The Richburg Lab

Richburg Lab ImagesThe longstanding focus of my research program is to decipher the molecular and cellular mechanisms by which exposure to certain environmental agents (e.g., phthalate acid ester-based plasticizers) or clinical chemotherapeutic drugs (e.g., cisplatin) can result in disruption of male reproduction. Specifically, the unifying theme of the research conducted in my laboratory is targeted at understanding the paracrine cellular signaling mechanisms between the Sertoli cells and germ cells in the testis that regulate the death (and/or survival) of germ cells by the process of apoptosis.

Recent experimental findings in my laboratory have suggested key roles of distinct macrophage subtypes in the sequence of events instigated by phthalate-induced testicular injury during the pubertal period in rodents. The species- (rat more than mice) and age- (pubertal more than adult age) dependent sensitivity to phthalate-induced testicular injury is well-recognized . Our findings have established that monocyte infiltration parallels the extent of phthalate-induced testicular injury. A particularly intriguing observation is an increase in the number, regional localization and morphological alteration of a distinctive subtype of testicular macrophages, peritubular macrophages, in response to MEHP exposure. These cells have been reported to be enriched in regions overlying undifferentiated spermatogonia and express factors known to positively influence spermatogonial proliferation and differentiation. However, the role of these cells in responding to testicular injury is not yet understood. Therefore, this work is expected to provide. novel insights into mechanisms underlying the susceptibility of individuals to MEHP-induced disruption of spermatogenesis that will be useful for predicting and preventing vulnerable individuals to phthalate-associated testicular disease.

John H. Richburg, Ph.D.

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.

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