Home » ... » - Faculty » Faculty Pages » Peterson, Richard E.
Peterson, Richard E.

 Richard E. Peterson, PhD
 Professor

Research Area:AhR Signaling. Reproductive and Developmental Toxicology. Mouse and zebrafish, Dioxin (TCDD), Prostate Growth, Develoment and Cancer, Heart Development, Nanotoxicology.

Home Dept: School of Pharmacy
Affiliated Depts: Molecular and Environmental Toxicology; Molecular and Cellular Pharmacology; Pharmaceutical Sciences

Address
5109 Rennebohm Hall
777 Highland Avenue
Madison, WI 53705
608/263-5453 - Email

 Milestones
2000-MERIT R37 - Research on the developmental reproductive toxicity of TCDD

 Research
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitous environmental contaminant which elicits a wide range of toxic responses. The developing male rat reproductive system is 100 times more sensitive to TCDD than is its adult counterpart. In utero and lactational exposure to a single low dose delays testis descent and preputial separation, decreases testis, epididymis, and accessory sex organ weights, and decreases daily sperm production, epididymal sperm reserves, and ejaculated sperm numbers throughout development. The mechanism underlying the spectrum of toxic responses elicited by TCDD is poorly understood. TCDD binds the aryl hydrocarbon receptor (AhR), which translocates to the nucleus and dimerizes with the AhR nuclear translocator (ARNT). This complex, a ligand-activated transcription factor, binds to enhancer elements (DREs) in the 5' regulatory region of genes and activates transcription. Although none of the TCDD-responsive genes identified to date have been directly linked to toxicity, it is thought that induction or repression of transcription of genes which have not yet been identified may play a key role in eliciting toxic responses. To better understand the mechanism by which TCDD selectively impairs the developing male reproductive system, we are characterizing the ontogeny and distribution of the AhR and ARNT within this organ system. In addition, we are working to identify genes that are transcriptionally modulated by in utero and lactational TCDD exposure in the prostate and epididymis, two organs which are particularly sensitive to this treatment. The identification of a TCDD-responsive gene(s) with known function may provide insight into the mechanism by which TCDD affects growth and/or function of the prostate, epididymis, and perhaps other organs as well. Novel genes will require characterization before mechanistic hypotheses can be formulated.

