Volume 14, No 1, Feb 2004
ISSN: 1001-0602
EISSN: 1748-7838 2018
impact factor 17.848*
(Clarivate Analytics, 2019)
Volume 14 Issue 1, February 2004: 54-59
ORIGINAL ARTICLES
Impaired reproduction in transgenic mice overexpressing γ-aminobutyric acid transporter I (GAT1)
Jia Hua HU1,*, Jin Fu ZHANG2,*, Ying Hua MA1, Jie JIANG1, Na YANG1, Xin Bo LI3, Zhi Guang YU CHI4, Jian FEI1, 5, Li He GUO1
1Laboratory of Molecular Cell Biology, Institute of Bi??hemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
2Department of Urology, Tongji Hospital, Tongji University, 389 Xincun Road, Shanghai 200065, China.
3New Drug R & D Center, North China Pharmaceutical Group Corporation, 388 Heping East Road, Shijia Zhuang 050015, Hebei, China.
4School of life sciences, Fudan University, 220 Handan Road, Shanghai 200433, China.
5Shanghai Research Center for Biomodel Organism, Shanghai 201203, China.
Correspondence: Li He GUO(mhzhang@sunm.shcnc.ac.cn )
It is well documented
that
γ-aminobutyric
acid (GABA) system existed in reproductive organs. Recent researches showed
that GABAA and GABAB receptors were present in testis
and sperm, and might mediate the acrosome reaction induced by GABA and
progesterone. GABA transporter I (GAT1) also existed in testis and sperm,
but its physiological function was unknown. In the present study, we used
GAT1 overexpressing mice to explore GAT1 function in male reproductive
system. We found that the expression level of GAT1 continuously increased
in wild-type mouse testis from 1 month to 2 months after birth. GAT1 overexpression
in mouse affected testis development, which embodied reduced testis mass
and slowed spermatogenesis in transgenic mice. Moreover, transgenic mice
showed increase of the percentage of broken sperm. The further study revealed
that the reproductive capacity was impaired in GAT1 overexpressing mice.
In addition, testosterone level was significantly low in transgenic mice
compared with that in wild-type mice. Our findings provided the first
evidence that abnormal expression of GAT1 could result in dysgenesis,
and indicated that GAT1 might be therapeutically targeted for contraception
or dysgenesis treatment.
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