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HENRY JAY FORMAN, PhDProfessor
School of Natural Sciences
Email: hforman@ucmerced.edu
Phone: (209)228-4370
Fax: (509)757-4370
Associate Editor, Free Radical Biology & Medicine
Treasurer, International Society for Free Radical Research
Co-Director, Atmospherics Aerosols and Health Research Program
B.A. Chemistry, Queens College, New York
Ph.D. Biochemistry, Columbia University
Personal website
Research Interests (View)
Research Interests (View)
Our laboratory focuses on the molecular biology and biochemistry of signal transduction and cellular adaptation to reactive oxygen species and other electrophiles relevant to the response of the lung to environmental pollution.
Signal transduction: In response to the types of particles in air pollution, lung macrophages generates reactive oxygen species (ROS). ROS can cause direct cell injury. More interestingly, ROS also signal for the activation of transcription factors, which regulate cytokine production and produce inflammation in lung diseases. The underlying mechanisms involve hydrogen peroxide acting as a second messenger in multiple signaling pathways in which activation of protein kinases, reversible inactivation of protein tyrosine phosphatases, and transient elevation of intracellular free calcium concentration play key roles. The mechanisms of activation of these processes and their interactions are being pursued.
Gene regulation in antioxidant defense: In response to toxicants and oxidative stress, such as in tobacco smoke, cells increase their defenses through increased synthesis of protective enzymes. These so-called Phase II enzymes include those responsible for the synthesis of glutathione (GSH), the major antioxidant in mammalian cells, which also increases. The induction of Phase II enzymes and GSH allows greater resistance to subsequent challenge by toxicants. Increased transcription, translation and mRNA stability of Phase II enzymes have been demonstrated. Our research focuses primarily on the signaling pathways that regulate transcription of the Phase II genes.
Funding for graduate students is available through the Atmospheric Aerosols and Health (AAH) Lead Campus program (a joint program between UC Merced and UC Davis http://aah.ucdavis.edu or contact me directly.
Representative Publications (View)Signal transduction: In response to the types of particles in air pollution, lung macrophages generates reactive oxygen species (ROS). ROS can cause direct cell injury. More interestingly, ROS also signal for the activation of transcription factors, which regulate cytokine production and produce inflammation in lung diseases. The underlying mechanisms involve hydrogen peroxide acting as a second messenger in multiple signaling pathways in which activation of protein kinases, reversible inactivation of protein tyrosine phosphatases, and transient elevation of intracellular free calcium concentration play key roles. The mechanisms of activation of these processes and their interactions are being pursued.
Gene regulation in antioxidant defense: In response to toxicants and oxidative stress, such as in tobacco smoke, cells increase their defenses through increased synthesis of protective enzymes. These so-called Phase II enzymes include those responsible for the synthesis of glutathione (GSH), the major antioxidant in mammalian cells, which also increases. The induction of Phase II enzymes and GSH allows greater resistance to subsequent challenge by toxicants. Increased transcription, translation and mRNA stability of Phase II enzymes have been demonstrated. Our research focuses primarily on the signaling pathways that regulate transcription of the Phase II genes.
Funding for graduate students is available through the Atmospheric Aerosols and Health (AAH) Lead Campus program (a joint program between UC Merced and UC Davis http://aah.ucdavis.edu or contact me directly.
- Forman, H.J. Use and abuse of exogenous H2O2 in studies of signal transduction. Free Radic. Biol. Med. 42: 926-932, 2007.
- Liu, H., Zhang, H. and Forman, H.J. Silica induces macrophage cytokines through phosphatidylcholine-specific phospholipase C with H2O2. Am. J. Respir. Cell Mol. Biol. doi:10.1165/rcmb.2006-0297OC
- lles, K.E., Dickinson, D.A., Wigley, A,F., Welty, N.E., Blank, V. and Forman, H.J. HNE increases HO-1 through activation of the ERK pathway in pulmonary epithelial cells. Free Radic. Biol. Med. 39: 355-364, 2005.
- Forman, H.J., Fukuto, J.M., and Torres, M. Redox signaling - thiol chemistry defines which reactive oxygen and nitrogen species can act as second messengers. Am. J. Physiol: Cell Physiol. 287: C246-C256, 2004.
- Dickinson, D.A., Iles, K.E., Zhang, H., Blank, V. and Forman, H.J. Curcumin alters EpRE and AP-1 binding complexes and elevates glutamate-cysteine ligase gene expression. Faseb J. (January 2, 2003) 10.1096/fj.02-0566fje (Full text - online). Faseb J. 17: 473-475, 2003 (Print version summary).