INDIVIDUAL RESEARCHER

Mohamed Trebak , Ph.D.
Assistant Professor
e-mail: trebakm(at)mail.amc.edu

Phone: 518-262-4682

Education

1998 - Ph.D. from Université de Liège, Belgium

Current Research

Calcium signaling and vascular function

Calcium signaling in cells is usually initiated after stimulation of membrane receptors to hormones, chemokines and growth factors. These stimuli induce an elevation of intracellular free calcium which is essential for cell survival andfunction. Calcium channels at the plasma membrane are under tight control and function as gates that open in response to membrane receptor stimulation to allow calcium to enter the cells from the extracellular space. The dysfunction in calcium homeostasis can result in diseases such as immune deficiency, cancer, neurodegenerative and cardiovascular diseases.

Figure: Calcium signaling controls a variety of cell functions. Calcium signaling is typically initiated by ligation of membrane receptors that couple to isoforms of phospholipase C (PLC). Calcium entry from the extracellular space is achieved through a variety of cation channels such as STIM/Orai and TRPC channels.

We use a variety of biochemical, biophysical and imaging techniques to gain insights into the activation and regulation mechanisms of native ion channels in vascular cells such as endothelial cells and smooth muscle cells. We are particularly interested in two classes of ion channels: the transient receptor potential canonical (TRPC) channels and the recently discovered components of the store-operated calcium entry (SOCE) pathway, STIM/Orai as they pertain to vascular function such as smooth muscle migration and endothelial permeability and angiogenesis. Our basic research approaches are complemented by the use of animal models of vascular disease as well as knockout mice that are deficient for a single ion channel molecule. The basic science studies provide the foundation for the translational studies in animals that are necessary to validate the use of TRPC and STIM/Orai as targets for therapy of vascular disease such as hypertension and atherosclerosis.

Lab Members

PhD Students:

-Rajender K Motiani: motianr(at)mail.amc.edu

-Jose C Gonzalez: gonzalj1(at)mail.amc.edu

MSc Students:

-Jonathan M Bisaillon: Bisailj(at)mail.amc.edu

Postdoctoral Fellows:

-Arti Shinde, PhD: Shindea(at)mail.amc.edu

-Wei Zhang, PhD: zhangw(at)mail.amc.edu

Trebak lab Members from left to right: Rajender Motiani, Mohamed Trebak, Jose Gonzalez, Arti Shinde, Wei Zhang, Jonathan Bisaillon

PubMed Publications

Potier M and Trebak M. New developments in the signaling mechanisms of the store-operated calcium entry pathway.Pflugers Arch. 2008 Nov;457(2):405-15. Epub 2008 Jun 7.

House SJ, Potier M, Bisaillon J, Singer HA, and Trebak M. The non-excitable smooth muscle: calcium signaling and phenotypic switching during vascular disease.Pflugers Arch. 2008 Aug;456(5):769-85. Epub 2008 Mar 26.

Abdullaev IF, Bisaillon JM, Potier M, Gonzalez JC, Motiani RK and Trebak M. Stim1 and Orai1 mediate CRAC currents and store-operated calcium entry important for endothelial cell proliferation. Circ Res. 2008 Nov 21;103(11):1289-99. Epub 2008 Oct 9.

Potier M, Gonzalez JC, Motiani RK, Abdullaev IF, Bisaillon JM, Singer HA and Trebak M. Evidence for STIM1- and Orai1-dependent store-operated calcium influx through ICRAC in vascular smooth muscle cells: role in proliferation and migration.FASEB J. 2009 Aug;23(8):2425-37. Epub 2009 Apr 13.

Bisaillon JM, Motiani RK, Gonzalez-Cobos JC, Potier M, Halligan KE, Alzawahra WF, Barroso M, Singer HA, Jourd’heuil D and Trebak M. Essential Role for STIM1/Orai1-Mediated Calcium Influx in PDGF-Induced Smooth Muscle Migration. 2010. Am J Physiol-Cell Physiol. 2010. Epub January 27