenna extending out into the extra cellular fluid. These finger-like appendages expand the area of extracellular contact and provide an enriched signaling mechanism by which a cell can sense and be influenced by its environment. Cilia themselves are found on almost every cell type including endothelial cells lining blood vessels and the collecting duct of the kidney. Their ability to function as a sensory organelle correlated with their length. Cilia length in turn, facilitates the ability of cells to sense mechanical or chemical stress. Cilia participate in cellular sensing of mechanical stresses (mechansensor) like blood flow and chemical stresses (chemosensor) like growth factors, hormones, as well as osmolarity. The sensory functions of cilia lead to the activation of multiple kinase pathways in addition to changes in eNOS and Ca+2 storage and release. Defects or the absence of cilia have been shown to contribute to multiple disease state, which has lead to the term ciliopathies. Some of these disease states include polycystic kidney disease, infertility, and respiratory disease, and secondary hypertension.
