Corticotropin-releasing hormone, also called corticotropin-releasing factor (CRF), is a potent stimulator of synthesis and secretion of preopiomelanocortin-derived peptides. Human plasma contains a CRH-binding protein which inactivates CRH and which may prevent inappropriate pituitary-adrenal stimulation in pregnancy.
NCBI Summary:
Corticotropin-releasing hormone is a potent stimulator of synthesis and secretion of preopiomelanocortin-derived peptides. Although CRH concentrations in the human peripheral circulation are normally low, they increase throughout pregnancy and fall rapidly after parturition. Maternal plasma CRH probably originates from the placenta. Human plasma contains a CRH-binding protein which inactivates CRH and which may prevent inappropriate pituitary-adrenal stimulation in pregnancy.
General function
Extracellular binding protein
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Cellular localization
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Ovarian function
Oogenesis, Oocyte maturation
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Gene whose expression is detected by cDNA array hybridization: stress response, cell/cell communication.
Also, relative transcript level reproducibly decreases during IVM Gene whose expression is detected by cDNA array hybridization: stress response, cell/cell communication. Also, relative transcript level reproducibly decreases during IVM Rozenn Dalbis-Tran and Pascal Mermilloda
Expression regulated by
LH
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Discovery of LH-regulated genes in the primate corpus luteum Xu J, et al .
Department of Environmental & Biomolecular Systems, OGI School of Science & Engineering, Beaverton, Oregon 97006, USA; Division of Reproductive Sciences, Oregon National Primate Research Center, Beaverton, Oregon 97006, USA.
Circulating LH is essential for the development and function of the primate corpus luteum (CL) during the menstrual cycle. However, the cellular and molecular processes whereby LH controls luteal structure and function are poorly understood. Therefore, studies were initiated to identify gene products that are regulated by gonadotrophin in the monkey CL. Rhesus monkeys either were untreated (controls, CTRL; n=3) or received the GnRH antagonist Antide (ANT; 3 mg/kg body weight, n=3) to inhibit pituitary LH secretion on day 6 of the luteal phase in spontaneous menstrual cycles. The CL was removed 24 h later. RNA was extracted and converted to cDNA. The CTRL and ANT cDNA were differentially labelled with fluorescent dyes (Cy3-CTRL and Cy5-ANT) and hybridized onto microarrays containing 11 600 human cDNA. The selected cDNA were analysed further via semi-quantitative RT-PCR (a) to validate the microarray results and (b) to determine if their expression varies in the CL (n=3/stage) between the mid (day 6-8), late (day 14-16), or very late (day 18-19, menses) luteal phase of the natural cycle. After normalization of the fluorescence data, 206 cDNA (1.8% of the total) exhibited >/=2-fold change in expression after ANT. Of the 25 cDNA exhibiting a >/=6-fold change, 6 were up-regulated and 19 were down-regulated. Twenty-two of these 25 cDNA were validated by RT-PCR as differentially expressed in the ANT group, relative to the CTRL group, and 11 of 25 changed (P<0.05) correspondingly in the late-to-very late luteal phase. Thus, we have identified gene products that are regulated by gonadotrophin in the primate CL that may be important in luteal regression during the menstrual cycle. CRHBP was regulated by GnRH antagonist treatment.
Ovarian localization
Theca, Luteal cells
Comment
Asakura et al. (1997) found that the thecal compartment of the human ovary contains a CRF system endowed with CRF, CRF1 122561, and CRFBP.
Follicle stages
Corpus luteum
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Dynamic Expression and Regulation of the Corticotropin Releasing Hormone/Urocortin-Receptor-Binding Protein System in the Primate Ovary during the Menstrual Cycle Xu J, et al .
Context: Microarray analysis discovered that mRNA for CRH-binding protein(CRHBP) increased significantly in the primate corpus luteum(CL) following LH withdrawal. Objective: Determine if other components of the CRH/urocortin(UCN)-receptor(R)-BP system are expressed in the CL during the menstrual cycle and regulated by LH. Design: CL were collected from monkeys during the early (day 3-5 post LH surge) to very late (day 18-19) luteal phase and from controls or animals receiving GnRH antagonist (Antide, 3 mg/kg BW). CRH/UCN-R-BP system components were quantitated for mRNA levels by real-time PCR and analyzed for protein localization by immunohistochemistry. Results: All genes encoding the CRH/UCN-R-BP system, except for UCN3, were expressed in the CL. CRH mRNA levels did not change during the luteal phase, whereas expression of UCN, UCN2, CRHR1 and CRHR2 was maximal at early or mid luteal phase before declining (P < 0.05) at the later stages. CRHBP mRNA levels were lowest at mid and increased (P < 0.05) in the late luteal phase. Suppressing gonadotropin secretion reduced UCN2 (P < 0.05) and increased CRHBP (P < 0.05) mRNA levels, without altering the expression of other ligands or receptors. CRH, UCN, UCN2 and their receptors were localized to the granulosa-lutein cells of the CL, whereas CRHBP was limited to the theca and theca-lutein cells of the preovulatory follicle and CL. Conclusions: A local CRH/UCN-R-BP system exists in the macaque CL that is dynamically expressed and LH-regulated during the luteal phase of the menstrual cycle. Ligand-receptor activity may regulate luteal structure-function, at this point in an unknown manner, in primates.