Publications
More Publications
Reduced RhoA activity mediates acute alcohol intoxication-induced inhibition of lymphatic myogenic constriction despite increased cytosolic [Ca(2+) ]. Souza-Smith FM, Molina PE, Breslin JW. Microcirculation. 2012 Dec 13. doi: 10.1111/micc.12032. [Epub ahead of print] PMID: 23237297
Measurement of cytosolic Ca2+ in isolated contractile lymphatics. Souza-Smith FM, Kurtz KM, Breslin JW. J Vis Exp. 2011 Dec 8;(58). doi:pii: 3438. 10.3791/3438. PMID: 22214883
ISG15 disrupts cytoskeletal architecture and promotes motility in human breast cancer cells. Desai SD, Reed RE, Burks J, Wood LM, Pullikuth AK, Haas AL, Liu LF, Breslin JW, Meiners S, Sankar S. Exp Biol Med (Maywood). 2012 Jan 1;237(1):38-49. doi: 10.1258/ebm.2011.011236. Epub 2011 Dec 20. PMID: 22185919
Study of the actin cytoskeleton in live endothelial cells expressing GFP-actin. Doggett TM, Breslin JW. J Vis Exp. 2011 Nov 18;(57). doi:pii: 3187. 10.3791/3187. PMID: 22126853
ROCK and cAMP promote lymphatic endothelial cell barrier integrity and modulate histamine and thrombin-induced barrier dysfunction. Breslin JW. Lymphat Res Biol. 2011 Mar;9(1):3-11. doi: 10.1089/lrb.2010.0016. PMID: 21417762
Memberships
Gulf Coast Physiological Society,
Treasurer;
2011 - 2012
American Heart Association,
Member;
2008 - present
American Association for the Advancement of Science,
Member;
2005 - present
American Society for Cell Biology,
Member;
2003 - present
American Physiological Society,
Member;
2001 - present
New York Academy of Sciences,
Member;
2001 - 2003
The Microcirculatory Society, Inc.,
Member;
2001 - present
Peer Review Positions
ZRG1 DKUS D 57; PAR Panel: Lymphatics in Health and Disease in the Digestive, Urinary, Cardiovascular and Pulmonary Systems D , National Institutes of Health; 2012 - 2012
Microcirculation, Editorial Board, The Microcirculatory Society, Inc.; 2011 - 2015
Technologies
Competitive Advantages:
Increased endothelial cell anaerobic glycolysis, Edema prevention, Enhanced endothelial barrier function,
A potential treatment for many diseases.
Disclosed are compositions and methods for modulating endothelial barrier functionUSF inventors have developed a method which utilizes agents that activate s1. The activation of s1 encourages the metabolic production of ATP to be shifted from oxidative mechanisms to anaerobic glycolysis. Our data show for the first time that s1 activation leads to enhanced glycolytic ATP production which is tightly linked to endothelial barrier integrity. Therefore, s1 can be utilized as a novel therapeutic target for ameliorating endothelial barrier dysfunction caused by ischemia. This invention is applicable to any disease involving endothelial dysfunction, including but not limited to diabetes, peripheral vascular disease, heart disease, hypertension, venous thrombosis, insulin resistance, ischemic diseases of the gut, stroke, sepsis, chronic inflammatory diseases, and severe viral diseases.
