Impaired female fertility in tubulointerstitial Antigen-Like 1-Deficient mice

Akihito Takahashi, Ajalli Rahim, Miki Takeuchi, Emiko Fukui, Midori Yoshizawa, Kuniaki Mukai, Makoto Suematsu, Hidetoshi Hasuwa, Masaru Okabe, Hiromichi Matsumoto

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Tubulointerstitial nephritis antigen-like 1 (Tinagl1, also known as adrenocortical zonation factor 1 [AZ-1] or lipocalin 7) is a matricellular protein. Previously, we demonstrated that Tinagl1 expression was restricted to extraembryonic regions during the postimplantation period and detected marked expression in mouse Reichert’s membranes. In uteri, Tinagl1 is markedly expressed in the decidual endometrium during the postimplantation period, suggesting that it plays a physical and physiological role in embryo development and/or decidualization of the uterine endometrium during pregnancy. In the present study, in order to determine the role of Tinagl1 during embryonic development and pregnancy, we generated Tinagl1-deficient mice. Although Tinagl1–/– embryos were not lethal during development to term, homologous matings of Tinagl1–/– females and Tinagl1–/– males showed impaired fertility during pregnancy, including failure to carry pregnancy to term and perinatal lethality. To examine ovarian function, ovulation was induced with equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG); the number of ovulated oocytes did not differ between Tinagl1–/–and Tinagl1flox/ flox. In vitro fertilization followed by embryo culture also demonstrated the normal developmental potential of Tinagl1-null embryos during the preimplantation period. Our results demonstrate that Tinagl1 deficiency affects female mice and results in subfertility phenotypes, and they suggest that although the potential of Tinagl1–/– oocytes is normal, Tinagl1 is related to fertility in adult females but is not essential for either fertilization or preimplantation development in vitro.

Original languageEnglish
Pages (from-to)43-49
Number of pages7
JournalJournal of Reproduction and Development
Volume62
Issue number1
DOIs
Publication statusPublished - 2016 Feb 20

Fingerprint

female fertility
pregnancy
antigens
endometrium
mice
embryo (animal)
oocytes
embryogenesis
equine chorionic gonadotropin
nephritis
embryo culture
human chorionic gonadotropin
in vitro fertilization
fertilization (reproduction)
uterus
ovulation
phenotype
proteins

Keywords

  • Mouse
  • Pregnancy
  • Subfertility
  • Tubulointerstitial nephritis antigen-like 1 (Tinagl1)

ASJC Scopus subject areas

  • Animal Science and Zoology

Cite this

Takahashi, A., Rahim, A., Takeuchi, M., Fukui, E., Yoshizawa, M., Mukai, K., ... Matsumoto, H. (2016). Impaired female fertility in tubulointerstitial Antigen-Like 1-Deficient mice. Journal of Reproduction and Development, 62(1), 43-49. https://doi.org/10.1262/jrd.2015-109

Impaired female fertility in tubulointerstitial Antigen-Like 1-Deficient mice. / Takahashi, Akihito; Rahim, Ajalli; Takeuchi, Miki; Fukui, Emiko; Yoshizawa, Midori; Mukai, Kuniaki; Suematsu, Makoto; Hasuwa, Hidetoshi; Okabe, Masaru; Matsumoto, Hiromichi.

In: Journal of Reproduction and Development, Vol. 62, No. 1, 20.02.2016, p. 43-49.

Research output: Contribution to journalArticle

Takahashi, A, Rahim, A, Takeuchi, M, Fukui, E, Yoshizawa, M, Mukai, K, Suematsu, M, Hasuwa, H, Okabe, M & Matsumoto, H 2016, 'Impaired female fertility in tubulointerstitial Antigen-Like 1-Deficient mice', Journal of Reproduction and Development, vol. 62, no. 1, pp. 43-49. https://doi.org/10.1262/jrd.2015-109
Takahashi, Akihito ; Rahim, Ajalli ; Takeuchi, Miki ; Fukui, Emiko ; Yoshizawa, Midori ; Mukai, Kuniaki ; Suematsu, Makoto ; Hasuwa, Hidetoshi ; Okabe, Masaru ; Matsumoto, Hiromichi. / Impaired female fertility in tubulointerstitial Antigen-Like 1-Deficient mice. In: Journal of Reproduction and Development. 2016 ; Vol. 62, No. 1. pp. 43-49.
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