Bagnell C A, Zhang Q, Downey B, Ainsworth L
Department of Animal Sciences, Rutgers University, New Brunswick, NJ 08903.
J Reprod Fertil Suppl. 1993;48:127-38.
Although the major source of relaxin in pigs is the corpus luteum of pregnancy, there is now evidence for relaxin gene expression and translation into protein in the theca interna cells of the preovulatory follicle, the corpus luteum of the cycle and the uterus. The theca interna cells retain their ability to express the relaxin gene and protein following ovulation. During the early stages of development of the corpus luteum, the theca-derived small lutein cells are the source of the relaxin transcript. As the corpus luteum becomes fully functional, there is a switch in the site of relaxin synthesis from small theca-derived lutein cells to large granulosa-derived cells. In the absence of luteolysis, this switch is accompanied by a dramatic rise in relaxin synthesis. Relaxin has been identified in boar seminal plasma and can maintain or increase sperm motility. However, a source of relaxin in the boar has not been identified. Relaxin is an important regulator of uterine function during pregnancy acting systemically to suppress myometrial activity and promote cervical dilation at parturition. The changes in thecal relaxin production during follicle development and its ability to promote growth and changes in proteolytic enzyme activity of granulosa cells in vitro have led to the concept of an autocrine or paracrine role for relaxin within the follicle. Uterotrophic effects of relaxin have been reported in rodents and swine and support the hypothesis that relaxin promotes uterine growth and expansion in early pregnancy to accommodate the growing fetuses. Mammotrophic effects of relaxin in rodents have now been extended to pigs, with evidence that relaxin is necessary for normal mammary parenchymal development in late pregnancy. In most instances the mechanisms responsible for, and the physiological significance of, these diverse biological effects remain to be elucidated.
虽然猪体内松弛素的主要来源是妊娠黄体,但现在有证据表明,在排卵前卵泡的内膜细胞、周期黄体和子宫中,松弛素基因能够表达并翻译为蛋白质。排卵后,内膜细胞仍保留表达松弛素基因和蛋白质的能力。在黄体发育的早期阶段,来自内膜的小黄体细胞是松弛素转录本的来源。随着黄体功能完全成熟,松弛素的合成部位从小的、来自内膜的黄体细胞转变为大的、来自颗粒层的细胞。在没有黄体溶解的情况下,这种转变伴随着松弛素合成的显著增加。已在公猪精液中鉴定出松弛素,它可以维持或增加精子活力。然而,公猪体内松弛素的来源尚未确定。松弛素是孕期子宫功能的重要调节因子,它通过全身作用抑制子宫肌层活动,并在分娩时促进子宫颈扩张。卵泡发育过程中内膜松弛素产生的变化,以及其在体外促进颗粒细胞生长和蛋白水解酶活性变化的能力,引发了关于松弛素在卵泡内具有自分泌或旁分泌作用的概念。在啮齿动物和猪身上已报道了松弛素对子宫的营养作用,这支持了松弛素在妊娠早期促进子宫生长和扩张以容纳不断生长的胎儿这一假说。现在,松弛素对啮齿动物乳腺的营养作用已扩展到猪身上,有证据表明,松弛素是妊娠后期乳腺实质正常发育所必需的。在大多数情况下,这些不同生物学效应的作用机制和生理意义仍有待阐明。