 Publications
  • Vezina, C.M., Allgeier, S.H., Moore, R.W., Lin, T.M., Bemis, J.C., Gasiewicz, T.A., and Peterson, R.E.: Spatiotemporal Patterns of Aryl Hydrocarbon Receptor Signaling and Prostatic Budding in 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Exposed Mice. Toxicol. Sci. 2008. (Submitted)
  • King Heiden, T.C., Wiecinski, P., Mangham, A., Metz, K.M., Nesbit, D., Pedersen, J.A., Hamers, R.J., Heideman, W., and Peterson, R.E.: Developmental Toxicity of Quantum Dots in Zebrafish Embryos: Shedding Light on Potential Ecotoxicological Risks of Engineered Nanoparticles. Env. Sci. Technol. . 2008. (Submitted).
  • Mehta, V., Peterson, R.E., and Heideman, W.: 2,3,7,8-Tetrachlorodibenzo-p-dioxin exposure prevents cardiac valve formation in developing zebrafish. Toxicol. Sci. : - , 2008. (In Press).
  • Fritz, W.A., Lin, T.L., and Peterson, R.E.: The aryl hydrocarbon receptor (AhR) inhibits vanadate-induced vascular endothelial growth factor (VEGF) production in TRAMP prostates. Carcinogenesis : - , 2008. (In Press)
  • Tillitt, D.E., Cook, P.M., Giesy, J.P., Heideman, W. and Peterson, R.E.: Reproductive impairment of Great Lakes lake trout by dioxin-like chemicals. In: The Toxicology of Fishes, Unit IV, Case Studies, (Di Giulio, R.T. and Hinton, D., eds.), CRC Press, Boca Raton, FL, Chapter 21, pp 819-875, 2008.
  • Lipinski, R.J., Hutson, P.R., Hannam, P.W., Nydza, R.J., Washington, I.M., Moore, R.W., Girdaukas, G.G., Peterson, R.E. and Bushman, W.: Dose- and route-dependent teratogenicity, toxicity, and pharmacokinetic profiles of the Hedgehog signaling antagonist cyclopamine in the mouse. Toxicol. Sci. 104: 189-197, 2008.
  • Vezina, C.M., Allgeier, S.H., Fritz, W.A., Moore, R.W., Strerath, M., Bushman, W., and Peterson, R.E.: Retinoic acid induces prostatic bud formation. Dev. Dyn. 237: 1321-1333, 2008.
  • Mukai, M., Lin, T.M., Peterson, R.E., Cooke, P.S., and Tischkau, S.A.: Behavioral rhythmicity of mice lacking AhR and attentuation of light-induced phase shift by 2,3,7,8-tetrachlorodibenzo-pdioxin. J. Biol. Rhyth. 23: 200-210, 2008.
  • Chen, J., Carney, S.A., Peterson, R.E., and Heideman, W.: Comparative genomics identifies genes mediating cardiotoxicity in the embryonic zebrafish heart. Physiol. Genomics 33: 148-158, 2008
  • Lipinski, R.J., Dengler, E., Kiehn, M., Peterson, R.E. and Bushman, W.: Identification and characterization of several dietary alkaloids as weak inhibitors of hedgehog signaling. Toxicol. Sci. 100 (2): 456-463, 2007.
  • King Heiden, T.C., Dengler, E. Kao, W.J., Heideman, W. and Peterson, R.E.: Developmental toxicity of low generation PAMAM dendrimers in zebrafish. Toxicol. Appl. Pharmacol. 225: 70-79, 2007
  • Kim, K.H., Antkiewicz, D.S., Kim, T.G., Heideman, W., Peterson, R.E., and Lee, Y.: Lrrc10 is required for early heart development and function in zebrafish. Dev. Biol. 308(2): 494-506, 2007. 3
  • Cook, C., Vezina, C.M., Hicks, S.M., Shaw, A., Yu, M., Peterson, R.E., and Bushman, W.; Noggin is required for normal lobe patterning and ductal budding in the mouse prostate. Dev. Biol. 312(1): 217-230, 2007
  • Fritz, W.A., Lin, T.-M., Cardiff, R.D. and Peterson, R.E.: The aryl hydrocarbon receptor inhibits prostate carcinogenesis in TRAMP mice. Carcinogenesis 28(2): 497-505, 2007.
  • Antkiewicz, D.S., Peterson, R.E., Heideman, W.: Blocking expression of AHR2 and ARNT1 in zebrafish larvae protects against cardiac toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol. Sci. 94: 175 -182, 2006.
  • van den Berg, M., Birnbaum, L., Denison, M., De Vito, M., Farland, W., Feeley, M., Fiedler, H., Hakansson, H., Hanberg, A., Haws, L., Rose, M., Safe, S., Schrenk, D., Tohyama, C., Tritscher, A., Tuomisto, J., Tysklind, M., Walker, N., and Peterson, R.E.: The 2005 World Health Organization re-evaluation of human and mammalian toxic equivalency factors for dioxins and dioxin-like compounds. Toxicol. Sci. 93: 223-241, 2006.
  • Carney, S.A., Chen, J., Burns, C.G., Xiong, K.M., Peterson, R.E., and Heideman, W.: AHR activation produces heart-specific transcriptional and toxic responses in developing zebrafish. Mol. Pharmacol. 70: 1-13, 2006.
  • Prasch, A.L., Tanguay, R.L., Mehta, V., Heideman, W., and Peterson, R.E.: Identification of zebrafish ARNT1 homologs: TCDD developmental toxicity in zebrafish requires ARNT1. Mol. Pharmacol. 69: 776-787, 2006.
