Dr. Lindon Young is an Associate Professor in the Department of Pathology, Microbiology, Immunology and Forensic Medicine at the Philadelphia College of Osteopathic Medicine. He received his PhD in Pharmacology from the Philadelphia College of Pharmacy and Science in 1998, and held postdoctoral positions at the University of the Sciences in Philadelphia, Department of Pharmacology/Toxicology, and at Thomas Jefferson University in the Department of Physiology, before coming to PCOM in 2002. Dr. Young has been a member of the American Physiological Society since 2002.
Research
Dr. Young's research involves examining reperfusion injury in animal models. Specifically, the role of polymorphonuclear leukocytes (PMNs) that infiltrate into post-reperfused tissues, and related biochemical mechanisms associated with reperfusion tissue injury, are evaluated in the settings of femoral, myocardial, and splanchnic ischemia/reperfusion (I/R). The in vivo femoral I/R model evaluates hydrogen peroxide (H2O2) and nitric oxide (NO) release in femoral veins. The ex vivo myocardial and in vivo splanchnic I/R models evaluate cardiac function and PMN vascular adherence and infiltration in heart and mesenteric tissues, respectively.
The laboratory personnel are investigating the role of tetrahydrobiopterin (BH4) and protein kinase C (PKC) as they pertain to the regulation of endothelial nitric oxide synthase (eNOS) function and PMN infiltration during reperfusion. BH4 is an essential co-factor of eNOS and PKC is a key enzyme in the regulation of eNOS function. The product profile of eNOS can shift from producing NO to superoxide when BH4 is oxidized to BH2, a condition referred to as eNOS uncoupling. Superoxide and H2O2 are produced in excess amounts during reperfusion of blood flow to a previously ischemic organ and are injurious to the tissues. The data obtained from this research would potentially be used to develop new treatment options to help patients receiving an organ transplant in obtaining a better quality of life post-procedurally.
Awards
NIH (R15; pending)
In vivo and ex vivo mechanisms related to eNOS uncoupling during reperfusion
NIH (R15); 3/18/04 - 2/28/07
Protein Kinase C isoform inhibition in cardiac ischemia/reperfusion
Publications (Click
here for a full list of Dr. Young's publications.)
Protein kinase C (PKC) isoform peptide activator/inhibitors exert cardioprotective
effects in polymorphonuclear leukocyte (PMN)-induced ischemia/reperfusion
(I/R) injury. Young LH, Phillipson A, Omiyi D, Atkinson N, Jivani M, Adams J, Peterman
EE, Taormina PII, Brue RJ and Harvey M. 2006. Understanding Biology Using Peptides,
Proceedings of the 19th American Peptide Symposium SE Blondelle, Editor 457-458.
Go 6983: A fast acting protein kinase C inhibitor that attenuates myocardial
ischemia/reperfusion injury. Young, L.H., B. J. Balin, and M. T. Weis. 2005.
Cardiovascular Drug Reviews 23: 255-272.
Protein kinase C beta II (PKC-βII) peptide inhibitor exerts cardioprotection in
polymorphonuclear leukocyte (PMNs) induced ischemia/reperfusion (I/R)
injury. Omiyi D, Brue R, Taormina P, Harvey M, Atkinson NK and Young, LH. 2005. J
Pharmacol Exp Thera 314: 542-551.
Protein kinase C zeta inhibition exerts cardioprotective effects in
ischemia/reperfusion injury. Phillipson A., E. E. Peterman, P. Taormina II, M. Harvey,
R. J. Brue, N. Atkinson, D. Omiyi, U. Chukwu, and L. H. Young. 2005. Am. J. Physiol.
289:H898-907.
Go 6983 exerts cardioprotective effects in myocardial ischemia/reperfusion.
Peterman, E. E., P. Taormina II, M. Harvey, and L. H. Young. 2004. J. Cardiovasc.
Pharmacol. 43: 645-656.
Inhibiting long chain fatty Acyl CoA synthetase increases basal and agonist-
stimulated NO synthesis in endothelium. Weis, M. T., J. L. Crumley, L. H. Young, and
J. N. Stallone. 2004. Cardiovasc. Res. 63:338-346.
Rosuvastatin, a new HMG-CoA reductase inhibitor, protects ischemic reperfused
myocardium in normocholesterolemic rats. Ikeda, Y., L. H. Young, and A. M. Lefer.
2003. J. Cardiovasc. Pharmacol. 41:649-656.
Protein kinase inhibition exerts cardioprotective effects in myocardial
ischemia/reperfusion via inhibition of superoxide release. Young, L. H., Y.
Ikeda, and A. M. Lefer. 2001. Methods Find. Exp. Clin. Pharmacol. 23:107-114.
Caveolin-1 peptide exerts cardioprotective effects in myocardial ischemia-
reperfusion via nitric oxide mechanism. Young, L. H., Y. Ikeda, and A. M. Lefer.
2001. Am. J. Physiol. Heart Circ. Physiol. 280:H2489-95.
Wortmannin, a potent antineutrophil agent, exerts cardioprotective effects in
myocardial ischemia/reperfusion. Young, L. H., Y. Ikeda, R. Scalia, and A. M. Lefer.
2000. J. Pharmacol. Exp. Ther. 295:37-43.
