Sources and biological actions of relaxin in pigs

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.