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NIH - Funded Training in Cell Signaling & Lung Pathobiology
 

Nutan Prasain, M.S.
Phone: (251) 460-7158
Fax: (251) 460-6798
np302@jaguar1.usouthal.edu

 
EDUCATIONAL HISTORY

Institution/Location

Degree

Year Conferred 

Field

University of South Alabama

Ph.D.

In Progress

Lung Biology

Mobile, Alabama

 

 

 

 

 

 

 

University of South Alabama

M.S. 

2004

Biology

Mobile, Alabama

 

 

 

 

 

 

 

Rajeev Gandhi University of Health Sciences, Bangalore, India

Bachelor of Pharmacy
(graduated with distinction)

2002

Pharmacy

 

 

Tribhuvan University, Kathmandu, Nepal 

Intermediate of Science (I.Sc.)

1997

Biology

 
RESEARCH EXPERIENCE

2005 - present

Graduate research assistant
Department of pharmacology/Center for Lung Biology
University of South Alabama, Mobile, AL

 

 

2003 – 2004

Graduate research assistant at Dr. Warren Zimmer Lab
Department of Cell biology and Neuroscience
University of South Alabama, Mobile, AL

HONORS AND AWARDS

2006 Research Recognition Award sponsored by the American Physiological Society Respiratory Section
2005 Outstanding Scholastic Achievement Award, University of South Alabama
2004 Member Phi Beta Delta Honor Society
 
RESEARCH INTERESTS
I am interested in understanding how cAMP, a second messenger, mediates paradoxical endothelial barrier protective as well as disruptive functions. Endothelial cells line the pulmonary vasculature and function as a semipermeable barrier regulating movement of fluids, solutes and macromolecules between the blood and the interstitium. High cAMP concentrations in membrane strengthen; whereas high cAMP concentrations in cytosol disrupt the endothelial barrier. Endothelial cell shape and consequently barrier integrity, is determined by cross-talk between the actin cytoskeleton and microtubules. The cortical actin cytoskeletal networks are highly concentrated in a region just beneath the plasmalemella, and are associated with a large number of membrane adhesive proteins including adhering and focal adhesion complex proteins that are responsible for generating tethering forces that keep cells in juxtaposition to each other and to the matrix. Like the cortical actin networks, individual tubulin subunits polymerize into organized cytoskeleton networks to form microtubules. Disruption of microtubule results in endothelial barrier dysfunction that increases endothelial cell permeability. Polymerized microtubules are stabilized by a family of proteins known as microtubule assembly proteins. Interestingly, cAMP-dependent protein kinase A phosphorylation of microtubule assembly proteins depolymerizes microtubules, potentially leading to an increase in endothelial cell permeability. We therefore hypothesize that cAMP produced at the cell membrane has the potential to stabilize cortical actin and strengthen the endothelial cell barrier integrity, while cAMP produced in the cytosol has the potential to destabilize microtubules and weaken the endothelial cell barrier.
 
ABSTRACT

Prasain N, Wu S, Goodman SR, Stevens, T. Disruption of spectrin-f-actin binding is sufficient to induce inter-endothelial gaps. FASEB J., 20 (4): A748, 2006.

 
PRESENTATIONS AND CONFRENCES
  • Abstract selected for presentation in a special session entitled "Graduate Student Highlights in Respiration Physiology" sponsored by the American Physiological Society Respiratory Section at Experimental Biology 2006
  • Research in Progress, Center of Lung Biology, University of South Alabama, October 2005, and May 2006  
  • Workshop on “A Field Guide to GenBank and NCBI Molecular Biology Resources”, National Center for Biotechnology Information January 2006
 
Last update: June 23, 2006