Decreased Ornithine Decarboxylase Activity in the Kidneys of Dahl Salt-Sensitive Rats.

Hayashi, Takeshi; Tsujino, Takeshi; Iwata, Sachiyo; Nonaka, Hidemi; Emoto, Noriaki; Yano, Yoshihisa; Otani, Shuzo; Hayashi, Yoshitake; Itoh, Hiroshi; Yokoyama, Mitsuhiro

doi:10.1291/hypres.25.787

Cited by 10 publications

(8 citation statements)

References 31 publications

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“…In this model, systemic hypertension induces left ventricular hypertrophy 17 and renal hypertrophy with glomerulosclerosis, 18,19 which is consistent with our Levels of mRNA were determined by Northern blot analysis as described in Methods. Autoradiographs from representative Northern blots are shown.…”

Section: Mohri Et Al Clock Genes In Dahl Salt-sensitive Rats 191supporting

confidence: 78%

Alterations of Circadian Expressions of Clock Genes in Dahl Salt-Sensitive Rats Fed a High-Salt Diet

et al. 2003

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Abstract-In mammals, behavioral and physiologic processes display 24-hour rhythms that are regulated by a circadian system consisting of central and peripheral oscillators. Because various cardiovascular functions show diurnal variations and abnormal patterns of circadian blood pressure variation carry a high risk of cardiovascular complications, we investigated whether the expression of clock genes is altered in an animal model of hypertension. In Dahl salt-sensitive rats fed a high-salt (4% NaCl) diet for 6 weeks (DS-H), radiotelemetry monitoring showed increased amplitude of circadian variations in blood pressure. The ratio of heart weight to body weight and the ratio of kidney weight to body weight were higher in DS-H. Echocardiographic data showed that the wall thickness of the left ventricle was greater in DS-H. Northern blot analysis and single cosinor analysis revealed that the amplitudes of circadian expression changes of the clock genes (mPer2, Bmal1, and dbp) in the heart, liver, and kidney were significantly decreased in DS-H rats compared with a normal-salt-diet group, except for Bmal1 in the liver. The circadian expression changes of plasminogen activator inhibitor-1, a clock-regulated gene, were attenuated in the hearts of DS-H. Key Words: circadian rhythm Ⅲ hypertension, experimental Ⅲ hypertrophy Ⅲ molecular biology Ⅲ rats, Dahl T he circadian clock system is responsible for the daily timing of physiologic processes. 1-4 Several genes essential for mammalian circadian clock function have been identified. These include homologues of the Drosophila gene period (mPer1, mPer2, and mPer3), cryptochrome isoforms (mCry1 and mCry2), and PAS helix-loop-helix transcription factors (Clock and Bmal1). The products of these genes constitute a model of a molecular oscillator, which is based on interconnected positive and negative transcriptionaltranslational feedback loops. Clock-controlled genes, including dbp, whose products show circadian accumulation but are not required for clock oscillation, can be regulated by the same feedback loops.The mammalian central clock is located in the suprachiasmatic nucleus (SCN) within the hypothalamus in the brain. However, circadian expression of the clock and clockcontrolled genes is observed not only in the SCN but also in most peripheral tissues. Recent evidence suggests that the circadian clock system has a hierarchical organization: a central pacemaker located in the SCN directs peripheral oscillators that are present in most tissues. Although central and peripheral clocks share important features in their molecular make-up, only the central clock is self-sustained. This suggests that SCN-derived signals synchronize peripheral oscillations to prevent the dampening of circadian gene expression. It appears that multiple signaling pathways consisting of hormonal and/or neuronal factors are used for entraining peripheral oscillators.Cardiovascular or hemodynamic parameters, such as heart rate (HR) and blood pressure (BP), exhibit variations consistent with circadian rhy...

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Section: Mohri Et Al Clock Genes In Dahl Salt-sensitive Rats 191supporting

confidence: 78%

Alterations of Circadian Expressions of Clock Genes in Dahl Salt-Sensitive Rats Fed a High-Salt Diet

et al. 2003

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“…A few studies have previously investigated the effects of chronic oral treatment with DFMO in different models of hypertension such as genetic hypertension [30,31], coarctation hypertension [32], angiotensin II-induced hypertension [33], deoxycorticosterone acetate-salt hypertension [34], or in Dahl salt-sensitive hypertensive rats [35]. These studies were conducted only with the aim of assessing the potential role of polyamines in the alterations in vascular structure and the subsequent blood pressure changes.…”

Section: Discussionmentioning

confidence: 99%

Arginase inhibition reduces endothelial dysfunction and blood pressure rising in spontaneously hypertensive rats

Demougeot¹,

Prigent‐Tessier

Marie

et al. 2005

Journal of Hypertension

141

130

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“…ODC-1 is the first enzyme in polyamine synthesis and is essential for normal development and tissue repair in mammals. In addition, both ODC1 mRNA expression and its activity might be affected by changes in osmolarity (Hayashi et al, 2002). We therefore studied whether p38 affected ODC1 RNA binding to hDlg under osmotic stress.…”

Section: Identification Of Mrna Bound To Hdlg And/or Psfmentioning

confidence: 99%

p38γ regulates interaction of nuclear PSF and RNA with the tumour-suppressor hDlg in response to osmotic shock

Sabio

Cerezo-Guisado

Reino

et al. 2010

Journal of Cell Science

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Activation of p38γ modulates the integrity of the complex formed by the human discs large protein (hDlg) with cytoskeletal proteins, which is important for cell adaptation to changes in environmental osmolarity. Here we report that, in response to hyperosmotic stress, p38γ also regulates formation of complexes between hDlg and the nuclear protein polypyrimidine tract-binding protein-associated-splicing factor (PSF). Following osmotic shock, p38γ in the cell nucleus increases its association with nuclear hDlg, thereby causing dissociation of hDlg-PSF complexes. Moreover, hDlg and PSF bind different RNAs; in response to osmotic shock, p38γ causes hDlg-PSF and hDlg-RNA dissociation independently of its kinase activity. These findings identify a novel nuclear complex and suggest a previously unreported function of p38γ, which is independent of its catalytic activity and could affect mRNA processing and/or gene transcription to aid cell adaptation to osmolarity changes in the environment.

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Decreased Ornithine Decarboxylase Activity in the Kidneys of Dahl Salt-Sensitive Rats.

Cited by 10 publications

References 31 publications

Alterations of Circadian Expressions of Clock Genes in Dahl Salt-Sensitive Rats Fed a High-Salt Diet

Alterations of Circadian Expressions of Clock Genes in Dahl Salt-Sensitive Rats Fed a High-Salt Diet

Arginase inhibition reduces endothelial dysfunction and blood pressure rising in spontaneously hypertensive rats

p38γ regulates interaction of nuclear PSF and RNA with the tumour-suppressor hDlg in response to osmotic shock

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