Studies performed in the Goligorsky laboratory in the last five years have established a) the role of premature cell senescence in endothelial dysfunction; b) contribution of endothelial progenitor cells (EPC) to rescuing the kidney from ischemia/reperfusion injury; c) the pathways of EPC mobilization and engraftment post-ischemia; d) the role of renal resident mesenchymal stem cells in renoprotection; e) the role of glial cell-derived neurotrophic factor in stimulating migration and antiapoptotic properties of mesenchymal stem cells; f) proteomic analysis of the urine in recipients of kidney transplant. Currently, Dr. Goligorsky is exploring the mechanism whereby alarm signaling, an innate immune response, mobilizes stem cells to the post-ischemic tissue/organ, the mechanisms of premature senescense of stem cells, and the proteomic phenotype of dysfunctional endothethial cells and their progenitors.
O'Riordan E, TN Orlova, N Mendelev, D Patschan, R Kemp, PN Chander, R, Hu, G, Hao, SS Gross, RV Iozzo, V Delaney, MS Goligorsky. Urinary proteomic analysis of chronic allograft nephropathy. Proteomics - Clinical
Applications. 2: 1025-1035, 2008
Patschan S, Chen J, Gealekman O, Krupincza K, Wang M, Shu L, Shayman JA, Goligorsky MS. Mapping mechanisms and charting the time course of premature cell senescence and apoptosis: lysosomal dysfunction and ganglioside accumulation in endothelial cells. Am J Physiol Renal Physiol. 2008 Jan;294(1):F100-9. Epub 2007 Oct 10.
Kuo MC, Patschan D, Patschan S, Cohen-Gould L, Park HC, Ni J, Addabbo F, Goligorsky MS. Ischemia-Induced Exocytosis of Weibel-Palade Bodies Mobilizes Stem Cells.
J Am Soc Nephrol. 2008 Aug 20. [Epub ahead of print]