Samson Jamesdaniel (fn2963)

6135 Woodward, IBio Rm. 2127
Detroit, MI 48202

Dr. Jamesdaniel has a joint appointment with the Institute for Environmental Health Sciences (IEHS). Dr. Jamesdaniel's research is focused on understanding the redox sensitive molecular mechanisms underlying the ototoxic effects of physical and chemical stressors. Noise, a pervasive environmental stressor, induces oxidative stress to affect physiological as well as psychological well-being. Its interaction with environmental ototoxicants, such as lead and cadmium, can potentiate the damage to the auditory system. His laboratory is interested in delineating these interactions and associated signaling mechanisms. In addition, he is also investigating the nitrative stress mechanism in cisplatin-induced hearing loss. He teaches FPH 7420 Principles of Environmental Health.

 Please see Dr. Jamesdaniel's CV. 

MPH

Redox sensitive molecular mechanisms play an important role in the regulation of cellular damage in acquired hearing loss induced by ototoxic environmental exposures, drugs, and aging.

1)  Noise, a pervasive environmental stressor, induces oxidative stress to affect the physiological as well as psychological well-being. My laboratory employs omics approaches to elucidate redox sensitive signaling mechanisms/pathways that regulate noise-induced hearing impairment as well as stress response. We are also interested in evaluating the interactions of environmental chemicals, such as lead and cadmium, that may play an important role in determining the susceptibility to noise-induced hearing loss.

2)  Cisplatin is a widely used anti-cancer drug, whose major side-effects include ototoxicity. Cisplatin induces nitration of cochlear proteins, an indicator of oxidative damage to proteins, and we identified the most abundant nitrated cochlear protein as LMO4, a transcriptional regulator. My laboratory is interested in delineating the signaling mechanism by which nitration of LMO4 alters its biological activity to induce cellular apoptosis and mediate cochlear cell death.

Rosati R, Shahab M, Ramkumar V, Jamesdaniel S. Lmo4 Deficiency Enhances Susceptibility to Cisplatin-Induced Cochlear Apoptosis and Hearing Loss. Mol Neurobiol. 2021. 58: 2019-2029.

Shahab M, Rosati R, Meyers D, Sheilds J, Crofts E, Baker TR, Jamesdaniel S. Cisplatin-induced hair cell loss in zebrafish neuromasts is accompanied by protein nitration and Lmo4 degradation. Toxicol Appl Pharmacol. 2021. 410: 115342.

Rosati, R., Jamesdaniel, S. Environmental exposures and hearing loss. Int J Environ Res Public Health. 2020. 17: 4879.

Rosati R, Shahab M, Neumann WL, Jamesdaniel S. Inhibition of protein nitration prevents cisplatin-induced inactivation of STAT3 and promotes anti-apoptotic signaling in organ of Corti cells. Exp Cell Res. 2019. 381: 105-111.

Jamesdaniel S, Elhage KG, Rosati R, Ghosh S, Arnetz B, Blessman J. Tinnitus and Self -Perceived Hearing Handicap in Firefighters: A Cross-Sectional Study. Int. J. Environ. Res. Public Health. 2019. 16: 3958.

Jamesdaniel S, Rosati R, Westrick J, Ruden DM. Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss. Toxicol Lett. 2018. 292: 175-180.

Rathinam R, Rosati R, Jamesdaniel S. CRISPR/Cas9-mediated knockout of Lim- domain only 4 retards organ of Corti cell growth. J Cell Biochem. 2018. 119: 3545-3553.

Jamesdaniel S, Rathinam R, Neumann WL. Targeting nitrative stress for attenuating cisplatin-induced downregulation of cochlear LIM domain only 4 and ototoxicity. Redox Biol. 2016. 10: 257-265.

Rathinam R, Ghosh S, Neumann WL, Jamesdaniel S. Cisplatin-induced apoptosis in auditory, renal, and neuronal cells is associated with nitration and downregulation of LMO4. Cell Death Discovery. 2015. 1, 15052.

Jamesdaniel S, Coling D, Hinduja S, Ding D, Li J, Cassidy L, Seigel M, Qu J, Salvi R. Cisplatin-induced ototoxicity is mediated by nitroxidative modification of cochlear proteins characterized by nitration of Lmo4. J Biol Chem. 2012. 287: 18674-18686.

Jamesdaniel S, Hu B, Habiby Kermany M, Jiang H, Ding D, Coling D, Salvi R. Noise induced changes in the expression of p38/MAPK signaling proteins in the sensory epithelium of the inner ear. J Proteomics. 2011. 75: 410-424.

