Cyrine Ben Dhaou was honored  with the American Heart Association (AHA) Fellowship Award in December 2025.

Dr. Cyrine Ben Dhaou received a NAVBO Travel Award to Vascular Biology 2025, Cape Cod, MA.

Dr. Cyrine Ben Dhaou was accepted into NASA’s STAR program. The Spaceflight Technology, Applications, and Research (STAR) program is NASA’s space biosciences training program.

Dr. Cyrine Ben Dhaou won Second Place Poster Award in the Postdoctoral Fellow category at the Feist Cardiovascular Research Symposium, LSUHS, Shreveport, LA.

Matthew Scott received the Malcom Feist Postdoctoral Transition Award from the CCDS and was promoted to Instructor in July 2025.

A. Wayne Orr, PhD, received a $300,000 Transformational Pathway Award from the American Heart Association in July 2025 for his work on “Integrin-dependent endothelial priming in atherosclerosis”.

A. Wayne Orr, PhD, was elected to serve as President of the North American Vascular Biology Organization starting in July 2025

Breanna Pearson-Gallion defended her dissertation titled EphA2 signaling in Nonalcoholic Fatty Liver Disease and received her PhD (and the Dean’s Award) in May 2025.

A. Wayne Orr, PhD, was an invited speaker for the NAVBO Mechanotransduction Workshop in February 2025, discussing his work on “ER stress in the endothelial response to flow”.

A. Wayne Orr, PhD, took over as chair of the Irvine H. Page Award committee for the ATVB council of the American Heart Association in July 2024 and serves as a member of the ATVB Leadership Council.

Dr. Cyrine Ben Dhaou was selected as the 2024 Outstanding Postdoctoral Fellow in the Pathology Department based on the Trainee Achievement Metrics document.

Dr. Cyrine Ben Dhaou received the CCDS Malcolm Feist Cardiovascular Research Postdoctoral Fellowship.

A. Wayne Orr, PhD, was an invited speaker for the Gordon Research Conference on Biomechanics in Vascular Biology and Disease in August 2023, discussing his work on “Integrin signaling in the endothelial response to flow.

A. Wayne Orr, PhD, received a five-year $2,876,200 R01 grant from the NIH National Heart, Lung, and Blood Institute for his project, "EphA2 regulation of atherosclerotic smooth muscle phenotype." 

Brenna Pearson-Gallion received the Second Place Poster in the Graduate Student category at the Feist Cardiovascular Research Symposium for her poster entitled: Altered EphA2 signaling in Nonalcoholic Fatty Liver Disease Progression”.

Dr. Syrine Ben Dhaou received the Second Place Poster award in the Postdoctoral Fellow category at the Feist Cardiovascular Research Symposium for her poster entitled: “Targeting endothelial Nck1 reduces atherosclerosis”.

Dr. Matthew Scott received the First Place Poster award at the Gordon Research Conference: Vascular Biology in Ventura, California for his poster entitled: The Role of EphA2 in Vascular Smooth Cell Proliferation, Migration, and Mitogenic Signaling.  (View Poster)

Brenna Pearson-Gallion was recently awarded a NIDDK F31 Predoctoral Fellowship award to fund her research on “EphA2 in Nonalcoholic Fatty Liver Disease.”

Dr. Wayne Orr and Dr. Karen Stokes were recently awarded an NIH T32 grant to establish a program for Multidisciplinary Training in Cardiovascular Pathophysiology (MTCP). The MTCP program is the only T32 training program in the state of Louisiana focused on cardiovascular disease.

Working with Dr. Andrew Yurochko, Dr. Orr organized the LSU Health Shreveport Faculty Development Workshops, a series of lectures aimed at assisting new faculty with starting a biomedical research laboratory.

