Transcriptome analysis of nicotine-exposed cells from the brainstem of neonate spontaneously hypertensive and Wistar Kyoto rats

Ferrari, Merari F. R.; Reis, Eduardo M.; Matsumoto, J P P; Fior-Chadi, Débora Rejane

doi:10.1038/tpj.2009.42

Cited by 2 publications

(1 citation statement)

References 56 publications

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“…The identification of neuropeptide and neurotransmitter systems is supported by work done in adult male SD, WKY, and SHR rats, as prolactin receptor, neuropeptide Y1 and Y5 receptors, glucagon-like peptide-1 receptor, cannabinoid 1 receptor, and adiponectin receptor are involved in HTN (25). In addition, following nicotine treatment, transcriptomics in the brain stem of WKY and SHR showed that animals may respond differently in the brain stem and involve cellular pathways related to neurotransmitter secretion and intracellular trafficking (16). Thus, the meta-analyses supports the notion that neuro-hormone transcripts related to feeding are associated with HTN.…”

Section: Murine Data Suggest That Gut-brain Neuropeptides Are Associated With Neurogenic Htnmentioning

confidence: 97%

Transcriptional networks in rodent models support a role for gut-brain communication in neurogenic hypertension: a review of the evidence

Zubcevic

Baker

Martyniuk

2017

Physiological Genomics

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Hypertension (HTN) is the most prevalent condition observed in primary health care. Hypertension shows complex etiology, and neuroinflammation, overactive sympathetic drive, and the microbiome are each associated with the disease. To obtain mechanistic perspective into neurogenic HTN, we first constructed a framework for transcriptional regulators of the disease using the Comparative Toxicogenomics Database. This approach yielded a core group of 178 transcripts that are prevalent in studies of HTN, including leptin and neuropeptide Y. We then conducted a meta-analysis for transcriptome data generated in brain tissue from HTN studies. Eight expression studies were reanalyzed, in which transcriptomics was conducted in hypertensive animal models [spontaneously hypertensive rats (SHR) and high blood pressure (BPH/2J) Schlager mice] (140 microarrays). Most strikingly, a gut-brain connection was a dominant theme in both rodent models of HTN. The transcriptomic data in the rat CNS converged on processes that included gastrointestinal motility and appetite, among others. In the mouse model, pathways converged on gastrointestinal transit. Thus, our data provide a powerful review of current molecular evidence of the interplay between gut and brain in HTN. Analyses of meta-genome data also suggested that transcriptome networks related to natriuresis, thermoregulation, reproduction (lactation and pregnancy), and vasoconstriction were associated to HTN, supporting physiological observations in independent studies by others. Lastly, we present novel transcriptome networks that may contribute to a neurogenic origin of HTN. Using this framework, new therapeutic targets can be proposed and investigated in treatment strategies.

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Section: Murine Data Suggest That Gut-brain Neuropeptides Are Associated With Neurogenic Htnmentioning

confidence: 97%

Transcriptional networks in rodent models support a role for gut-brain communication in neurogenic hypertension: a review of the evidence

Zubcevic

Baker

Martyniuk

2017

Physiological Genomics

View full text Add to dashboard Cite

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Adenosine receptor type 2a is differently modulated by nicotine in dorsal brainstem cells of Wistar Kyoto and spontaneously hypertensive rats

2010

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Hypertension can result from neuronal network imbalance in areas of central nervous system that control blood pressure, such as the nucleus tractus solitarius (NTS). There are several neurotransmitters and neuromodulatory substances within the NTS, such as adenosine, which acts on purinoreceptors A(2a) (A(2a)R). The A(2a)R modulates neurotransmission in the NTS where its activation may induce decrease in blood pressure by different mechanisms. Nicotine is a molecule that crosses the hematoencephalic barrier and acts in several areas of central nervous system including the NTS, where it may interact with some neurotransmitter systems and contributes to the development of hypertension in subjects with genetic predisposition to this disease. In this study we first determined A(2a)R binding, protein, and mRNA expression in dorsomedial medulla oblongata of neonate normotensive (WKY) and spontaneously hypertensive rats (SHR). Subsequently, we analyzed the modulatory effects of nicotine on A(2a)R in cell culture in order to evaluate its possible involvement in the development of hypertension. Data showed a decreased A(2a)R binding and increased protein and mRNA expression in tissue sample and culture of dorsal brainstem from SHR compared with those from WKY rats at basal conditions. Moreover, nicotine modulated A(2a)R binding, protein, and mRNA expression in cells from both strains. Interestingly, nicotine decreased A(2a)R binding and increased protein levels, as well as, induced a differential modulation in A(2a)R mRNA expression. Results give us a clue about the mechanisms involved in the modulatory effects of nicotine on A(2a)R as well as hypothesize its possible contribution to the development of hypertension. In conclusion, we demonstrated that A(2a)R of SHR cells which differ from WKY and nicotine differentially modulates A(2a)R in dorsal brainstem cells of SHR and WKY.

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Transcriptome analysis of nicotine-exposed cells from the brainstem of neonate spontaneously hypertensive and Wistar Kyoto rats

Cited by 2 publications

References 56 publications

Transcriptional networks in rodent models support a role for gut-brain communication in neurogenic hypertension: a review of the evidence

Transcriptional networks in rodent models support a role for gut-brain communication in neurogenic hypertension: a review of the evidence

Adenosine receptor type 2a is differently modulated by nicotine in dorsal brainstem cells of Wistar Kyoto and spontaneously hypertensive rats

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