The critical role of the kidney in maintaining fluid and electrolyte balance, and the disorders of homeostasis that are accompany diseases of the kidney and associated loss of renal function underscore the importance of this organ. Our increasing ability to both identify and modify the gene products that are responsible for maintaining normal homeostatic balance offers new and powerful approaches to examine the contributions of individual proteins to the maintenance of normal renal function and the consequences of loss of renal function. The objective of the Pittsburgh Center for Kidney Research is to both reinforce and expand interactions among investigators at the University of Pittsburgh and colleagues at Mount Sinai School of Medicine who have had a longstanding history of research in areas related to the identification and characterization of cellular processes within the kidney that are associated with normal physiology and with path physiological states, to develop new directions of investigation using electrophysiological, cell biological, molecular, and genetic tools, and to attract new investigators to renal-related research. The Center will be focused on four main cores, which will support the work of investigators at the University of Pittsburgh and Mount Sinai School of Medicine. Core A is a cellular physiology core, led by Dr. Hallows. Core B is a single nephron and metabolomics core, led by Drs. Jackson and Satlin. Core C is a kidney imaging core, led by Dr. Apodaca. Core D will focus on the use of model organisms and is led by Drs. Brodsky and Hukriede. The Center will support four pilot and feasibility projects. An administrative core, led by Drs. Kleyman and Weisz, will provide administrative oversight of the core facilities, the pilot and feasibility project program and the educational activities of the center. All research cores are specifically structured to serve as nation-wide resources for investigators. Our Center is designed to realize our goal of continuing to advance our understanding of normal renal function, of cellular mechanisms that contribute to kidney disease, and of the myriad of altered cellular functions that occur in the setting of renal insufficiency.
The goals of the Pittsburgh Center for Kidney Research are to develop and facilitate multidisciplinary research, training and information transfer related to kidney physiology, cell biology, pharmacology and pathophysiology.
|Chang, Andy; Yeung, Steven; Thakkar, Arvind et al. (2015) Prevention of skin carcinogenesis by the ?-blocker carvedilol. Cancer Prev Res (Phila) 8:27-36|
|Jackson, Edwin K; Cheng, Dongmei; Verrier, Jonathan D et al. (2014) Interactive roles of CD73 and tissue nonspecific alkaline phosphatase in the renal vascular metabolism of 5'-AMP. Am J Physiol Renal Physiol 307:F680-5|
|Novitskaya, Tatiana; McDermott, Lee; Zhang, Ke Xin et al. (2014) A PTBA small molecule enhances recovery and reduces postinjury fibrosis after aristolochic acid-induced kidney injury. Am J Physiol Renal Physiol 306:F496-504|
|Morrell, Eric D; Kellum, John A; Hallows, Kenneth R et al. (2014) Epithelial transport during septic acute kidney injury. Nephrol Dial Transplant 29:1312-9|
|Prakasam, H Sandeep; Gallo, Luciana I; Li, Hui et al. (2014) A1 adenosine receptor-stimulated exocytosis in bladder umbrella cells requires phosphorylation of ADAM17 Ser-811 and EGF receptor transactivation. Mol Biol Cell 25:3798-812|
|Schuler, P J; Saze, Z; Hong, C-S et al. (2014) Human CD4+ CD39+ regulatory T cells produce adenosine upon co-expression of surface CD73 or contact with CD73+ exosomes or CD73+ cells. Clin Exp Immunol 177:531-43|
|Chen, Jingxin; Kleyman, Thomas R; Sheng, Shaohu (2014) Deletion of ?-subunit exon 11 of the epithelial Na+ channel reveals a regulatory module. Am J Physiol Renal Physiol 306:F561-7|
|Hecht, Karen A; O'Donnell, Allyson F; Brodsky, Jeffrey L (2014) The proteolytic landscape of the yeast vacuole. Cell Logist 4:e28023|
|Nirmal, J; Wolf-Johnston, A S; Chancellor, M B et al. (2014) Liposomal inhibition of acrolein-induced injury in rat cultured urothelial cells. Int Urol Nephrol 46:1947-52|
|Yao, Mingyi; Rogers, Natasha M; Csányi, Gábor et al. (2014) Thrombospondin-1 activation of signal-regulatory protein-? stimulates reactive oxygen species production and promotes renal ischemia reperfusion injury. J Am Soc Nephrol 25:1171-86|
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