Estrogen decreases the expression of claudin-5 in vascular endothelial cells in the murine uterus

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Author(s)

    • Hata Masaki
    • Department of Pathology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan
    • Yamanegi Koji
    • Department of Pathology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan
    • Yamada Naoko
    • Department of Pathology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan
    • Ohyama Hideki
    • Department of Pathology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan
    • Yukitatsu Yoriko
    • Department of Pathology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan |Department of Otolaryngology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan
    • Nakasho Keiji
    • Department of Pathology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan
    • Okamura Haruki
    • Department of Tumor Immunology and Cell Therapy, Hyogo College of Medicine, Nishinomiya 663-8501, Japan
    • Terada Nobuyuki
    • Department of Pathology, Hyogo College of Medicine, Nishinomiya 663-8501, Japan

Abstract

Vascular endothelial (VE)-cadherin and claudin-5 are major components of the adherens and tight junctions of vascular endothelial cells, respectively, and decreases in their expression are associated with increases in endothelial paracellular permeability. In the uterus, estrogen induces endometrial edema. However, the <i>in vivo</i> effect of estrogen on endothelial paracellular permeability is unknown. Therefore, we studied the expression of VE-cadherin and claudin-5 in vascular endothelial cells in murine uteri stimulated by estrogen or progesterone. Ovariectomized mature mice were injected with estradiol-17β (1 μg/mouse) or progesterone (1 mg/mouse) at intervals of 24 hours for 6 days. The frozen transverse sections of the uteri of these mice and untreated mice were stained for CD31 (vascular endothelial cell marker) plus VE-cadherin or claudin-5 using a double-immunofluorescence method. Then, the percentages of VE-cadherin- or claudin-5-positive vessels among CD31-positive vessels were examined in the uterine endometria. VE-cadherin and claudin-5 were expressed in most CD31-positive vessels in the endometria of the untreated mice. Progesterone did not affect the expression of both VE-cadherin and claudin-5 and estradiol-17β also did not affect the VE-cadherin expression, but estradiol-17β significantly decreased the claudin-5 expression. This decreasing effect of estradiol-17β was detected from 24 hours later when the water content per a uterus significantly increased. The present study indicates that estrogen, but not progesterone, decreases the expression of claudin-5 in vascular endothelial cells in the murine uterine endometrium from 24 hours later, suggesting that the decrease in the claudin-5 expression contributes to the endometrial edema late after the estrogen stimulation.

Journal

  • Endocrine Journal

    Endocrine Journal 61(7), 705-715, 2014

    The Japan Endocrine Society

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