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Dev Reprod. 2015 Jun;19(2):69-77. doi: 10.12717/DR.2015.19.2.069.

Modification of Gene Expression of Connexins in the Rat Corpus Epididymis by Estradiol Benzoate or Flutamide Exposure at the Early Neonatal Age.

Development & reproduction

Ki-Ho Lee

Affiliations

  1. Dept. of Biochemistry and Molecular Biology, College of Medicine, Eulji University, Daejeon 301-746, Korea.

PMID: 27004263 PMCID: PMC4801050 DOI: 10.12717/DR.2015.19.2.069

Abstract

Cell-cell direct communication through channel-forming molecules, connexin (Cx), is essential for a tissue to exchange signaling molecules between neighboring cells and establish unique functional characteristics during postnatal development. The corpus epididymis is a well-known androgen-responsive tissue and involves in proper sperm maturation. In the present research, it was attempted to determine if expression of Cx isoforms in the corpus epididymis in the adult is modulated by exposure to estrogenic or anti-androgenic compound during the early postnatal period. The neonatal male rats at 7 days of age were subcutaneously injected by estradiol benzoate (EB) at low-dose (0.015 mg/kg body weight) or high-dose (1.5 mg/kg body weight) or flutamide (Flu) at low-dose (500 mg/kg body weight) or high-dose (50 mg/kg body weight). The corpus epididymis collected at 4 months of age was subjected to evaluate expressional changes of Cx isoforms by quantitative real-time PCR. Treatment of low-dose EB resulted in increases of Cx32, Cx37, and Cx45 transcript levels, while exposure to high-dose EB decreased expression of Cx26, Cx30.3, Cx31, Cx31.1, Cx32, Cx40, Cx43, and Cx45. Treatments of Flu caused significant decreases of expression of all examined Cx isoforms, except Cx37 and Cx43 shown no expressional change with high-dose Flu treatment. These findings imply that expression of most Cx isoforms present in the corpus epididymis would be transcriptionally regulated by actions of androgen and/or estrogen during postnatal period.

Keywords: Connexin; Corpus epididymis; Estradiol benzoate; Flutamide; Gene expression

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