Cellular & Integrative Physiology

Babu Padanilam, Ph.D.

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ACADEMIC DEGREES:
Graduate School: Medical College of Georgia, Augusta, Georgia
Postdoctoral Training: University of Iowa, Iowa City, Iowa

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Contact Name: Babu Padanilam, Ph.D.
Phone Number: (402) 559-3575
e-mail address: bpadanil@unmc.edu

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• GRANT SUPPORT (last 3 years):

NIH- Protein Kinase C in Ischemic Renal Injury and Repair, 1999 -2004
UNMC-New Grant-CD27 mediated cell death in renal ischemia 2003-2004
Nebraska Kidney Foundation, Role of PARP in Renal Ischemia, 2003-2004
Nebraska Kidney Foundation, PARP mediated type 2 diabetes mellitus, 2004-2005

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• PUBLICATIONS (last 3-5 years):

Kishor Devalaraja-Narasimha, Kurinji Singaravelu and Babu J. Padanilam. Poly (ADP-Ribose) Polymerase mediated cell injury in acute renal failure (Invited review)  Pharmacolgical Research: 52: 44-59; 2005

Jianfeng Zheng, Kishor Devalaraja-Narasimha, Kurinji Singaravelu and Babu J. Padanilam. Poly (ADP-Ribose) Polymerase gene ablation protects mice from ischemic renal injury . Am J Physiol Renal Physiol. 288:F387-98; 2005.

Peilin Wei P, Pascale PH, Lane JT,  Padanilam BJ and  Sansom SC. Glomerular structural and functional changes in a high fat diet mouse model of early-stage type 2 diabetes.  Diabetologia  47:1541-1549, 2004

Wang X, Pluznick JL, Wei P, Padanilam BJ, Sansom SC. TRPC4 forms store-operated Ca2+ channels in mouse mesangial cells.  Am J Physiol Cell Physiol. 287:C357-64; 2004.

Kudlacek P, Pluznick J, Padanilam BJ and SC Sansom. Role of H[[beta]]1 in activation of human mesangial BK channels by cGMP-kinase. Am J Physiol Renal Physiol. 285:F289-F294; 2003. 

Padanilam BJ.  Cell death induced by acute renal injury: A perspective on the contributions of apoptosis and necrosis. Am. J. Physiol Vol. 284, Issue 4, F608-F627, April 2003

Dina Polosukhina, Kurinji Singaravelu and Padanilam, BJ.  Activation of protein kinase C isozymes protects llcpk1 cells from H2O2 induced necrotic cell death. American  Journal of Nephrology 23: 380-389, 2003

Padanilam, BJ.  Induction and subcellular localization of PKC isozymes following renal ischemia.  Kidney Int’l  59:1789-1797, 2001.

Lewington, A.J.P., B.J. Padanilam, D.R. Martin and M.R. Hammerman.  Expression of CD44 and its ligands in kidney following acute ischemic injury in the rat.  Am. J. Physiol. 278:R247-R254, 2000.

Martin, D.R., A.J.P. Lewington, M.R. Hammerman and B.J. Padanilam.  Inhibition of poly (ADP-ribose) polymerase attenuates ischemic renal injury in rats.  Am. J. Physiol., 279:R1834-R1840, 2000.

Martin, D.R., A.J.P. Lewington, M.R. Hammerman and B.J. Padanilam.  Inhibition of poly (ADP-ribose) polymerase attenuates ischemic renal injury in rats.  J. Am. Soc. Nephrol. 10:A3225, 1999.

Padanilam, B.J. and A.J.P. Lewington.  Molecular mechanisms of cell death and regeneration in acute ischemic renal injury.  Current Opinion in Nephrology & Hypertension.  8:15-19, 1999.

Lewington, A.J.P., B.J. Padanilam, D.R. Martin and M.R. Hammerman.  Expression of CD44 and its ligands in kidney following acute ischemic injury in the rat.  J. Am. Soc. Nephrology 10:A3218, 1999.

Padanilam, B.J. and M.R. Hammerman.  Ischemia/rreperfusion-induced expression of CD27 and its ligand Siva in rat kidneys.  Kidney Int’l 54:1967-1975, 1998.

Padanilam, B.J. and M.R. Hammerman.  Ischemia/reperfusion-induced expession of CD27 and its ligand Siva in rat kidneys.  J. Am. Soc. Nephrology 9:A2275, 1998.

Miller, S.B. and B.J. Padanilam.  Molecular responses and growth factors.  In: Atlas of Diseases of the Kidney, Ed. 1, edited by R.W. Schrier, Current Medicine, Philadelphia, pp. 17.1-17.16,1998.

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• PREVIOUS GRADUATE STUDENTS/POST-DOCTORAL FELLOWS (present location):

Kurinji Singaravelu
Kishor Devalaraja-Narasimha

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• CURRENT RESEARCH PROJECTS:

Acute renal failure (ARF) is the most costly kidney disease in hospitalized patients.  Its high mortality has changed little despite the progress made in the practice of hemodialysis.  At present, there are no clinically accepted pharmaceutical agents to treat ARF.  My laboratory is studying the molecular response of the kidney following an ischemic episode and identifying key molecules involved in the injury and repair process.  Specifically, we are looking at the role of various molecules involved in cell death {poly (ADP-ribose)-polymerase (PARP), p53 and its transcriptional targets,  Protein Kinase C (PKC)} pathways and the role of stem cells in regeneration of the kidney post ischemia. We use pharmacological inhibitors, overexpression of wild type and mutant genes, transgenic and knock out models to study the role of these molecules in renal ischemia. 

A second major interest in the laboratory is in elucidating the molecular mechanisms of the development of type 2 diabetes in obese adolescents.  Recently, poly (ADP-ribose)-polymerase (PARP) has been implicated in the reactive oxygen species mediated activation of various signaling pathways.  We are investigating the role of PARP in the development of type 2 diabetes.

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• SPECIALIZED LABORATORY/CLINICAL RESEARCH RESOURCES:

Animal models for studying both acute renal failure and type 2 diabetes.
Cell culture studies using epithelial, endothelial and stem cells
Gene expression studies in in vitro and in vivo models of renal ischemia