  • Prasch, A.L., Tanguay, R.L., Mehta, V., Heideman, W., and Peterson, R.E.: Identification of zebrafish ARNT1 homologs: TCDD developmental toxicity in zebrafish requires ARNT1. Mol. Pharmacol. 69: 776-787, 2006.
  • Carney, S.A., Prasch, A.L., Heideman, W., and Peterson, R.E.: Understanding dioxin developmental toxicity using the zebrafish model. Birth Defects Research, Part A: Clinical and Molecular Teratology 76: 7 -18, 2006.
  • Doles, J.D., Vezina, C.M., Lipinski, R.J., Peterson, R.E., and Bushman, W.: Growth,morphogenesis, and differentiation during mouse prostate development in situ, in renal grafts,and in vitro. Prostate 65 (4): 390-399, 2005.
  • Fritz, W.A., Lin, T.-M., Moore, R.W., Cooke, P.S., and Peterson, R.E.: In utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure: Effects on the prostate and its response to castration in senescent C57BL/6J mice. Toxicol. Sci. 86: 387-395, 2005.
  • Lipinski, R.J., Cook, C.H., Barnett, D.H., Gipp, J.J., Peterson, R.E., and Bushman, W.: Sonic hedgehog signaling regulates the expression of Insulin-like growth factor binding protein-6 during fetal prostate development. Dev. Dyn. 233: 829-836, 2005.
  • Heideman, W., Antkiewicz, D.S., Carney, S.A., and Peterson, R.E.: Zebrafish and cardiac toxicology. Cardiovasc. Toxicol. 5: 203-214, 2005.
  • Mukai, M., Dong, Q., Hardy, M.P., Kiyokawa, H., Peterson, R.E., and Cooke, P.S.: Altered prostatic epithelial proliferation, apoptosis, prostatic development and serum testosterone in mice lacking cyclin-dependent kinase inhibitors. Biol. Repro. 73, 951-958, 2005.
  • Hill, A.J., Teraoka, H., Heideman, W. and Peterson, R.E.: Zebrafish as a model vertebrate for investigating chemical toxicity. Toxicol.Sci. 86: 6-19, 2005. 2
  • Antkiewicz, D.S., Burns, G.C., Carney, S.A., Peterson, R.E., and Heideman, W.: Heart malformation is an early response to TCDD in embryonic zebrafish. Toxicol. Sci. 84: 1-10, 2005.
  • Carney, S.A., Peterson, R.E., and Heideman, W.: 2,3,7,8-Tetrachlorodibenzo-p-dioxin activation of the aryl hydrocarbon/aryl hydrocarbon receptor nuclear translocator pathway causes developmental toxicity through a CYP1A-independent mechanism in zebrafish. Mol. Pharmacol. 66: 512-521, 2004.
  • Prasch, L., Heideman, W., and Peterson, R.E.: ARNT2 is not required for TCDD developmental toxicity in zebrafish. Toxicol. Sci. 82: 250-258, 2004.
  • Ito, T., Tsukumo, S., Suzuki, N., Motohashi, H., Yamamoto, M., Fuji-Kuriyama, Y., Mimura, J.,Lin, T.M., Peterson, R..E., Tohyama, C., and Nohara, K.: A constitutively active aryl hydrocarbon receptor induces growth inhibition of Jurkat T cells through changes in the expression of genes related to apoptosis and cell cycle arrest. J. Biol. Chem. 279: 25204-25210, 2004.
  • Simanainen, U., Haavisto, T., Tuomisto, J., Paranko, J., Toppari, J., Tuomisto, J., Peterson,R.E., and Viluksela, M.: Pattern of male reproduction system effects after in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in three differentially TCDD sensitive rat lines. Toxicol Sci. 80: 101-108, 2004.
  • Hill, A.J., Bello, S.M., Prasch, A.L., Peterson, R.E. and Heideman, W.: Water permeability and TCDD-induced edema in zebrafish early-life stages. Toxicol. Sci. 78: 78-87, 2004.
  • Ko, K., Theobald, H.M., Moore, R.W., and Peterson, R.E.: Evidence that inhibited prostatic epithelial bud formation in 2,3,7,8-tetrachlorodibenzo-p-dioxin-exposed C57BL/6J fetal mice is not due to interruption of androgen signaling in the urogenital sinus. Toxicol. Sci. 79: 360-369, 2004.
  • Bello, S.M., Heideman, W., and Peterson, R.E.: 2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibits regression of the common cardinal vein in developing zebrafish. Toxicol. Sci. 78: 258-266, 2004.
  • Ko, K., Moore, R.W., and Peterson, R.E.: Aryl hydrocarbon receptors in urogenital sinus mesenchyme mediate the inhibition of prostatic epithelial bud formation by 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicol. Appl. Pharmacol. 196: 149-155, 2004.
  • Lin, T.-M., Rasmussen, N., Moore, R.W., Albrecht, R.M., and Peterson, R.E.: 2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibits prostatic epithelial bud formation by acting directly on the urogenital sinus. J. Urol. 172: 365-368, 2004.
  • Prasch, A.L., Andreasen, E.A., Peterson, R.E., and Heideman, W.: Interactions between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and hypoxia signaling pathways in zebrafish: Hypoxia decreases responses to TCDD in zebrafish embryos. Toxicol. Sci. 78: 68-77, 2004

Date Last Updated: 07/09/2008 webteam@med.wisc.edu