Clonidine-Induced Enhancement of iNOS Expression Involves NF-κB

Su, Nuan Yen; Tsai, Pei Shan; Huang, Chun Jen

doi:10.1016/j.jss.2007.11.725

Cited by 11 publications

(2 citation statements)

References 29 publications

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“…In our study, the inflammatory molecule TNF‐α did not change iNOS expression in the endothelial cell/trophoblast co‐cultured cells, indicating that iNOS is not involved in this in vitro model. While clonidine has been reported to induce iNOS expression in macrophage cells none of the selected medications had any effect on iNOS expression in this study.…”

Section: Discussioncontrasting

confidence: 56%

Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor‐α inhibited endothelial nitric oxide synthase expression in endothelial‐trophoblast cellular networks

Bobek

Makris

et al. 2017

Clin Exp Pharma Physio

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Medications used to control hypertension in pregnancy also improve trophoblast and endothelial cellular interaction in vitro. Tumour necrosis factor-α (TNF-α) inhibits trophoblast and endothelial cellular interactions and simultaneously decreases endothelial nitric oxide synthase (eNOS) expression. This study investigated whether antihypertensive medications improved these cellular interactions by modulating eNOS and inducible nitric oxide synthase (iNOS) expression. Human uterine myometrial microvascular endothelial cells (UtMVECs) were pre-incubated with (or without) low dose TNF-α (0.5 ng/mL) or TNF-α plus soluble fms-like tyrosine kinase-1 (sFlt-1) (100 ng/mL). The endothelial cells were cultured on Matrigel. After endothelial cellular networks appeared, trophoblast derived HTR-8/SVneo cells were co-cultured in the presence of clinically relevant doses of methyldopa, labetalol, hydralazine or clonidine for 24 hours. Cells were retrieved from the Matrigel to extract mRNA and eNOS and iNOS expression were examined by quantitative PCR. Methyldopa, labetalol, hydralazine and clonidine reversed the inhibitory effect of TNF-α on eNOS mRNA expression. After pre-incubating endothelial cells with TNF-α and sFlt-1, all the medications except methyldopa lost their effect on eNOS mRNA expression. In the absence of TNF-α, antihypertensive medications did not change eNOS expression. The mRNA expression of iNOS was not affected by TNF-α or any medications. This study shows that selected antihypertensive medications used in the treatment of hypertension in pregnancy increase eNOS expression in vitro when induced by the inflammatory TNF-α. The anti-angiogenic molecule sFlt-1 may antagonise the potential benefit of these medications by interfering with the NOS pathway.

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Section: Discussioncontrasting

confidence: 56%

Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor‐α inhibited endothelial nitric oxide synthase expression in endothelial‐trophoblast cellular networks

Bobek

Makris

et al. 2017

Clin Exp Pharma Physio

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“…Clonidine, an anti-hypertension agent is effectively used as adjunct to anesthesia/sedation and pain management. It has shown to enhance iNOS expression in endotoxin-activated macrophages via induction of NFκB 24 . Since PKC is associated with NFκB activation by a variety of stimuli.…”

Section: Resultsmentioning

confidence: 99%

Transcription Factor Target Gene Network governs the Logical Abstraction Analysis of the Synthetic Circuit in Leishmaniasis

Mol

Kosey

Boppana

et al. 2018

Sci Rep

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With the advent of synthetic biology in medicine many synthetic or engineered proteins have made their way to therapeutics and diagnostics. In this paper, the downstream gene network of CD14-TNF-EGFR pathway in leishmaniasis, a tropical disease, is reconstructed. Network analysis showed that NFkB links the signaling and gene network, used as a point of intervention through a synthetic circuit embedded within the negative autoregulatory feedback loop. A chimeric protein kinase C (PKC) is incorporated in the synthetic circuit, under the transcriptional regulation of Lac repressor and IPTG, as an inducer. The chimeric PKC_ζα via IκKb phosphorylation activates NFκB, and modulates the gene expression from an anti-inflammatory to a pro-inflammatory phenotype in in vitro L. major infected macrophage model. This is the first ever report of a synthetic device construction in leishmania.

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Immunohistochemistry on Rodent Circulatory System: Its Possible Use in Investigating Hypertension

Kamisah

Jaarin

2015

Technical Aspects of Toxicological Immunohistochemistry

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Clonidine-Induced Enhancement of iNOS Expression Involves NF-κB

Cited by 11 publications

References 29 publications

Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor‐α inhibited endothelial nitric oxide synthase expression in endothelial‐trophoblast cellular networks

Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor‐α inhibited endothelial nitric oxide synthase expression in endothelial‐trophoblast cellular networks

Transcription Factor Target Gene Network governs the Logical Abstraction Analysis of the Synthetic Circuit in Leishmaniasis

Immunohistochemistry on Rodent Circulatory System: Its Possible Use in Investigating Hypertension

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