Granulocyte colony stimulating factor prevents loss of spermatogenesis after sterilizing busulfan chemotherapy

Spermatogenesis can be destroyed by alkylating chemotherapies. In this study, spermatogenesis and undifferentiated spermatogonia in mice treated with busulfan were protected by treatment with granulocyte colony-stimulating factor.

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Authors

Roberto Benavides-Garcia, Rose Joachim, Nancy A. Pina, B.S., Kazadi N. Mutoji, Ph.D., Matthew A. Reilly, Ph.D., Brian P. Hermann, Ph.D.

Volume 103, Issue 1, Pages 270-280

Abstract

Objective:

To determine whether granulocyte colony-stimulating factor (G-CSF) could prevent loss of spermatogenesis induced by busulfan chemotherapy via protection of undifferentiated spermatogonia, which might serve as an adjuvant approach to preserving male fertility among cancer patients.

Design:

Laboratory animal study.

Setting:

University.

Animal(s):

Laboratory mice.

Intervention(s):

Five-week-old mice were treated with a sterilizing busulfan dose and with 7 days of G-CSF or vehicle treatment and evaluated 10 weeks later (experiment 1) or 24 hours after treatment (experiment 2).

Main Outcome Measure(s):

Experiment 1: testis weights, epididymal sperm counts, testis histology. Experiment 2: PLZF immunofluorescent costaining with apoptotic markers. Molecular analysis of G-CSF receptor expression in undifferentiated spermatogonia.

Result(s):

Ten weeks after treatment, busulfan-treated mice that also received treatment with G-CSF exhibited significantly better recovery of spermatogenesis and epididymal sperm counts than animals receiving busulfan alone. G-CSF led to increased numbers of PLZF+ spermatogonia 24 hours after treatment that was not accompanied by changes in apoptosis. To address the cellular target of G-CSF, mRNA for the G-CSF receptor, Csf3r, was found in adult mouse testes and cultured THY1+ (undifferentiated) spermatogonia, and cell-surface localized CSF3R was observed on 3% of cultured THY1+ spermatogonia.

Conclusion(s):

These results demonstrate that G-CSF protects spermatogenesis from gonadotoxic insult (busulfan) in rodents, and this may occur via direct action on CSF3R+ undifferentiated spermatogonia. G-CSF treatment might be an effective adjuvant therapy to preserve male fertility in cancer patients receiving sterilizing treatments.

Read the full text at: http://www.fertstert.org/article/S0015-0282(14)02200-6/fulltext


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Editorial Office, American Society for Reproductive Medicine

Fertility and Sterility® is an international journal for obstetricians, gynecologists, reproductive endocrinologists, urologists, basic scientists and others who treat and investigate problems of infertility and human reproductive disorders. The journal publishes juried original scientific articles in clinical and laboratory research relevant to reproductive endocrinology, urology, andrology, physiology, immunology, genetics, contraception, and menopause. Fertility and Sterility® encourages and supports meaningful basic and clinical research, and facilitates and promotes excellence in professional education, in the field of reproductive medicine.

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