Catechol-O-methyltransferase: potential relationship to idiopathic hypertension

Mantione, Kirk J.; Kream, Richard M.; Stefano, George B.

doi:10.5114/aoms.2010.14246

Cited by 6 publications

(8 citation statements)

References 35 publications

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“…Intrarenal COMT levels of normotensive rats were lower than those of spontaneously hypertensive rats . The intracellular COMT mRNA levels were increased by administration of epinephrine and decreased by administration of morphine that suppressed sympathetic nerve activity . These results were considered by negative feedback against sympathetic nerve activity.…”

Section: Discussionmentioning

confidence: 93%

Effects of Sleeve Gastrectomy on Blood Pressure and the Renal Renin–Angiotensin System in Rats with Diet‐Induced Obesity

Yoshida

Gotoh

Masaki

et al. 2019

Obesity

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Objective Sleeve gastrectomy (SG) has been reported to decrease blood pressure (BP), although the reason has not been revealed. The present study aimed to establish the reason why SG decreases BP. Methods Male Sprague–Dawley rats were subjected to surgical (sham operation or SG) and dietary interventions (fed a normal diet or high‐fat diet ad libitum or fed by pair‐feeding [PF]). Systolic BP (SBP), urinary sodium excretion, and endocrine parameters were examined 4 weeks after surgery. Results Both SG and PF rats had reduced body weight compared with SO rats fed normal diet or high‐fat diet ad libitum. SG rats exhibited a reduction in SBP compared with PF, which was associated with a reduction in renal renin, angiotensin II, and catechol‐O‐methyltransferase levels (P < 0.01 for each). SG increased plasma cholecystokinin (CCK) levels compared with PF (P < 0.0001 for each), whereas glucagon‐like peptide 1 and peptide YY were not changed in fasting. Exogenous administration of CCK reduced renal catechol‐O‐methyltransferase (P = 0.0233), renin (P < 0.0001), and angiotensin II (P < 0.0001) levels and SBP (P = 0.0053). Conclusions SG reduced SBP, at least in part, through suppression of sympathetic nerve action by elevation of CCK, which was followed by suppression of the intrarenal renin–angiotensin system.

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Section: Discussionmentioning

confidence: 93%

Effects of Sleeve Gastrectomy on Blood Pressure and the Renal Renin–Angiotensin System in Rats with Diet‐Induced Obesity

