PMID- 11700863
OWN - NLM
STAT- MEDLINE
DCOM- 20020502
LR  - 20191105
IS  - 0196-3635 (Print)
IS  - 0196-3635 (Linking)
VI  - 22
IP  - 6
DP  - 2001 Nov-Dec
TI  - Impairment of spermatogenesis in transgenic mice with selective overexpression of 
      Bcl-2 in the somatic cells of the testis.
PG  - 981-91
AB  - To explore the functional role of Bcl-2 in germ cell development, transgenic mice 
      carrying 6 kilobases of the inhibin-alpha promoter were generated to express 
      human bcl-2 gene product in the gonads. Although female transgenic mice 
      demonstrated decreased follicle apoptosis, enhanced folliculogenesis, and 
      increased germ cell tumorigenesis, the adult males exhibited variable impairment 
      of spermatogenesis. The degree of damage ranged from tubules with intraepithelial 
      vacuoles of varying sizes to near atrophied tubules consisting of Sertoli cells 
      and a few spermatogonia. Although there was no significant change in body weight, 
      an approximately 34% decrease in testicular weights was noted in transgenic 
      animals compared with wild-type mice. Gamete maturation, assessed by determining 
      the percentage of tubules with advanced (steps 13-16) spermatids, was decreased 
      to 44.4% of the values measured in the wild-type animals. The incidence of germ 
      cell apoptosis increased 3.8-fold in the transgenic animals and was associated 
      with a marked loss of germ cells. Electron microscopy of the testes further 
      revealed large vacuoles in the Sertoli cell cytoplasm and dilations of the 
      intracellular spaces between adjacent Sertoli cells, spermatid malformations, and 
      increased germ cell apoptosis in the transgenic animals. There was no evidence of 
      Sertoli cell death either by terminal deoxynucleotidyl transferase-mediated dUTP 
      nick end labeling (TUNEL) assay or electron microscopy. Leydig cell 
      ultrastructure, cell size and numbers, and plasma levels of testosterone were not 
      different between normal and the transgenic animals. Collectively, these results 
      support the critical role of Bcl-2 in male germ cell development and are 
      consistent with the gender-specific role of the Bcl-2 family members in 
      reproduction.
FAU - Yamamoto, C M
AU  - Yamamoto CM
AD  - Department of Medicine, Harbor-UCLA Medical Center and Research and Education 
      Institute, Torrance, California 90509, USA.
FAU - Hikim, A P
AU  - Hikim AP
FAU - Lue, Y
AU  - Lue Y
FAU - Portugal, A M
AU  - Portugal AM
FAU - Guo, T B
AU  - Guo TB
FAU - Hsu, S Y
AU  - Hsu SY
FAU - Salameh, W A
AU  - Salameh WA
FAU - Wang, C
AU  - Wang C
FAU - Hsueh, A J
AU  - Hsueh AJ
FAU - Swerdloff, R S
AU  - Swerdloff RS
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Androl
JT  - Journal of andrology
JID - 8106453
RN  - 3XMK78S47O (Testosterone)
RN  - 9002-68-0 (Follicle Stimulating Hormone)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Body Weight
MH  - Female
MH  - Follicle Stimulating Hormone/blood
MH  - *Gene Expression Regulation
MH  - *Genes, bcl-2
MH  - Male
MH  - Mice
MH  - *Mice, Transgenic
MH  - Organ Size
MH  - Ovarian Follicle/cytology
MH  - Sertoli Cells/cytology
MH  - Spermatogenesis/*genetics
MH  - Spermatozoa/abnormalities
MH  - Testis/anatomy & histology/*physiology/ultrastructure
MH  - Testosterone/blood
MH  - Vacuoles/ultrastructure
EDAT- 2001/11/10 10:00
MHDA- 2002/05/03 10:01
CRDT- 2001/11/10 10:00
PHST- 2001/11/10 10:00 [pubmed]
PHST- 2002/05/03 10:01 [medline]
PHST- 2001/11/10 10:00 [entrez]
AID - 10.1002/j.1939-4640.2001.tb03439.x [doi]
PST - ppublish
SO  - J Androl. 2001 Nov-Dec;22(6):981-91. doi: 10.1002/j.1939-4640.2001.tb03439.x.