Jennifer H. Shaw

Jennifer H. Shaw, Assistant Professor

Intercellular signaling in the coronary vessel wall; Physiology & Pharmacology instruction

Ph.D., 2000, University of Montana

Phone: 405-744-5555

Email: This e-mail address is being protected from spambots. You need JavaScript enabled to view it

Specific Interests

I am primarily interested in studying the mechanisms for communication within the coronary vessel wall in healthy versus unhealthy vasculature. A critical determinant for survival following an acute coronary event caused by atherosclerotic vascular occlusion is the ability to develop coronary collateral arteries. In tissues (such as the heart) containing pre-existing collateral vessels, occlusion of an upstream supply artery results in diversion of blood flow through these vessels, protecting the distal tissue from ischemia. The sudden rise in blood flow through collateral vessels exerts shear stress upon the vessel wall, thereby providing the initial stimulus for arteriogenesis. Arteriogenesis, the structural expansion of collateral circulation, involves smooth muscle cell (SMC) proliferation which leads to increased vessel diameter and wall thickness. Since shear is sensed at the level of endothelial cells (EC), communication from EC to the underlying SMC must occur as part of this process.

Working with Dr. Pamela Lloyd (Center for Veterinary Health Sciences, Dept of Physiological Sciences) we previously reported that EC exposed to shear stress release hydrogen peroxide (H₂O₂), and that H₂O₂ can signal vascular SMC to increase gene and protein expression of placenta growth factor (PLGF), a known mediator of arteriogenesis (Shaw, JH et al, American Journal of Physiology Cell Physiology 300, C349-C355). In follow up studies, we found that H₂O₂ regulates PLGF at the post-transcriptional level and relies, in part, on p38 MAPK, JNK and ERK1/2 pathways in human coronary artery smooth muscle (Shaw, JH & Lloyd, PG, Microvascular Research 84: 155-160). Future studies will focus on communication within the vessel wall via connexins, also known as gap junctions, under healthy and pathological conditions such as oxidative stress, low shear stress, hyperglycemia and hypercholesterolemia.

In the classroom, I have the privilege to teach students in Mammalian Physiology (ZOO 4215) each spring semester where I strive to build concrete analogies to make abstract physiological concepts easier to digest and facilitate critical thinking to prepare students for a future in the health sciences. Other courses that I have taught include lectures on pharmacodynamics, anti-inflammatory drugs, anti-arrhythmic drugs, respiratory drugs and gastrointestinal drugs in Veterinary Pharmacology (VMED 7333, 7432) as well as lectures on skeletal, smooth and cardiac muscle in Veterinary Physiology (VMED 7114).

Selected Publications

Shaw JH, Lloyd PG. Post-transcriptional regulation of placenta growth factor mRNA by hydrogen peroxide. Microvascular Research 84 (2012) 155-160.
Shaw JH, Lloyd PG. PLGF is regulated by hydrogen peroxide at the post-transcriptional, but not the transcriptional, level in vascular smooth muscle. FASEB Journal Mar 2012, 26:863.5.
Shaw JH, Xiang L, Shah A, and Lloyd PG. Placental growth factor expression is regulated by hydrogen peroxide in vascular smooth muscle cells. American Journal of Physiology 2011 Feb; 300(2):C349-55.
Shaw JH and Lloyd PG. Hydrogen peroxide increases PLGF mRNA half-life via a p38 and ERK1/2 kinase dependent mechanism. FASEB Journal Mar 2011, 25:821.36.
Rasdan NA, Soulek JJ, Shaw JH, and Lloyd PG. PLGF expression in coronary artery smooth muscle cells is sensitive to changes in shear stress. FASEB Journal Mar 2011, 25:1b462.
Rubenstein DA, Mujib T, Shaw JH, Lloyd PG and Yin W. Altered gravity promotes platelet-endothelial cell interactions that precede cardiovascular diseases. FASEB Journal Mar 2011, 25:668.5.
Shaw JH and Lloyd PG. Reactive oxygen species regulate PlGF and VEGF expression in human coronary artery smooth muscle cells. FASEB Journal Apr 2010, 24:1031.9.
Shaw J, Grund V, Durling L, Crane D, Caldwell HD. Infect Immun. 2002 Mar: 70(3): 1097-105. Dendritic cells pulsed with a recombinant chlamydial major outer membrane protein antigen elicit a CD4(+) type 2 rather than type 1 immune response that is not protective.
Shaw JH, Grund VR, Durling L, Caldwell HD. Infect Immuno. 2001 Jul: 69(7):4667-72. Expression of genes encoding Th1 cell-activating cytokines and lymphoid homing chemokines by chlamydia-pulsed dendritic cells correlates with protective immunizing efficacy.