Disease relevance of LOC443482

• Exposure to gestational undernutrition (R-R and C-R groups), however, resulted in a stimulation in the relative level of expression of MC2R mRNA (P=0.001) and StAR mRNA (P=0.007) in the fetal adrenal during late gestation [1].

High impact information on LOC443482

• In addition, cortisol modulates the mechanism by which ACTH activates fetal adrenal function, possibly through an action at the level of the ACTH receptor [2].
• Thus, the effects of TGF beta on ACTH receptor content are likely another important negative action of this peptide on adrenocortical cell differentiation [3].
• The variations in ACTH receptor number were associated with parallel changes on acute ACTH-induced cyclic AMP production [3].
• Plasma changes were not associated with altered adrenal P450c17, ACTH receptor, beta-hydroxysteroid dehydrogenase, or glucocorticoid receptor mRNA levels [4].
• ACTH-R mRNA levels were significantly higher in ACTH-infused fetuses in both the 118 and 138 dGA groups [5].

Biological context of LOC443482

• There was a significant increase in the StAR mRNA and protein between 100 and 142 days of gestation, but there were no significant age-related changes in ACTH-R mRNA and protein levels [6].
• This study examined how ACTH affects ACTH-R and StAR mRNA expression, and cortisol production in adrenocortical cells isolated from fetuses of varying gestational age (dGA) [7].
• Sustained hypoxaemia resulted in an upregulation of mRNA encoding for ACTH-R, but only in older fetuses and in association with a sustained increase in plasma cortisol [8].
• MC2-R expression progressively increases from day 60 to day 140 of gestation (x3), then more rapidly before parturition and remains constant in the newborn [9].
• Expression of the melanocortin receptors MC2-R (ACTH-receptor) and MC5-R during embryonic development of ovine adrenals [9].

Anatomical context of LOC443482

• The mRNA levels for StAR and ACTH-R were assessed by RNase protection assay (RPA) and protein levels were measured by Western blot in placentas from pregnant ewes (100-105 days of gestation, n = 8; 120 days of gestation, n = 5; 135-142 days of gestation, n = 8) [6].
• Whole adrenal glands were removed from fetal sheep, lambs and adult sheep at different stages of development for measurement of ACTH-R mRNA [8].
• Therefore, we quantitated ACTH receptor expression in the ovine adrenal cortex during development and after manipulations to better understand the regulation of the adrenal receptor in vivo [10].
• Hypophysectomy (HX) did not alter the expression of MC2R mRNA; however, the abundance of SF-1 mRNA fell by approximately 50% following the removal of the pituitary gland [11].

Associations of LOC443482 with chemical compounds

• In addition, because cortisol is secreted by the placenta, we also examined the expression of adrenocorticotropic hormone receptor (ACTH-R) to determine if it was present and if the pattern of expression changed as gestation proceeded [6].
• Real-time PCR was used to quantify mRNA for steroidogenic acute regulatory protein, 17alpha-hydroxylase (CYP17), 21-hydroxylase (CYP21), cholesterol side-chain cleavage (CYP11A1), 3beta-hydroxysteroid dehydrogenase type II (HSD3B2), and the ACTH receptor [12].
• Developmental changes in adrenocorticotrophin (ACTH)-induced expression of ACTH receptor and steroid acute regulatory protein mRNA in ovine fetal adrenal cells [7].
• Neither dexamethasone nor ACTH modified ACTH receptor mRNA half-lives [13].
• Testosterone did not modify, while high concentrations of 17 beta-estradiol decreased, ACTH receptor mRNA levels [13].

Analytical, diagnostic and therapeutic context of LOC443482

• At approximately 138 days of gestation, fetuses were killed, and adrenals were removed for cell culture and analyses of ACTH-R mRNA and protein [14].
• ACTH-R mRNA was detected by northern blotting using a cDNA cloned in our laboratory and by in situ hybridisation [8].

References