The Richburg Lab

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The longstanding focus of the Richburg Laboratory is to decipher the molecular and cellular mechanisms by which exposure to environmental toxicants (e.g., phthalates) or clinical chemotherapeutic agents (e.g., cisplatin) can result in the disruption in spermatogenesis. Specifically, the unifying theme of my research program is to reveal the paracrine cellular signaling mechanisms between cells in the testis that regulate the balance between survival and death of germ cells. It is anticipated that mechanistic insights garnered from research in the laboratory will provide foundational cellular and mechanistic insights underlying the sensitivity of the testis to environmental toxicants that can be exploited in developing strategies to prevent the long-term disruption of male fertility from exposure to these agents.

Recent Laboratory News: A 5 -year NIH/NIEHS R01 grant has been received to delineate the functional contribution of cells of the innate immune system (macrophages & monocytes) in the sequence of events that occur in the pubertal rodent testis after exposure to the environmental toxicant, mono-(2-ethylhexyl) phthalate (MEHP). The work of this research proposal is relevant to human health as it is anticipated to provide mechanistic insights that will be valuable for predicting and preventing human reproductive health risks to environmental toxicants. Assessing the individual susceptibility to interactions of environmental toxicants with the immune system is consistent with goals of the NIEHS 2018-2023 strategic plan. Click to see more.

Recent Peer-Reviewed Publications:

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  • Gillette, R, Tiwary, R, Voss, JJLP and Richburg, JH (2019). Peritubular macrophages and spermatogonia are sequentially increased in the testis of rats after mono-(2-ethylhexyl) phthalate exposure. BioRXiv. Posted online Sep. 12, 2019; doi: 10.1101/767707
  • Ghaffari, R, and Richburg, JH (2019). Mice with a Sertoli cell-specific knockout of the Ctr1 gene exhibit a reduced sensitivity to cisplatin-induced testicular germ cell apoptosis. Toxicology Research. 8, 972-978. PMC7344760
  • Ghaffari, R, Di Bona, KR, Riley, CL and Richburg, JH (2019). Copper transporter 1 (CTR1) expression by mouse testicular germ cells, but not Sertoli cells, is essential for functional spermatogenesis. PlosOne. 14 (4) PMC6474593
  • Voss, JJLP, Stermer, AR, Ghaffari, R, Tiwary, R, and Richburg, JH (2018). MEHP-induced rat testicular inflammation does not exacerbate germ cell apoptosis. Reproduction. 156 (1): 35-46. PMCID: PMC6021206
  • Bao, J, Perez, CJ, Kim, J, Zhang, H, Murphy, CJ, Hamidi, T, Jaubert, J, Platt, C, Deng, M, Gaitán-Peñas, H, Guénet, J-L, Chen, T, Bedford, MT, Dent, SYR, Richburg, JH, Estévez, R, Pan, H-L, Geha, RS, Shi, Q, and Benavides, F (2018). Deficient LRRC8A-dependent volume-regulated anion channel activity is associated with male infertility in mice. Journal of Clinical Investigation Insight. 3(16) e99767. PMCID: PMC6141173

Male Fertility: Richburg Lab Research in the News

Dr. Richburg speaks with KXAN News about his research in how male fertility can be affected by environmental toxins found in everyday plastic products, and by chemotherapy in the treatment of testicular cancer (OK, a little dated now – but still fun to watch!)..


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