Centro de Estudios Biomédicos Básicos, Aplicados y Desarrollo (CEBBAD) Universidad Maimónides, Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina.
PLoS One. 2022 Jul 8;17(7):e0271067. doi: 10.1371/journal.pone.0271067. eCollection 2022.
Reactivation of the hypothalamic-pituitary-ovarian (HPO) axis triggered by the decline in serum progesterone in mid-gestation is an uncommon trait that distinguishes the vizcacha from most mammals. Accessory corpora lutea (aCL) developed upon this event have been proposed as guarantors of the restoration of the progesterone levels necessary to mantain gestation. Therefore, the steroidogenic input of primary CL (pCL) vs aCL was evaluated before and after HPO axis-reactivation (BP and AP respectively) and in term pregnancy (TP). Nonpregnant-ovulated females (NP) were considered as the pCL-starting point group. In BP, the ovaries mainly showed pCL, whose LH receptor (LHR), StAR, 3β-HSD, 20α-HSD, and VEGF immunoexpressions were similar or lower than those of NP. In AP, luteal reactivity increased significantly compared to the previous stages, and the pool of aCL developed in this stage represented 20% of the ovarian structures, equaling the percentage of pCL. Both pCL and aCL luteal cells shared similar histological features consistent with secretory activity. Although pCL and aCL showed equivalent labeling intensity for the luteotropic markers, pCL were significantly larger than aCL. Towards TP, both showed structural disorganization and loss of secretory characteristics. No significant DNA fragmentation was detected in luteal cells throughout gestation. Our findings indicate that the LH surge derived from HPO axis-reactivation targets the pCL and boost luteal steroidogenesis and thus progesterone production. Because there are many LHR-expressing antral follicles in BP, they also respond to the LH stimuli and luteinize without extruding the oocyte. These aCL certainly contribute but it is the steroidogenic restart of the pCL that is the main force that restores progesterone levels, ensuring that gestation is carried to term. Most importantly, the results of this work propose luteal steroidogenesis reboot as a key event in the modulation of vizcacha pregnancy and depict yet another distinctive aspect of its reproductive endocrinology.
血清孕激素在妊娠中期下降触发下丘脑-垂体-卵巢（HPO）轴的重新激活，这是一种不常见的特征，将兔形目动物与大多数哺乳动物区分开来。在此事件后形成的副黄体（aCL）被认为是保证恢复维持妊娠所需孕激素水平的保障。因此，在 HPO 轴重新激活前后（分别为 BP 和 AP）以及足月妊娠（TP）时，评估了初级黄体（pCL）与 aCL 的甾体生成输入。未怀孕排卵的雌性（NP）被认为是 pCL 的起始点组。在 BP 中，卵巢主要显示 pCL，其 LH 受体（LHR）、StAR、3β-HSD、20α-HSD 和 VEGF 免疫表达与 NP 相似或更低。在 AP 中，黄体反应性与前几个阶段相比显著增加，在此阶段形成的 aCL 池代表卵巢结构的 20%，与 pCL 的百分比相等。pCL 和 aCL 的黄体细胞都具有相似的组织学特征，表明具有分泌活性。尽管 pCL 和 aCL 的黄体生成标记物的标记强度相似，但 pCL 明显大于 aCL。随着向 TP 的发展，它们都表现出结构紊乱和分泌特征丧失。在整个妊娠期，黄体细胞中未检测到明显的 DNA 片段化。我们的研究结果表明，HPO 轴重新激活产生的 LH 峰靶向 pCL，并促进黄体甾体生成，从而促进孕激素的产生。由于 BP 中有许多表达 LHR 的窦前卵泡，它们也对 LH 刺激做出反应并黄体化，而不会排出卵母细胞。这些 aCL 肯定有贡献，但恢复孕激素水平的主要力量是 pCL 的甾体生成重新启动，确保妊娠足月。最重要的是，这项工作的结果提出黄体甾体生成重新启动是调节兔形目动物妊娠的关键事件，并描绘了其生殖内分泌学的另一个独特方面。
