Dr. Standley trained as a vascular physiologist at Wayne State University School of Medicine in Detroit, Michigan. His first faculty appointments were in the Departments of Physiology and Internal Medicine where he continued his work investigating the vascular effects of insulin and its actions as a calcium channel blocking agent. Upon his arrival to Arizona in 1996, he helped found and develop a new innovative medical physiology curriculum at Midwestern University. During his tenure at MWU, his research gained new focus in the field of biophysical regulation of gene expression in vascular smooth muscle. In 2006, Dr. Standley was recruited to the University of Arizona College of Medicine - Phoenix to help found its new medical school track. He currently serves as Director of Preclinical Block Curriculum and the Block Director for the Cardiovascular/Pulmonary/Renal Block in the year I medical curriculum. He also holds appointments as a professor at Arizona State University’s School of Life Sciences and A.T. Still University. Dr. Standley follows a student-centric philosophy and takes great passion in helping mentor individuals to pursue advancement and excellence in their educational goals. He has taught medical students in all disciplines of medical physiology for 20 years. In 2009 he was awarded both the Virginia and Vernon Furrow Award for Excellence in Basic Science Teaching for Medical Students and Outstanding Teaching by a Professor- Class of 2012. Dr. Standley also shares a strong passion for research. He received the 2006 Irvin M. Korr National Research Award for Outstanding Basic Science Researcher and the 2008 George W. Northup Award in Medical Writing – JAOA Research Paper of the Year. He is a gifted speaker and is invited to present at several national and international conferences each year to share research with his colleagues. He is a member of numerous professional organizations including the American Heart Association, the American Society of Hypertension, and the American Physiological Society. His current NIH- and AOA- funded research focuses on the biophysical regulation of gene expression and cell growth in vascular smooth muscle, fibroblasts and skeletal muscle cells.

Beneath the fascia lie skeletal muscle, the source of hypertonicity and clinically palpable restrictions resulting from immobilization, anatomical strains, and injury. Recent reports suggest that skeletal muscle myoblast differentiation into functional muscle, as well as skeletal muscle contraction, are modulated by a variety of paracrine and systemic cytokines and growth factors. As we have shown that fascial fibroblasts - which exist under injurious and treatment-directed biomechanical strains - are a rich source of such modulators, we are currently investigating how injurious biomechanical strain induces human fibroblast cytokine and growth factor secretion that, in turn, locally retard human skeletal muscle differentiation and inappropriately enhance skeletal muscle cell sensitivity to contractile stimuli, and that IL-6 is the key mediator of these responses. Further, we are investigating whether fibroblasts exposed to modeled MMT attenuate or reverse these skeletal muscle responses to injurious strain in a similar paracrine manner. To test these hypothesizes we have developed a co-culture system that strains human fibroblasts and allows resulting paracrine secretory products to be within diffusible range of human skeletal myoblasts and myotubes. We are currently determining potential regulation of (a) myoblast differentiation into myotubes, (b) skeletal muscle contractility in response to contractile agonists, and (c) acetylcholine receptor (AChR) content and clustering.
Collaborating with Sarver Heart Center in Tucson and Theregen Inc. we are investigating a novel approach to cell-based therapy for heart failure wherein we implant a bioabsorbable vicryl patch embedded with dermal fibroblasts onto the infarcted heart to provide a support structure for new blood vessel formation and cell growth. This 3-deminsional fibroblast construct (3DFC) secretes cytokines and angiogenic growth factors that may potentially mediate new blood vessel formation in-vivo. Using microarrays we are analyzing the soluble products secreted from the 3DFC when strained in manners modeling the biophysics of the cardiac cycle. The 3DFC does not generate an immune response and is currently used clinically as a skin graft for diabetic foot ulcers and is the subject of two Phase I clinical trials in CABG patients and in patients with left ventricular assist devices (LVADs).
Cell proliferation is a hallmark of vascular neointimal formation observed, for example, post angioplasty as well as post vein grafting. The clinical consequences of untreated reocclusion are dire and an understanding of the mechanisms responsible for it is crucial. To this end, our laboratory models tissue-specific strain profiles and investigates, using a variety of techniques, changes in VSMC growth, proliferation and apoptosis. Further, we assess gene expression and secretory profiles of suspect growth factors and inflammatory cytokines by protein arrays and subsequently inhibit their expression and actions utilizing a variety of methodologies. Our work in this area has shown that strain-induced autocrine insulin-like growth factor 1 (IGF-1), nitric oxide, and vascular endothelial growth factor (VEGF) appear to reciprocally mediate VSMC hyperplasia, and perhaps clinical neointimal formation, in environments of increased cyclic mechanical strain. Also in response to mechanical strain is the observation that VSMC align in a manner perpendicular to the dominant strain vector presumably to establish an ideal energy efficient conformation. We have investigated various signaling pathways potentially responsible for this occurrence, and it appears that these are separate and distinct from those regulating the hyperproliferative response. Our work has expanded to include investigation of the putative mechanotransducer responsible for VSMC signaling. Stretch activated calcium channels (SACCs) appear to play an important proximal step in strain-mediated gene expression by coding for intracellular calcium pulses that result in gene activation and vesicle release.
Please contact Dr. Standley at Standley@email.arizona.edu for further information and collaborative opportunities.