To find a doctor, call 800-667-5356 or click below:

Find a Doctor

Request an Appointment

left banner
right banner
Smaller Larger

Ruhul Abid, MD, PhD

Assistant Professor of Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School

330 Brookline Avenue, RN-232
Boston, MA 02215

Office: 617-667-1025
Fax: 617-667-2913
Email: rabid@bidmc.harvard.edu

Education/Training/Appointments

Ruhul Abid is an Assistant Professor of Medicine, Harvard Medical School, and a researcher in the Division of Molecular and Vascular Medicine at BIDMC. He obtained his MD degree from Dhaka University and PhD in Molecular Biology and Biochemistry from Nagoya University, Japan. Ruhul joined Dr. Aird"s lab at BIDMC as a post-doctoral fellow in 1999 and was promoted to the position of Instructor in Medicine in 2002. Ruhul was promoted to Assistant Professor of Medicine, Harvard Medical School in 2006 and became a member of the CVBR.

Research Interests

Redox and Signal Transduction in the Endothelium

Basic Research

Our research projects are mainly aimed at elucidation of the mechanism of signal transduction and redox signaling that modulate phenotype of the endothelium in health and disease.

Using physiological growth factors as ligands, we study the intracellular signal transduction events that determine the growth of new blood vessels, the maintenance of vascular integrity, and hemostasis in health and inflammatory conditions.

Redox Signaling in the Endothelium

Our studies demonstrate that NADPH oxidase-derived ROS selectively modulate some (PI3K-Akt-forkhead signaling) but not all (e.g. ERK1/2 activation) the effects of VEGF on endothelial cell phenotype. These findings argue against a global sensitivity of VEGF signal transduction pathways to the redox state of the cell, and suggest that therapeutic modulation of ROS will selectively influence the effect of VEGF on endothelial cell phenotypes.

Signal Transduction

Our lab studies signaling events that occur at the endothelial cell-surface leading to activation of intracellular signaling intermediates and induction of gene expression. We study the VEGF-PI3K-Akt-forkhead signaling axis in vascular biology, and provide evidence for the existence of a subset of VEGF-responsive genes whose expression is both dependent on and modulated by forkhead activity in the endothelium.

Translational Research

In collaborartion with Christianne Ferran, we have shown in a rat balloon carotid arterial injury model, adenovirus-mediated gene transfer of forkhead caused an increase in the expression of p27kip1 in the VSMC and inhibition of neointimal hyperplasia. These data suggest that FoxO activity inhibits VSMC proliferation and activation and that this signaling axis may represent a therapeutic target in vasculopathic disease states. In addition, our study demonstrates that endocan (ESM-1) is preferentially expressed in tumor endothelium in vivo and that its expression is regulated by tumor-derived factors.

New and Noteworthy Publications

View all publications via PubMed >>

  1. Abid MR*, Nadeau RJ, Spokes KC, Minami T, Li D, Shih SC, Arid WC. (2008) Hepatocyte growth factor inhibits VEGF-forkhead-dependent gene expression in endothelial cells. Arterioscler Thromb Vasc Biol. In Press.*Corresponding Author. This study describes that physiological agonists of PI3K-Akt signaling pathway may modulate VEGF-FKHR/FOXO1-dependent gene expression in endothelial cells. In the present study, we tested the hypothesis that preconditioning of endothelial cells with the PI3K-AKT agonist, HGF would affect the ability of VEGF to activate Class II genes by limiting the availability of FKHR/FOXO1 in the nucleus (the functional equivalent of FKHR/FOXO1 knockdown). We show that HGF does indeed attenuate VEGF induction of FKHR-dependent genes. These findings add a new level of complexity to forkhead signaling in endothelial cells.

  2. Abid MR*, Spokes KC, Shih SC, Aird WC. (2007) NADPH oxidase activity selectively modulates vascular endothelial growth factor signaling pathways. J Biol Chem. 282, p35373. *Corresponding author. This study suggests that NADPH oxidase-derived ROS selectively modulate some (PI3K-Akt-forkhead signaling) but not all (e.g. ERK1/2 activation) the effects of VEGF on endothelial cell phenotype. The findings argue against a global sensitivity of VEGF signal transduction pathways to the redox state of the cell, and suggest that therapeutic modulation of ROS will selectively influence the effect of VEGF on endothelial cell phenotypes.

  3. Abid MR*, Shih SC, Otu HH, Spokes KC, Okada Y, Curiel DT, Minami T, Aird WC. (2006) A novel class of vegf-responsive genes that require forkhead activity for expression. J Biol Chem. 281, p35544. *Corresponding author. This study demonstrates that the VEGF-forkhead signaling axis plays an important role in vascular biology, over and above its ability to inhibit pro-apoptotic/cell cycle arrest genes. Here, we provide evidence for the existence of a subset of VEGF-responsive genes whose expression is both dependent on and modulated by forkhead activity in ECs.

  4. Abid MR, Yano K, Guo S, Patel VL, Shrikande G, Spokes KC, FerranC, Aird WC. (2005) Forkhead Transcription Factors Inhibit Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia. J Biol Chem. 280, p29064. In a rat balloon carotid arterial injury model, adenovirus-mediated gene transfer of FKHRL1 caused an increase in the expression of p27kip1 in the VSMC and inhibition of neointimal hyperplasia. These data suggest that FoxO activity inhibits VSMC proliferation and activation and that this signaling axis may represent a therapeutic target in vasculopathic disease states.

Contact Information

Nicole Magner, Administrative Assistant
Center for Vascular Biology Research
Beth Israel Deaconess Medical Center
Research North
99 Brookline Avenue
Boston, MA 02215
617-667-0654
info.cvbr@bidmc.harvard.edu