Research Faculty

622 West 168th Street
PH 17-102
New York, NY 10032

Phone: 212-305-0793
Fax: 212-305-8088
Education and Training
M.D., 1984, Fujian Medical University, China
Ph.D., 1995, New York Medical College

Fangming Lin, M.D., Ph.D.
Associate Professor of Pediatrics and Pathology and Cell Biology
Research Summary

The Lin Laboratory uses mouse models to study renal tubular epithelial response to injuries resulting from ischemic insult or urinary tract obstruction. Currently, we focus on autophagy as one of the major response mechanisms to stress and injury. Using newly generated autophagy reporter mice (CAG-RFP-GFP-LC3), which allow us to track autophagic process, we are able to reveal the dynamics of renal tubular autophagy in post-ischemic kidneys and show that autophagic cells are less likely to be progenitors for tubular repair. We demonstrate that mTOR activation plays an important role in the resolution of autophagy and subsequent tubular regeneration. Although autophagy is a mechanism for cell survival, prolonged and excessive autophagy under pathological conditions may result in over destruction of vital components, thus causing cellular catastrophe. We have evidence to show that autophagy in the kidneys with persistent urinary tract obstruction is associated with tubular atrophy, which is a common finding in chronic kidney disease. Furthermore, we study the interaction between stress-responsive molecules, specifically the involvement of FoxO3a and mTOR in the kidneys with congenital urinary tract obstruction. These studies may shed light onto the regulation of epithelial autophagy and help in designing therapeutic interventions to prevent and/or slow down the progression of renal tubular atrophy.
Selected Publications

Li, L, Wang ZV, Hill JA and Lin F. New Autophagy Reporter Mice Reveal Dynamics of Proximal Tubular Autophagy, J Am Soc Nephrol., online publication Oct. 30, 2013

Li L, Black R, Yang Q, Wang A, Ma Z and Lin F. Use of Mouse Hematopoietic Stem and Progenitor Cells to Treat Acute Kidney Injury, Am J Physiol Renal Physiol. 2012 Jan;302(1):F9-F19

Li L, Zepeda-Orozco D, Black R, and Lin F. Autophagy is a component of epithelial cell fate in obstructive uropathy. Am J Pathol., 2010, 176(4):1767-78

Li L, Zepeda-Orozco D, Patel V, Truong P, Karner M, Carroll T, and Lin F. Aberrant planar cell polarity induced by obstructive uropathy. Am. J. Physiol. Renal Physiol., 2009, 297: F1526-F1533

Patel V, Li L, Cobo-Stark P, Shao X, Somlo S, Lin F., and Igarashi P. Acute kidney injury and aberrant planar cell polarity induce cyst formation in mice lacking renal cilia. Hum Mol Genet., 2008, 17(11):1578-90

Li, L, Truong, P, Igarashi, P and Lin, F. Renal and bone marrow cells fuse after renal ischemic injury. J Am Soc Nephrol., 2007, 18(12):3067-77

Lin F, Moran A, and Igarashi P. Intrarenal Cells, not Bone Marrow-Derived Cells, are the Major Sources for Kidney Regeneration Following Ischemia-Reperfusion Injury. J. Clin. Invest., 2005, 115(7):1756-64

Lopez-Rodriguez C, Antos CL, Shelton JM, Richardson, JA, Lin F, Novobrantseva TI, Bronson RT, Igarashi P, Rao A, Olson EN. Loss of NFAT5 results in renal atrophy and lack of tonicity-responsive gene expression. Proc Natl Acad Sci USA, 2004, 101 (8):2392-2397

Lin F, Hiesberger T, Cordes K, Sinclair A, Somlo S, Goldstein LSB, and Igarashi P. Inactivation of the kif3a subunit of kinesin-II inhibits renal ciliogenesis and produce polycystic kidney disease. Proc Natl Acad Sci USA, 2003, 100: 5286-5291

Lin F, Cordes K, Hood L, Li L, Couser WG, Shankland S, and Igarashi P. Hematopoietic stem cells contribute to the regeneration of renal tubules following ischemia/reperfusion injury. J. Am. Soc. Nephrol. , 2003, 14 (5):1188-1199

Park IK, He Y, Lin F, Laerum O, Tian Q, Bumgarner R, Klug CA, Li K, Kuhr C, Doyle M, Xie T, Schummer M, Sun Y, Goldsmith A, Clark M, Weissman I, Hood L, and Li L. Differential gene expression profiling of adult murine hematopoietic stem cells. Blood, 2002, 99 (2):488-498

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