Ask about this productRelated genes to: PNMT antibody
- Gene:
- PNMT NIH gene
- Name:
- phenylethanolamine N-methyltransferase
- Previous symbol:
- PENT
- Synonyms:
- -
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-12
- Date modifiied:
- 2015-08-25
Related products to: PNMT antibody
Related articles to: PNMT antibody
- It has now been well established that gut microbiota significantly influences emotional and neuroendocrine responses to stress. Specifically, multiple pieces of evidence from various preclinical models indicate that gut microbiota regulates the response of the hypothalamic-pituitary-adrenocortical (HPA) axis to acute and chronic stress. In contrast, the influence of gut microbiota on the adrenomedullary tissue, which is responsible for the production and release of catecholamines-the first hormones released in response to stress-has received little attention. Therefore, our study aimed to explore whether adrenal corticosterone and catecholamine biosynthesis were differently regulated in germ-free (GF) and conventional, specific pathogen-free (SPF) male rats when exposed to unpredictable chronic mild stress, acute metabolic stress, or both. Results showed that both GF and SPF chronically stressed rats had significantly (p < 0.05) heavier adrenal glands (+30% for GF, +21% for SPF) compared to unstressed animals. Gene expression levels of corticosterone biosynthesis enzymes and plasma and adrenal corticosterone concentrations did not differ significantly between control rats and those exposed to chronic, acute, or both stress factors, whether in GF or SPF rats. The same result was observed for the genes encoding tyrosine hydroxylase and dopamine β-hydroxylase, two enzymes involved in catecholamine biosynthesis. By contrast, GF rats exhibited a 2.3-fold increase (p = 0.0271) in Pnmt gene expression (which encodes phenylethanolamine N-methyltransferase, the enzyme responsible for converting norepinephrine to epinephrine) and a 2.6-fold increase (p = 0.0786) in epinephrine concentration in the adrenal glands under combined stress conditions. This response was not observed in SPF rats. In these animals, chronic stress was found to reshape the composition and metabolic functions of the gut microbiota. Interestingly, this was accompanied by a 40% decrease in norepinephrine (p = 0.0364) and epinephrine (p = 0.0840) concentrations in their adrenal glands. This study highlights the gut microbiota as a regulator of adrenomedullary activity, enhancing our understanding of the interaction between peripheral and central stress circuitry. - Source: PubMed
Etienne CamilleBernat ClaireMonnoye MagaliAndry VirginiePhilippe CatherineMaudet ClaireMaximin EliseNaudon LaurentGoumon YannickHeberden ChristineGuérineau Nathalie CRabot Sylvie - Pheochromocytoma is a catecholamine-producing neuroendocrine tumor with unpredictable biological behavior. Neurotrophic Tropomyosin Receptor Kinase (NTRK), particularly tropomyosin-related receptor tyrosine kinase A (TrkA) encoded by , mediates neurotrophin signaling and contributes to cellular differentiation. Although TrkA (NTRK1) expression has been observed in pheochromocytoma, its pathological significance remains unclear. In this study, we examined 31 surgically resected pheochromocytomas using immunohistochemistry for NTRK1, S100, tyrosine hydroxylase (TH), dopamine β-hydroxylase (DBH), phenylethanolamine N-methyltransferase (PNMT), Ki-67, and succinate dehydrogenase complex iron sulfur subunit B (SDHB). The immunoreactive score was used to semiquantitatively evaluate the expression of NTRK1 and catecholamine-synthesizing enzymes, and their correlations with clinicopathological factors, including PASS and GAPP scores, were analyzed. NTRK1 immunoreactivity was detected in approximately 80% of tumors. High NTRK1 expression was significantly positively correlated with S100-positive sustentacular cells, TH, and DBH, but not with PNMT. In contrast, NTRK1 expression was inversely correlated with the Ki-67 labeling index. NTRK1 expression did not correlate with clinicopathological variables, PASS or GAPP scores, or SDHB status. These findings suggest that NTRK1 expression reflects structural and functional differentiation in pheochromocytoma, characterized by preserved sustentacular cell networks and catecholamine synthetic capacity rather than indicating malignant potential. Therefore, NTRK1 may serve as a differentiation-associated marker in pheochromocytoma, and further mechanistic and molecular investigations are warranted to elucidate its mechanistic role in chromaffin cell biology. - Source: PubMed
Publication date: 2026/05/18
Matsushita HarunaShimada HirokiHata ShukoSato NaomiOgata TomoakiTezuka YutaYamazaki YutoSuzuki TakashiNakamura Yasuhiro - Organophosphate flame retardants (OPFRs) are ubiquitous flame-retardant additives with endocrine-disrupting properties. Despite increasing evidence that OPFRs affect neurodevelopment, their effects on the neuroendocrine stress response remain poorly understood. To examine their long-term effect 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 (age 8-9 weeks) were then challenged with acute stressors, including 1-hour 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-hour 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-hour restraint in the hypothalamus (Crhr1, Crhr2, Ptpn5) and pituitary (Crhr1, Pomc, Nr3c1). Females demonstrated more differences in adrenal gene expression related to steroidogenesis (Mc2r, Cyp11b2) and catecholamine biosynthesis (Dbh, Pnmt), with OPFR-treated groups having blunted responses. OPFR AVS females displayed reduced corticosterone and Crh messenger RNA in the hypothalamus, and downregulated Pacap/Pac1r 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 Pacap and Pac1r 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
Rojas Catherine MDeLucca JuliaBrown Caylee AYasrebi AliChiou SavannahBello Nicholas TRoepke Troy A - Housing conditions, particularly environmental enrichment (EE), can influence experimental outcomes and welfare. While EE is generally regarded as beneficial, a male bias exists in research supporting this. This study investigated whether sex differences exist in levels of BDNF in the brain and peripheral tissues in environmentally enriched mice. Expression of the catecholamine biosynthetic enzymes of the adrenal glands, key to the sympathoadrenal medullary system and stress response, was also investigated. We showed that female mice exposed to EE exhibited increased anxiety-like behaviors. EE in male mice did not induce anxiety-like behavior, and it was associated with increased hippocampal and pituitary BDNF expression, suggestive of enhanced neurotrophic support. In the adrenal gland, the levels of adrenal catecholamine biosynthetic enzymes, specifically total tyrosine hydroxylase and PNMT levels, were increased in females, but not in males. In conclusion, EE may serve as a mild stressor in female mice. In male mice, EE may have induced neurotrophic support of the hippocampus since hippocampal BDNF levels were increased with minimal changes to adrenal catecholamine synthetic enzymes. This study highlights the importance of considering sex as a biological variable in translational neuroscientific research. - Source: PubMed
Herselman M FLuo S YLin L YZhou X FBobrovskaya L - To systematically identify potential pathological molecular and therapeutic targets for type 2 airway inflammatory diseases using Mendelian randomization (MR) and co-localization analysis. - Source: PubMed
Jiang ZihanMeng JuanLiu Shixi