Possible contribution of α2,6-sialylation to luteolysis in cows by inhibiting the luteotrophic effects of galectin-1
Possible contribution of α2,6-sialylation to luteolysis in cows by inhibiting the luteotrophic effects of galectin-1
复制标题
α2,6-唾液酸化可能通过抑制半乳糖凝集素-1的黄体营养作用对奶牛黄体溶解作出贡献
DOI：
10.1095/biolreprod.116.140194
复制
发表时间：
2016
影响因子：
3.6
通讯作者：
Okuda K
中科院分区：
文献类型：
--
作者：
Hashiba K;Nio-Kobayashi J;Sano M;Maeda M;Kimura Y;Yamamoto Y;Kimura K;Okuda K
黄体（CL）是建立妊娠所必需的。如果在发情周期内没有怀孕，则黄体溶解是由子宫分泌的前列腺素（PG）F2 α诱导的。半乳糖凝集素-1（Galectin-1）是一种abeta-半乳糖结合蛋白，表达于奶牛的功能性黄体中，通过修饰膜糖蛋白的功能来提高牛黄体类固醇生成细胞（LSC）的活力。半乳糖凝集素-1与糖蛋白的结合被糖缀合物的末端半乳糖残基的α 2，6-唾液酸化阻断，所述α 2，6-唾液酸化由唾液酸转移酶（ST 6 Gal-I）催化。然而，α 2，6-唾液酸在牛CL中的生理作用尚不清楚。牛CL的α 2，6-唾液酸化水平在黄体退化期高于其他黄体期。凝集素组织化学显示，α 2，6-唾液酸化糖缀合物定位于整个发情周期的黄体内皮细胞。此外，在退黄体期，α 2，6-唾液酸化糖缀合物浓缩到LSC的膜上。PGF 2 α处理72 h可增强中-LSC中ST 6 Gal-ImRNA的表达和α 2，6-唾液酸化糖蛋白的水平。晚期LSC（排卵后第15-17天）的α 2，6-唾液酸化糖蛋白水平高于中期LSC（排卵后第8-12天），并且半乳糖凝集素-1增加中期LSC的活力，但不增加晚期LSC的活力。此外，当α 2，6-唾液酸残基被神经氨酸酶去除时，半乳糖凝集素-1增加了晚期LSC的活力。总体结果表明，PGF 2 α刺激的α 2，6-唾液酸化通过抑制牛CL中半乳糖凝集素-1的促黄体作用而促进黄体溶解。
The corpus luteum (CL) is essential for establishing pregnancy. If pregnancy does not occur during the estrous cycle, luteolysis is induced by prostaglandin (PG) F2alpha secreted from the uterus. Galectin-1, abeta-galactose-binding protein, is expressed in the functional CL of cows and increases the viability of bovine luteal steroidogenic cells (LSCs) by modifying the functions of membrane glycoproteins. The binding of galectin-1 to glycoproteins is blocked by alpha2,6-sialylation of the terminal galactose residues of glycoconjugates, which is catalyzed by a sialyltransferase (ST6Gal-I). However, the physiological role of alpha2,6-sialic acid in bovine CL is unclear. The level of alpha2,6-sialylation of the bovine CL was higher during the regressed-luteal stage than in other luteal stages. Lectin histochemistry revealed that alpha2,6-sialylated glycoconjugates were localized to luteal endothelial cells throughout the estrous cycle. In addition, alpha2,6-sialylated glycoconjugates concentrated to the membrane of LSCs during the regressed-luteal stage. PGF2alpha treatment for 72 h enhanced the expression ofST6Gal-ImRNA and the level of alpha2,6-sialylated glycoproteins in mid-LSCs. The level of alpha2,6-sialylated glycoproteins of late-stage LSCs (Days 15–17 after ovulation) was higher than that of mid-stage LSCs (Days 8–12 after ovulation), and galectin-1 increased the viability of mid-LSCs but not that of late-stage LSCs. Furthermore, galectin-1 increased the viability of late-LSCs when alpha2,6-sialic acid residues were removed by neuraminidase. The overall findings suggest that alpha2,6-sialylation stimulated by PGF2alpha contributes to luteolysis by inhibiting the luteotropic effects of galectin-1 in bovine CL.