ACTH (Adrenocorticotropic Hormone) Antibody
- Known as:
- ACTH (Adrenocorticotropic Hormone) Antibody
- Catalog number:
- 20070
- Product Quantity:
- 100 µL
- Category:
- Antibodies
- Supplier:
- Immunostar
- Gene target:
- ACTH (Adrenocorticotropic Hormone) Antibody
Related genes to: ACTH (Adrenocorticotropic Hormone) Antibody
- Gene:
- MC2R NIH gene
- Name:
- melanocortin 2 receptor
- Previous symbol:
- -
- Synonyms:
- ACTHR
- Chromosome:
- 18p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-20
- Date modifiied:
- 2016-02-01
- Gene:
- POMC NIH gene
- Name:
- proopiomelanocortin
- Previous symbol:
- -
- Synonyms:
- MSH, POC, CLIP, ACTH, NPP, LPH
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: ACTH (Adrenocorticotropic Hormone) Antibody
Related articles to: ACTH (Adrenocorticotropic Hormone) Antibody
- The hypothalamic-pituitary-interrenal (HPI) axis mediates stress responses in fish. Previous work showed that dietary supplementation with B vitamins attenuated cortisol response to acute stress, whereas dietary genistein produced high basal levels of cortisol and altered stress responsiveness. In the present study, we investigated the expression of key genes of the HPI axis and selected hepatic targets to better characterize these responses. Cortisol was correlated with nr3c1 expression in the pituitary of control fish. Conversely, B vitamins supplementation was associated with changes in the relationship between plasma cortisol levels and nr3c1 expression across tissues, including higher basal higher basal expression expression in the head kidney. In parallel, lower hepatic oxidative stress following acute stress in this fish was associated with differences in cortisol levels and liver metabolic responses. Dietary genistein was associated with altered pituitary regulation of pomc paralogs, characterized by reduced pomcb and elevated pomca expression after stress. These expression patterns persisted 4.5 months after dietary exposure, with pomca becoming the only gene showing a positive association with plasma cortisol levels. In addition, genistein supplementation was associated with higher basal expression of the ACTH receptor (mc2r) in the head kidney. Stress challenges performed up to one year after the nutritional intervention revealed convergence of cortisol responses among dietary groups. Overall, these results indicate that dietary components can produce short-term changes in the regulation of the HPI axis. Further studies are required to clarify the mechanisms underlying the dietary effects observed in this study. - Source: PubMed
Publication date: 2026/02/19
Navarro-Guillén CarmenHuesa-Cerdán RubénHidalgo-Pérez Juan AntonioMartínez-Rodríguez GonzaloRodríguez-Viera LeandroMartos-Sitcha Juan AntonioBlanco-Benítez Juan JoséPerera Erick - Early-life infections have enduring effects on the immune and endocrine systems. Glucocorticoids (GCs) are produced by the adrenal glands and also produced by lymphoid organs (immunosteroids). We investigated the impacts of early-life lipopolysaccharide (LPS) challenge on GC and mineralocorticoid regulation in blood and lymphoid organs. We administered saline vehicle (nVEH) or LPS (50 µg/kg body wt, ip) (nLPS) to neonatal mice on postnatal day (PND) 4 and 6 ("first hit"). We then administered saline vehicle (aVEH) or LPS (50 µg/kg body wt, ip) (aLPS) to adults on PND90 ("second hit"), in a 2 × 2 design. We collected whole blood, bone marrow, thymus, and spleen 4 h after treatment at PND90. We measured nine steroids via liquid chromatography-tandem mass spectrometry and measured transcripts of steroidogenic enzymes (, , , and ), GC receptor, mineralocorticoid receptor, and hypothalamic-pituitary-adrenal axis components (, , , and ) via RT-qPCR. The nLPS treatment did not have significant effects on blood GC levels in adulthood. Nonetheless, nLPS treatment increased corticosterone and 11-dehydrocorticosterone levels in lymphoid organs of aLPS subjects. The nLPS treatment increased aldosterone levels in blood and bone marrow of aVEH females but decreased aldosterone levels in bone marrow and thymus of aVEH males. The nLPS treatment also increased transcripts for steroidogenic enzymes, especially the aldosterone-synthetic enzyme , and modulated transcripts for steroid receptors, especially mineralocorticoid receptors, in lymphoid organs of aVEH and aLPS subjects. These findings suggest that elevated local GC and aldosterone production in lymphoid organs is a mechanism for the enduring effects of early-life infections on immune function. Using a "two-hit" model in mice, we examined the effects of early-life lipopolysaccharide (LPS) administration on steroid regulation in blood and lymphoid organs. Mice received saline or LPS as neonates, and then saline or LPS as adults. Neonatal LPS heightened local glucocorticoid and systemic aldosterone responses to adult LPS treatment in bone marrow, thymus, and spleen. These data highlight the potential role of immunosteroids in developmental programming of immune function and health. - Source: PubMed
Publication date: 2026/01/07