Despite advances in treatments over the past several decades, cardiovascular disease remains the leading cause of death in developed countries worldwide. Atherosclerosis, a chronic inflammatory disease of the vessel wall, is responsible for more than 80% of all cardiovascular disease related deaths. Current models suggest that the local accumulation of low density lipoproteins (LDL, "bad cholesterol") in the vessel wall promotes an inflammatory response characterized by endothelial cell activation and leukocyte recruitment.  This early inflammatory response stimulates phenotypic changes in the underlying medial smooth muscle cells resulting in their proliferation and migration into the growing plaque, where they contribute both to plaque size and plaque stability.  Our lab studies how the arterial microenvironment, including soluble factors, vascular mechanics (stiffness, hemodynamics), and adhesive interaction, affects vascular cell function during atherosclerotic plaque formation. While current cardiovascular disease therapies target the systemic soluble risk factors, no therapeutics target the altered arterial microenvironment during atherosclerosis.  Through a better understanding of the molecular mechanisms regulating vascular cell function, we hope to identify novel therapeutic targets to limit cardiovascular disease. 

The subendothelial matrix in endothelial activation - Our research has shown an important role for matrix composition in modulating the cellular response to multiple atherogenic stimuli. Early during atherogenesis in vivo, wound-associated transitional matrix proteins (ex. fibronectin, fibrinogen) become deposited into the endothelial cell basement membrane. In vitro, these transitional matrix proteins enhance the ability of atherogenic stimuli, such as disturbed flow patterns and oxidized LDL, induce endothelial cell dysfunction, while components of the basement membrane (ex. collagen, laminin) limit endothelial cell dysfunction. We hypothesize that signals from cell-matrix interactions serve as a form of tissue memory, helping cells place atherogenic stimuli into a temporal context by indicating whether the tissue is actively remodeling.  Our current research seeks to understand the factors regulating matrix remodeling during atherogenesis (ex. hyperglycemia, oxidized LDL), to characterize how specific integrins (cell matrix receptors) contribute to endothelial activation in vitro and in vivo, and to characterize how integrin affinity modulation affects atherogenic endothelial activation.  

Nck adaptor proteins in atherogenic endothelial activation.  Work from our laboratory has shown that the Nck family of signaling adaptor proteins, Nck1 and Nck2, contribute to endothelial dysfunction under atherosclerotic conditions.  In response to shear or oxidant stress, Nck1/2 are recruited to tyrosine phosphorylated proteins at sites of cell-cell and cell-matrix adhesion, where they form specific signaling complexes to drive endothelial proinflammatory gene expression and vascular permeability.  Work from our group is currently characterizing the mechanisms regulating Nck1/2 recruitment following shear and oxidant stress and the role of individual Nck isoforms in endothelial activation in vitro and in vivo.   

Guidance Molecules in Atherogenic Remodeling - The ephrin and Eph family of cell-cell adhesion molecules are well characterized regulators of vascular and neuronal development and are implicated in numerous tissue remodeling responses in adult organisms. The Eph receptor EphA2 shows prominent expression in endothelial cells, macrophages, and synthetic smooth muscle cells, and we have demonstrated enhanced expression of EphA2 and its receptor ephrinA1 in both mouse models of atherosclerosis and human atherosclerotic plaques.  In endothelial cells, EphA2 signaling promotes proinflammatory endothelial activation, and EphA2 knockout mice show smaller plaques with reduced leukocyte recruitment.  However, EphA2 also contributes to smooth muscle growth, proliferation and extracellular matrix deposition, and plaques from EphA2 knockout mice show reduced markers of plaque stability.  Our current research seeks to characterize the dynamic interplay between smooth muscle EphA2 expression and matrix composition, determine the mechanisms by which EphA2 signaling affects smooth muscle proliferation and migration, and assess the role of EphA2 cell type-specific expression and signaling in atherosclerotic fibroproliferative remodeling.. 

