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Fertil Steril. 2015 Jan;103(1):270-80.e8. doi: 10.1016/j.fertnstert.2014.09.023. Epub 2014 Nov 5.

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

Author information

  • 1Department of Biology, University of Texas at San Antonio, San Antonio, Texas.
  • 2Department of Biomedical Engineering, University of Texas at San Antonio, San Antonio, Texas.
  • 3Department of Biology, University of Texas at San Antonio, San Antonio, Texas. Electronic address: brian.hermann@utsa.edu.

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.

KEYWORDS:

Spermatogonial stem cells; cancer therapy; cytokines; fertility preservation; infertility

PMID:
25439845
PMCID:
PMC4282609
DOI:
10.1016/j.fertnstert.2014.09.023
[PubMed - indexed for MEDLINE]
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