Salehzadeh MelodyMazurenko AnnaSoma Kiran K - Mild neonatal hypoxia (NH) can serve as a conditioning stimulus that persistently modulates stress systems. We tested whether brief neonatal hypobaric hypoxia induces long-term changes hypothalamic-pituitary-adrenal (HPA) regulation and adult behavior. Male Wistar rats received three 2 h hypobaric sessions on postnatal days 8-10. At 3 months, behavior was assessed. Biochemical measures included plasma/adrenal corticosterone (CORT), plasma ACTH, brain CORT, CRH/POMC/GR/11β-HSD2 protein, and HPA/steroidogenic gene expression. NH yielded a calmer, context-beneficial phenotype: startle latency increased, Morris water maze memory improved, whereas Barnes, recognition memory, and forced swim measures were unchanged. Hypothalamic CRH protein and pituitary/plasma ACTH were reduced, despite unchanged crh and Pomc mRNA, suggesting post-transcriptional control. Basal CORT in plasma and adrenals remained unchanged, but the CORT response to mild stress was larger and more sustained. In the adrenal glands, Cyp11b1 was selectively downregulated, whereas Mc2r, Cyp11a1, Hsd3b2, Cyp21a1 were unaffected. GR and 11β-HSD2 protein did not differ across tissues. In the brain, CORT decreased selectively in the amygdala. NH appears to act as developmental preconditioning, leading to persistent behavioral adaptations and altered HPA regulation in adulthood, characterized by reduced central drive at rest, preserved basal output, and efficient mobilization under challenge. - Source: PubMed
Publication date: 2026/01/07
Potapova SofiyaSafarova DianaTyulkova EkaterinaVetrovoy Oleg - Chronic stress alters hypothalamic-pituitary-adrenal (HPA) axis function, affecting corticosterone regulation and adaptive responses. Understanding individual variability in stress adaptation requires identifying distinct HPA axis response patterns. Here, we assessed HPA axis sensitivity in male C57BL6 mice exposed to 30 days of chronic social defeat stress (CSDS). Negative feedback integrity was evaluated using the dexamethasone suppression test (DST), with corticosterone measured after saline or low-dose dexamethasone administration at days 10 and 30. Behavioral testing (open field, elevated plus maze, social interaction test, partition, social defeat, forced swimming test, sucrose preference test) and qPCR analysis of HPA-axis-related genes in the hypothalamus (, , , , ), pituitary (, , , ), and adrenal glands (, , , , , , ) were performed. K-means cluster analysis identified three distinct response profiles differing in baseline and dexamethasone-suppressed corticosterone levels. Clusters also exhibited differences in behavioral phenotypes and HPA axis gene expression. Cluster 1 showed low basal corticosterone and an abnormal dexamethasone suppression response, without significant or dysregulation in the hypothalamus. Cluster 2 exhibited elevated basal corticosterone, a blunted dexamethasone response, anhedonia, and reduced immobility in the forced swim test; increased and reduced suggested enhanced glucocorticoid receptor sensitivity and sustained hypercortisolemia. Cluster 3, characterized by normal basal corticosterone and normal dexamethasone response, displayed upregulation of and , consistent with balanced and potentially adaptive HPA axis regulation under chronic stress. These results demonstrate that corticosterone response heterogeneity reflects distinct adaptive trajectories under chronic stress. Identifying behavioral and molecular markers of these strategies may advance understanding of stress vulnerability and resilience mechanisms, with implications for stress-related disorders. - Source: PubMed
Publication date: 2025/11/26
Ritter PolinaSalman RashaRyabushkina YuliyaBondar Natalya - Organophosphate flame retardants (OPFRs) are ubiquitous flame-retardant additives with endocrine-disrupting properties. Despite increasing evidence that OPFRs impact neurodevelopment, their effects on the neuroendocrine stress response remain poorly understood. To examine their long-term impact on stress regulation, we treated pregnant C57Bl/6J dams to a mixture of tris(1,3-dichloro-2-propyl) phosphate (TDCPP), triphenyl phosphate (TPP), and tricresyl phosphate (TCP; 1 mg/kg each) from gestational day (GD) 7 through postnatal day (PND) 14. Adult offspring (8-9 weeks of age) were then challenged with acute stressors, including 1 h restraint or a 6-day acute variable stress (AVS) paradigm. Perinatal OPFR exposure produced persistent, sex-specific alterations in the hypothalamic-pituitary-adrenal (HPA) axis and stress-related neurocircuitry. Following 1 h restraint, OPFR-treated females showed heightened serum corticosterone. In addition, gene expression analysis revealed sex-dependent disruptions in key stress-regulatory pathways after OPFR treatment and 1 h restraint in the hypothalamus () and pituitary (). Females demonstrated more differences in adrenal gene expression related to steroidogenesis () and catecholamine biosynthesis (), with OPFR-treated groups having blunted responses. OPFR AVS females displayed reduced corticosterone and downregulated expression in the bed nucleus of the stria terminalis (BNST), accompanied by increased behavioral avoidance and immobility. In males, OPFR exposure led to increased BNST and , expression, along with hyperactivity and avoidance behaviors. Together, these findings demonstrate that early-life OPFR exposure induces lasting, sex-specific dysregulation of the HPA axis and associated stress circuits, highlighting OPFRs as developmental neuroendocrine disruptors with implications for mood and stress-related disorders. - Source: PubMed
Publication date: 2025/10/14
Rojas Catherine MDeLucca JuliaBrown Caylee AYasrebi AliChiou SavannahBello Nicholas TRoepke Troy A