Disease relevance of Corpus Luteum

• The corpora lutea of pregnancy in the rat are highly dependent on the action of PRL and PRL-like hormones to hypertrophy and to produce progesterone needed for the maintenance of gestation [1].
• Hypothyroidism, however, like melatonin, resulted in a reduced number of developing and mature follicles and corpora lutea in the ovaries, and in reduced uterine weight [2].
• Enhanced secretion of prostaglandins produced by the cyclooxygenase pathway did not contribute to development of ovarian cysts but, unlike histamine, was required for formation of corpora lutea in prepubertal gilts treated with PMSG and hCG [3].
• Female YHR(+) mice undergo precocious puberty with early vaginal opening, accelerated uterine development, enhanced follicular development, including the presence of corpora lutea, and an increase in serum progesterone [4].
• Luteinizing hormone (LH) receptor concentrations in ovarian follicles and corpora lutea were measured in 51 patients with histologically proven endometriosis and in 41 control patients [5].

High impact information on Corpus Luteum

• Hysterectomy in these nonprimate species causes maintenance of the corpora lutea, whereas in primates, removal of the uterus does not influence the cyclical regression of the corpus luteum [6].
• Maturation of secondary ovarian follicles into corpora lutea, which express high levels of p27, was markedly impaired [7].
• When nonpregnant cycling female mice were chronically treated with AGM-1470, inhibition of endometrial maturation and corpora lutea was observed [8].
• C/EBP beta-deficient ovaries lack corpora lutea and fail to down-regulate expression of the prostaglandin endoperoxidase synthase 2 and P450 aromatase genes in response to gonadotropins [9].
• In contrast, levels of mRNA for P450scc increased only gradually in follicles but were markedly increased by the LH surge and high concentrations of cAMP and then appeared to be constitutively expressed in rat corpora lutea in a cAMP-independent manner [10].

Chemical compound and disease context of Corpus Luteum

• All technical MXC doses and estradiol increased the duration of vaginal cornification but only estradiol, 0.5, or 1.0 mg technical MXC induced ovarian atrophy, relative ovarian weight loss, and depletion of corpora lutea [11].
• At adulthood the animals were killed, the stage of vaginal estrus determined, the ovaries examined for the presence of corpora lutea and follicular cysts, and circulating levels of progesterone, E2, and testosterone were measured by radioimmunoassay (RIA) [12].

Biological context of Corpus Luteum

• Progesterone (P) is secreted by ovarian corpora lutea (CL) throughout gestation in the rat [13].
• Results showed that c-Ki-ras p21 is at its lowest level in the immature ovary and increases with development of the corpora lutea to its highest levels at day 16 of pregnancy, after which levels decline and then rise again during lactation [14].
• After superovulation treatment, the AR(-/-) ovaries produced fewer oocytes and also showed fewer corpora lutea [15].
• Similar to corpora lutea, the lesions were highly vascularized, although they did not express the luteinization marker Cyp11a1 [16].
• Cyclic AMP-dependent and -independent regulation of cholesterol side chain cleavage cytochrome P-450 (P-450scc) in rat ovarian granulosa cells and corpora lutea. cDNA and deduced amino acid sequence of rat P-450scc [17].

Anatomical context of Corpus Luteum

• Granulosa cells in the ovary establish quiescence within several hours after the ovulation-inducing luteinizing hormone surge, whereas they undergo differentiation into corpora lutea [18].
• Cyclic AMP-dependent protein kinase in mitochondria and cytosol from different-sized follicles and corpora lutea of porcine ovaries [19].
• A solubilized preparation of cytochrome P-450, obtained by treatment of mitochondria from bovine corpora lutea with phospholipase A, contained all of the necessary components for the cholesterol side chain cleavage activity [20].
• In membranes of bovine corpora lutea and of L cells stably expressing the murine LH receptor (LHR cells), human chorionic gonadotropin (hCG) led to incorporation of the label into alphas and alphai2 [21].
• Treatment with pregnant mare serum gonadotropin decreased STC1 transcript levels in theca cells of maturing follicles, whereas subsequent treatment with human chorionic gonadotropin led to sustained suppression in the corpora lutea [22].

Associations of Corpus Luteum with chemical compounds

• Rabbit corpora lutea were tested for the presence of phosphorylative responses sensitive to estrogen [23].
• Identification of fatty acid esters of pregnenolone and allopregnanolone from bovine corpora lutea [24].
• Immunohistochemical analyses demonstrated that corpora lutea of p27(Kip1), p21(Cip1) double-null mice showed large numbers of cells with bromodeoxyuridine incorporation and high proliferative cell nuclear antigen expression, which were more remarkable than those in p27(Kip1) single-deficient mice showing modest hyperproliferation [18].
• Conversely the levels of mRNA specific for the key regulatory enzyme in the conversion of pregnenolone or progesterone to androgen, namely 17 alpha-hydroxylase cytochrome P-450, were high in all antral follicles examined but were low in young corpora lutea and undetectable in more mature corpora lutea [25].
• Prostaglandin F2alpha binding sites in human corpora lutea [26].

Gene context of Corpus Luteum

• EG-VEGF expression in normal ovaries is dynamic and generally complementary to VEGF expression in both follicles and corpora lutea [27].
• Finally, Smad3-/- ovaries have no corpora lutea, and they do not ovulate after ovulatory induction with exogenous gonadotropins [28].
• Although wild-type and SF-1 KO ovaries were indistinguishable during embryogenesis and at birth, adult females were sterile and their ovaries lacked corpora lutea and contained hemorrhagic cysts resembling those in estrogen receptor alpha and aromatase KO mice [29].
• An intense signal for PAPP-A mRNA was also present in healthy corpora lutea (CL), being localized to a subset of large luteal cells [30].
• Specifically, the high level of 17 beta HSD1 is clearly localized to follicles and corpora lutea indicating involvement in the synthesis of estradiol [31].

Analytical, diagnostic and therapeutic context of Corpus Luteum

• Western blot analysis of soluble extracts obtained from follicles and corpora lutea at various time points after human chorionic gonadotropin (hCG) injection revealed a 6-10-fold increase in RI alpha protein by 5 h after hCG injection [32].
• By Northern analysis, high levels of 17 beta HSD1 messenger RNA were found in follicles, corpora lutea, and cortex, whereas low levels were detected in the postmenopausal stroma and in fetal ovaries by RT-PCR [31].
• Indirect immunofluorescence staining of ovarian tissues with specific monoclonal antibodies revealed that DPP IV was present in large and small luteal cells in corpora lutea [33].
• CRH immunoreactivity was localized by immunohistochemistry in the cytoplasm of thecal cells surrounding the ovarian follicles, in luteinized cells of the stroma, and in large granulosa-derived luteinized cells of developing corpora lutea [34].
• In situ hybridization of day 10 corpora lutea localized TIMP-1 mRNA predominantly to specific cells that were randomly dispersed throughout the luteal tissue [35].

References