Eric W. Howard

Contact Information:
Eric W. Howard


Howard, Eric W. (HSC)
Associate Professor

Department of:

College Of Medicine/Cell Biology -Associate Professor

Center of:


University of California   PhD  

Professional Interest/Expertise/Specializations:
The primary focus of the lab is to understand how vascular cells communicate with each other and their environment during blood vessel remodeling. Blood vessels are composed primarily of endothelial cells and perivascular cells such as vascular smooth muscle cells (VSMCs) or pericytes. These cells are capable of altering their phenotypes during angiogenesis, then reverting back to a quiescent state after vessel maturation. New blood vessel formation initiates with angiogenic sprouts from existing vessels, and proceeds with the recruitment of VSMCs or pericytes from the base of these sprouts towards the growing tip. Platelet-derived growth factor (PDGF) expressed by endothelial cells induces VMSCs to de-differentiate from a contractile state to a migratory, proliferative state, and is the factor critical for perivascular cell recruitment during vessel maturation. In contrast, physical contact between VSMCs and endothelial cells stimulates the production and activation of transforming growth factor (TGF)-ß, which plays an important role in VSMC re-differentiation back to the contractile state. The orchestration of all of these signals is not well understood, but somehow VSMCs need to overcome PDGF-mediated de-differentiation signals in order to participate in vessel maturation. At the same time, these cells need to overcome some of the anti-proliferative signals induced by TGF-ß in order to migrate and proliferate along the newly forming vessel. We have recently found that TGF-ß is able to selectively inhibit PDGF-mediated VSMC de-differentiation, but not by blocking many of the key signaling pathways initiated by PDGF-BB. At the same time, PDGF is able to suppress selected changes in gene expression induced by TGF-ß. Our goal is to understand how vascular cells respond to the simultaneous stimulation by multiple growth factors, and how the various signaling pathways converge at the promoters of target genes, leading to changes in gene expression.


Research Projects:

Selected Publications:

Myocardin-related Transcription Factors-A and -B are Key Regulators of the TGF-ß1-Induced Fibroblast to Myofibroblast Transition.
2011    Crider, B.J., Risinger, Jr., G.M., Haaksma, C.J., Howard, E.W., and Tomasek, J. J.
Invest. Dermatol.
Autocrine Production Of Activated TGF-ß Suppresses The Up-Regulation Of MMP-2 By Vascular Smooth Muscle Cells In Response To Platelet-Derived Growth Factor-BB.
2010    Risinger, Jr., G.M., Updike, D.L., Bullen, E.C., Tomasek, J.J., and Howard, E.W.
Am. J. Physiol.-Cell Physiol.
Toxoplasma gondii activates hypoxia inducible factor by stabilizing the HIF-1 alpha subunit via type I activin like receptor kinase receptor signaling.
2010    Wiley, M., Sweeney, K.R., Chan, D.A., Brown, K.M., McMurtrey, C., Howard, E.W., Giaccia, A.J., Blader, I.J.
J. Biol. Chem.
Identification of the RLBP1 Gene Promoter.
2007    Vogel, J.S., Bullen, E.C., Teygong, C.L., and Howard, E.W.
Invest. Ophtalmol.Vis. Sci.
Matrix Metalloproteinase-2 Expression By Vascular Smooth Muscle Cells Is Mediated By Both Stimulatory And Inhibitory Signals In Response To Growth Factors.
2006    Risinger, Jr., G.M., Hunt, T.S., Updike, D.L., Bullen, E.C., and Howard, E.W.
J. Biol. Chem.