Jamesdaniel S, Ding D, Habiby Kermany M, Jiang H, Salvi R, Coling D. Analysis of cochlear protein profiles of Wistar, Sprague-Dawley and Fischer 344 Rats having normal hearing function. J Proteome Res. 2009. 8: 3520-3528.

Jamesdaniel S, Ding D, Habiby Kermany M, Davidson B, Knight P, Salvi R, Coling D. Proteomic analysis of the balance between survival and cell death responses in cisplatin mediated ototoxicity. J Proteome Res. 2008. 7: 3516-3524.

Redox sensitive molecular mechanisms play an important role in the regulation of cellular damage in acquired hearing loss induced by noise exposure, ototoxic drugs, and aging.

1) Noise is a pervasive environmental stressor, which induces oxidative stress to affect the physiological as well as psychological well-being. Since proteins determine the functional state of a cell, my laboratory employs a proteomic approach to elucidate redox sensitive signaling mechanisms/pathways that regulate noise-induced hearing impairment as well as stress response. We are also interested in identifying the genetic and environmental factors that play an important role in determining the susceptibility to noise-induced hearing loss.

2) Cisplatin is a commonly used anti-cancer drug, whose major side-effects include ototoxicity. Cisplatin induces nitration of cochlear proteins, an indicator of oxidative damage to proteins, and we identified the most abundant nitrated cochlear protein as LMO4, a transcriptional regulator. My laboratory is interested in delineating the signaling mechanism by which nitration of LMO4 alters its biological activity to induce cellular apoptosis and mediate cochlear cell death.

6135 Woodward Avenue, IBio Rm. 2127
Detroit, MI - 48202

313-577-6578

Redox sensitive molecular mechanisms play an important role in the regulation of cellular damage in acquired hearing loss induced by noise exposure, ototoxic drugs, and aging.

1. Noise is a pervasive environmental stressor, which induces oxidative stress to affect the physiological as well as psychological well-being. My laboratory employs a proteomic approach to elucidate redox sensitive signaling mechanisms/pathways that regulate noise-induced hearing impairment as well as stress response. We are also interested in identifying the interaction between genetic and environmental factors that play an important role in determining the susceptibility to noise-induced hearing loss.
    
2. Cisplatin is a commonly used anti-cancer drug, whose major side-effects include ototoxicity. Cisplatin induces nitration of cochlear proteins, an indicator of oxidative damage to proteins, and we identified the most abundant nitrated cochlear protein as LMO4, a transcriptional regulator. My laboratory is interested in delineating the signaling mechanism by which nitration of LMO4 alters its biological activity to induce cellular apoptosis and mediate cochlear cell death.

Ph.D., (2006, Physiology) - University of Madras, Chennai, India.

M.D., (2001, Alternative Medicine) - Tamil Nadu Dr. MGR Medical University, Chennai, India.

• Jamesdaniel S, Rathinam R, Neumann WL. Targeting nitrative stress for attenuating cisplatin-induced downregulation of cochlear LIM domain only 4 and ototoxicity. Redox Biol. 2016. 10: 257-265.
• Manohar S, Jamesdaniel S, Ding D, Salvi R, Seigel G, Roth, J. Quantitative PCR analysis and protein distribution of drug transporter genes in the rat cochlea. Hear Res. 2016. 332, 46-54.
• Rathinam R, Ghosh S, Neumann WL, Jamesdaniel S. Cisplatin-induced apoptosis in auditory, renal, and neuronal cells is associated with nitration and downregulation of LMO4. Cell Death Discovery 2015. 1, 15052.
• Jamesdaniel S. Downstream targets of Lmo4 are modulated by cisplatin in the inner ear of Wistar rats. PLoS One. 2014. 9(12): e115263.
• Alagramam KN, Stepanyan R, Jamesdaniel S, Chen DH, Davis RR. Noise exposure immediately activates cochlear mitogen-activated protein kinase signaling. Noise Health. 2014. 16: 400-409.
• Jamesdaniel S, Manohar S, Hinduja S. Is S-nitrosylation of cochlear proteins a critical factor in cisplatin-induced ototoxicity? Antioxid Redox Signal. 2012. 17: 929- 933.  
• Jamesdaniel S, Coling D, Hinduja S, Ding D, Li J, Cassidy L, Seigel M, Qu J, Salvi R. Cisplatin-induced ototoxicity is mediated by nitroxidative modification of cochlear proteins characterized by nitration of Lmo4. J Biol Chem. 2012. 287: 18674-18686.