Selected Publications

1. Pearson-Gallion B.*, Finney A.C.*, Scott M.L., Connelly Z., Alam S., Peretik J.M., Bhuiyan M.S., Traylor J.G. Jr., DeGrado W.F., Jo. H., Yu X., Rom O., Pattillo C.B., Dhanesha N., Yurdagul A. Jr., and A.W. Orr. (2025) Fibronectin-dependent integrin signaling drives EphA2 expression in vascular smooth muscle cells. Am. J. Physiol. Cell Physiol., 328: C1623-C11636. *co-first author
2. Joshi D., Coon B.G., Chakraborty R., Deng H., Fernandez-Tussy P., Meredith E., Traylor J.G., Orr A.W., Fernandez-Hernando C., and M.A. Schwartz. (2024) Gamma protocadherins in vascular endothelial cells inhibit Klf2/4 to promote atherosclerosis. Nat. Cardiovasc. Res., 3: 1035-1048.
3. Ben Dhaou C., Scott M.L., and A.W. Orr. (2024) Advances in Understanding Cardiovascular Disease Pathogenesis Through Next-Generation Technologies. Am. J. Pathol., 194: 476-481.
4. Finney A.C.*, Scott M.L.*, Reeves K.A., Wang D.D., Alfaidi A., Schwartz J.C., Chitmon C.M., Acosta C.H., Murphy J.M., Alexander J.S., Pattillo C.B., Lim S.S., and A.W. Orr. (2021) EphA2 signaling within integrin adhesions regulates fibrillar adhesion elongation and fibronectin deposition. Matrix Biol., 103-104: 1-21. *co-first author
5. Al-Yafeai Z., Pearson B.H., Peretik J.M., Cockerham E.D., Reeves K.A., Bhattarai U., Wang D.D., Petrich B.G., and A.W. Orr. (2020) Integrin affinity modulation critically regulates atherogenic endothelial activation in vitro and in vivo. Matrix Biol., 96: 87-103.
6. Alfaidi M., Acosta C.H., Wang D., Traylor J.G., and A.W. Orr. (2020) Selective role of Nck1 in atherogenic inflammation and plaque formation. J. Clin. Invest., 130: 4331-4347.
7. Al-Yafaei Z.*, Yurdagul Jr. A.*, Peretik J.M., Alfaidi M., Murphy P., and A.W. Orr. (2018) Endothelial a5b1 integrins regulate fibronectin deposition, inflammation, and early atherosclerosis: a novel regulatory role for cell-derived fibronectin. Arterioscler. Thromb. Vasc. Biol., 38: 2601-2614. *co-authors
8. Yuan S.*, Yurdagul Jr. A.*, Peretik J.M., Alfaidi M., Al Yafeai Z., Pardue S., Kevil C.G., and A.W. Orr. (2018) Cystathionine g-lyase modulates flow-dependent vascular remodeling. Arterioscler. Thromb. Vasc. Biol., 38: 2126-2136. *co-authors
9. Finney A.C., Funk S.D., Green J.M., Yurdagul A. Jr., Rana M.A., Pistorius R., Henry M., Yurochko A.D., Pattillo C.B., Traylor J.G., Chen J., Woolard M.D., Kevil C.G., and A.W. Orr. (2017) EphA2 expression regulates inflammation and fibroproliferative remodeling in atherosclerosis. Circulation, 136: 566-582.
10. Yurdagul Jr. A., Finney A.C., Woolard M.D., and A.W. Orr. (2016) The Arterial Microenvironment: The Where and Why of Atherosclerosis. Biochem J., 473: 1281-1295.

Complete List of my Published Work in MyBibliography: LEARN MORE
 

ALUMNI

Post-doctoral Fellows

We are currently recruiting a Post-doctoral Fellow to study the role of vascular cell signaling mechanisms in atherosclerosis, ischemia/reperfusion injury, and angiogenesis. To enquire about opportunities, contact Dr. Orr at wayne.orr@lsuhs.edu.

Graduate Students

Graduate students interested in conducting research in the Orr lab should review the current laboratory research directions and contact Dr. Orr at wayne.orr@lsuhs.edu.

Undergraduate Research Assistants

We are not currently hiring any additional undergraduates. However, positions can become available during the summer.

Medical Students, Residents, and Fellows

The Orr laboratory has a number of research projects available for any Medical Students, Residents, and Fellows interested in performing atherosclerosis research. These projects can include the study of vascular cell biology, animal models of cardiovascular disease, and/or human atherosclerotic plaques.
 

Contact the Orr Lab

LSU Health Shreveport
Department of Pathology
Biomedical Research Institute Rm 6-21
1501 Kings Hwy
Shreveport, LA 71103

A. Wayne Orr, Phd
Email: wayne.orr@lsuhs.edu
Office: (318) 675-5462 
Lab: (318) 675-5463
Fax: (318) 675-8144