Yoshida

Gotoh

Masaki

et al. 2019

Obesity

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“…These enrichment analyses were used to explore the molecular mechanisms of enriched genes involved in the occurrence and advancement of HD. Signaling pathways include signaling by GPCR [56] [99], EGFR (epidermal growth factor receptor) [100], ABCA1 [101], CRHR2 [102], RND3 [103], COMT (catechol-Omethyltransferase) [104] and SMAD9 [105] plays an important role in the pathogenesis of hypertension. Studies have revealed that NEUROD4 [106], SOX10 [107], MOG (myelin oligodendrocyte glycoprotein) [108], NR5A2 [109], GLRA3 [110], FA2H [111], SERPINA [112], HOXB9 [113], TGM2 [114], LRRK2 [115], ROS1 [116] NKX6-1 [141], SLC22A3 [142], CADM2 [143], FREM1 [144], TWIST2 [145], WNT16 [146], KISS1 [147], TMEM176B [148], MYL9 [149], IL7R [150], MBP (myelin basic protein) [151], GPR37 [152], ACAN (aggrecan) [153], SHH (sonic hedgehog signaling molecule) [154], HOXD9 [155], PROK1 [156], AGTR1 [157], TIE1 [158], P2RX7 [159], NTSR1 [160], VTN (vitronectin) [161], SIRT2 [162], RBP4 [163] [178], HLA-DRB1 [179], NKX2-3 [180], CD74 [92], HLA-DRA [181], VWF (von Willebrand factor)…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Huntington's disease (HD) is the primary cause of progressive motor deficits, psychiatric symptoms, and cognitive impairment. The exact molecular mechanisms of HD pathogenesis are largely unknown. This investigation aims to identify the hub genes, miRNA and TFs in HD and explore their potential molecular regulatory network. Next generation sequencing (NGS) dataset (GSE105041) was extracted from the Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification of differentially expressed genes (DEGs), Gene ontology and REACTOME pathway enrichment analysis, protein-protein interaction (PPI) network and module analysis, miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network analysis, and receiver operating characteristic curve (ROC) analysis were applied to identify hub genes, miRNA and TFs, and key drivers of HD pathogenesis. We identified 958 DEGs in the discovery phase, consisting of 479 up regulated genes and 479 down regulated genes. GO and REACTOME enrichment analyses of the 479 up regulated genes and 479 down regulated genes showed that they were mainly involved in multicellular organismal process, developmental process, signaling by GPCR and MHC class II antigen presentation. Further analysis of the PPI network using Cytoscape and PEWCC plugins identified 10 hub genes, including LRRK2, MTUS2, HOXA1, IL7R, ERBB3, EGFR, TEX101, WDR76, NEDD4L and COMT. Possible target miRNAs and TFs, including hsa-mir-1292-5p, hsa-mir-4521, ESRRB and SREBF1, were predicted by constructing a miRNA-hub gene regulatory network analysis and TF-hub gene regulatory network. This investigation used bioinformatics methods to explore the molecular pathogenesis of HD, and identified potential molecular markers. These molecular markers might provide novel ideas and methods for the early diagnosis, treatment, and monitoring of HD.

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“…109 This is also somewhat evident from the COMT data, which involve ADHD behavioral states and EDs. 110 , 111 Taken together, although ADHD is complex and multifaceted as are EDs, it appears that they may represent a logical comorbidity. Hence, early diagnostic indicators for ADHD may be at hand in the form of novel discoveries in gene expression patterns.…”

Section: Discussionmentioning

confidence: 99%

Attention deficit hyperactivity disorder and disordered eating behaviors: links, risks, and challenges faced

Ptáček

Stefano

Weissenberger³

et al. 2016

NDT

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Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder that often persists in adulthood. It is defined by inattention and/or hyperactivity–impulsivity. ADHD is associated with many comorbidities, including eating disorders (EDs). In the last decade, studies have reported that ADHD is linked with binge EDs, bulimia nervosa, and anorexia nervosa. Many postulates have been proposed to explain the association: 1) impulsive behavior in ADHD patients leads to disordered eating behavior; 2) other psychologic comorbidities present in ADHD patients account for eating behavior; 3) poor eating habits and resulting nutritional deficiencies contribute to ADHD symptoms; and 4) other risk factors common to both ADHD and EDs contribute to the coincidence of both diseases. Additionally, sex differences become a significant issue in the discussion of EDs and ADHD because of the higher incidence of bulimia nervosa and anorexia nervosa in females and the ability of females to mask the symptoms of ADHD. Interestingly, both EDs and ADHD rely on a common neural substrate, namely, dopaminergic signaling. Dopaminergic signaling is critical for motor activity and emotion, the latter enabling the former into a combined motivated movement like eating. This linkage aids in explaining the many comorbidities associated with ADHD. The interconnection of ADHD and EDs is discussed from both a historical perspective and the one based on the revealing nature of its comorbidities.

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Catechol-O-methyltransferase: potential relationship to idiopathic hypertension

Cited by 6 publications

References 35 publications

Effects of Sleeve Gastrectomy on Blood Pressure and the Renal Renin–Angiotensin System in Rats with Diet‐Induced Obesity

Effects of Sleeve Gastrectomy on Blood Pressure and the Renal Renin–Angiotensin System in Rats with Diet‐Induced Obesity

Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis

Attention deficit hyperactivity disorder and disordered eating behaviors: links, risks, and challenges faced

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