Emmen J M, McLuskey A, Grootegoed J A, Brinkmann A O
Department of Endocrinology and Reproduction, Faculty of Medicine and Health Sciences, Erasmus University Rotterdam, The Netherlands.
Hum Reprod. 1998 May;13(5):1272-80. doi: 10.1093/humrep/13.5.1272.
The cranial suspensory ligament is located on the border of the cranial (mesonephric) mesentery in adult female mammals, which runs between the cranial pole of the internal genitalia and the dorsal abdominal wall. Absence of the cranial suspensory ligament in male mammals depends upon exposure of its primordium to fetal testicular androgens and is a prerequisite for testis descent. Female rats were exposed to 5alpha-dihydrotestosterone propionate at different stages of genital development, and cranial suspensory ligament development was studied in neonatal and in adult animals. Androgens suppressed cranial suspensory ligament development when exposure started during the early stages of genital development, until day 19 postconception (pc). Androgen receptor expression was immunohistochemically detected in the cranial mesentery of both sexes from day 16 pc onwards. A decrease of androgen receptor expression in female fetuses from day 18 pc onwards coincided with the appearance of a differentiated cranial suspensory ligament, as evidenced by the expression of two cell differentiation markers: alpha-smooth muscle (alpha-SM) actin and desmin. alpha-SM actin was located on the outer border of the cranial mesentery of both sexes at day 17 pc, and expression increased only in female fetuses. On day 19 pc, desmin expression was also detectable in the a-SM actin-positive cells. Proliferation and apoptosis indices of cells in the cranial mesentery, as analysed by 5'-bromodeoxyuridine incorporation and by detection of DNA strand breaks (TUNEL method) respectively, did not show any difference between the sexes, neither on day 17 nor on day 18 pc. Since primordial cells of the cranial suspensory ligament highly express the androgen receptor during the period of gestation when androgens can suppress cranial suspensory development, altered morphogenesis of these cells may be a direct consequence of androgen action.
颅悬韧带位于成年雌性哺乳动物颅侧（中肾）系膜的边缘，它在生殖器官的颅极与腹后壁之间延伸。雄性哺乳动物缺乏颅悬韧带取决于其原基暴露于胎儿睾丸雄激素，这是睾丸下降的先决条件。将雌性大鼠在生殖器官发育的不同阶段暴露于丙酸5α-双氢睾酮，并对新生和成年动物的颅悬韧带发育进行研究。当在生殖器官发育早期（直到受孕后第19天）开始暴露时，雄激素会抑制颅悬韧带的发育。从受孕后第16天起，在两性的颅系膜中均通过免疫组织化学检测到雄激素受体表达。从受孕后第18天起，雌性胎儿中雄激素受体表达的降低与分化的颅悬韧带的出现相吻合，这由两种细胞分化标志物α-平滑肌（α-SM）肌动蛋白和结蛋白的表达所证实。在受孕后第17天，α-SM肌动蛋白位于两性颅系膜的外侧边缘，且仅在雌性胎儿中表达增加。在受孕后第19天，在α-SM肌动蛋白阳性细胞中也可检测到结蛋白表达。分别通过5'-溴脱氧尿苷掺入法和DNA链断裂检测法（TUNEL法）分析的颅系膜中细胞的增殖和凋亡指数，在受孕后第17天和第18天，两性之间均未显示出任何差异。由于颅悬韧带的原始细胞在雄激素可抑制颅悬韧带发育的妊娠期高度表达雄激素受体，这些细胞形态发生的改变可能是雄激素作用的直接后果。
