Cigarette smoke extract induces HO‐1 expression in mouse cerebral vascular endothelial cells: Involvement of c‐Src/NADPH oxidase/PDGFR/JAK2/STAT3 pathway

Shih, Ruey Horng; Lee, I-Te; Hsieh, Hsi‐Lung; Kou, Yu Ru; Yang, Che‐Hua

doi:10.1002/jcp.22270

Cited by 28 publications

(31 citation statements)

References 42 publications

(49 reference statements)

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“…Regarding molecular mechanism of anti-inflammatory effect of nicotine, importance of Jak2-STAT3 signaling pathway has been reported (8). Activation of Jak2-STAT3 signal also plays a crucial role for HO-1 expression in various cells, including human macrophages (35,40,44). Therefore, whether the activation of Jak2-STAT3 by nicotine leads to HO-1 induction in macrophages needs further investigation.…”

Section: Anti-inflammation By Nicotine Involves Ho-1 2065mentioning

confidence: 99%

Stimulation of Alpha7 Nicotinic Acetylcholine Receptor by Nicotine Attenuates Inflammatory Response in Macrophages and Improves Survival in Experimental Model of Sepsis Through Heme Oxygenase-1 Induction

Tsoyi

Jang

Kim

et al. 2011

Antioxidants & Redox Signaling

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Activation of nicotinic acetylcholine receptor alpha7 subunit (α7nAChR) by nicotine leads to the improved survival rate in experimental model of sepsis. Previously, we demonstrated that heme oxygenase (HO)-1 inducers or carbon monoxide significantly increased survival of lipopolysaccharide (LPS)-induced and cecal ligation and puncture-induced septic mice by reduction of high mobility group box 1 release, a late mediator of sepsis. However, that activation of α7nAChR by nicotine provides anti-inflammatory action through HO-1 upregulation has not been elucidated. Here we show that HO-1-inducible effect by nicotine was mediated through sequential event-Ca(2+) influx, classical protein kinase C activation, and reactive oxygen species production-which activates phosphoinositol-3-kinase/Akt/Nrf-2 pathway. In addition, HO-1 is required for nicotine-mediated suppression of tumor necrosis factor-α, inducible nitric oxide synthase, and high mobility group box 1 expression induced by LPS in macrophages, as evidenced by the fact that nicotine failed to inhibit production of these mediators when HO-1 was suppressed. Importantly, nicotine-induced survival rate was reduced by inhibition of HO-1 in LPS- and cecal ligation and puncture-treated septic mice. Collectively, these data suggest that activation of α7nAChR by nicotine is critical in the regulation of anti-inflammatory process, which could be mediated through HO-1 expression. Thus, we conclude that activation of α7nAChR by nicotine provides anti-inflammatory action through HO-1 upregulation.

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Section: Anti-inflammation By Nicotine Involves Ho-1 2065mentioning

confidence: 99%

Stimulation of Alpha7 Nicotinic Acetylcholine Receptor by Nicotine Attenuates Inflammatory Response in Macrophages and Improves Survival in Experimental Model of Sepsis Through Heme Oxygenase-1 Induction

Tsoyi

Jang

Kim

et al. 2011

Antioxidants & Redox Signaling

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“…These enzymes contain common cis-acting elements, called electrophile response elements (EpRE) or antioxidant response elements (ARE) in their promoter regions [22]. The elements are activated by carcinogens or oxidative stress from endogenous and exogenous origins.…”

Section: Introductionmentioning

confidence: 99%

“…HO-1 is expressed in the major components of skin, including epidermal KC and dermal Wbroblast, and is known for its cytoprotective and antioxidant properties [27]. HO-1 was reported to be induced by environmental pro-oxidants, such as UV radiation (both types A and B), ozone, air pollution, and cigarette smoking [14,22,28]. NQO-1 has been mainly studied for its protective role during skin carcinogenesis in a mouse model [5,13].…”

Section: Introductionmentioning

confidence: 99%

Nrf2-dependent and Nrf2-independent induction of phase 2 detoxifying and antioxidant enzymes during keratinocyte differentiation

et al. 2012

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As antioxidant enzymes can be actively modulated during keratinocyte (KC) differentiation, this study was aimed to evaluate the modulation of a group of phase 2 detoxifying and antioxidant enzymes (phase 2 enzymes) during KC differentiation. In postconfluence-induced differentiation model of KC, heme oxygenase-1 (HO-1), NADP(H):quinone oxidoreductase-1 (NQO-1), and glutathione S-transferase pi (GSTpi) were up-regulated at a transcriptional level. In Western blot analysis, the phase 2 enzymes were up-regulated by H(2)O(2), but down-regulated by N-acetyl cysteine, indicating the active role of reactive oxygen species for their expression during KC differentiation. When a redox-sensitive NF-E2 related factor-2 (Nrf2), a key transcriptional factor for phase 2 enzymes, was knocked down by small interfering RNA transfection in differentiated KCs, only NQO-1 was down-regulated in both mRNA and protein levels. In human skin, expression levels of the phase 2 enzymes were up-regulated in the differentiated KC in the normal epidermis and keratotic foci in squamous cell carcinoma, further supporting the differentiation-dependent expression of phase 2 enzymes in vivo. This study demonstrates that a group of phase 2 enzymes are modulated during KC differentiation via either Nrf2-dependent (NQO-1) or Nrf2-independent (HO-1 and GSTpi) ways.

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“…One should point out, however, that reports also exist describing p38-MAPK and MSK1 involvement in HOX-1 regulation by various stimuli (28, 71). Src along with Nox have been shown to mediate HOX-1 up-regulation by lipotechoic acid in human tracheal smooth muscle cells (72) and by cigarette smoke particle in mouse brain endothelial cells (73). On the other hand, although neither ERK1/2 nor p38-MAPK activation was detected in insulin-exposed renal cells (19), ERK1/2 were shown to be activated by insulin in human skin fibroblasts, via a Nox-dependent mechanism (54).…”

Section: Discussionmentioning

confidence: 99%

Insulin-Induced Oxidative Stress Up-Regulates Heme Oxygenase-1 via Diverse Signaling Cascades in the C2 Skeletal Myoblast Cell Line

et al. 2011

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Impaired insulin sensitivity (insulin resistance) is a common denominator in many metabolic disorders, exerting pleiotropic effects on skeletal muscle, liver, and adipose tissue function. Heme oxygenase-1 (HOX-1), the rate-limiting enzyme in heme catabolism, has recently been shown to confer an antidiabetic effect while regulating cellular redox-buffering capacity. Therefore, in the present study, we probed into the mechanisms underlying the effect of insulin on HOX-1 in C2 skeletal myoblasts. Hence, insulin was found to suppress C2 myoblasts viability via stimulation of oxidative stress, with HOX-1 counteracting this action. Insulin induced HOX-1 expression in a time-and dose-dependent manner, an effect attenuated by selective inhibitors of ERK1/2 (PD98059), Src (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine), and c-Jun terminal kinases 1 and 2 (SP600125) pathways. Furthermore, nuclear factor-B role in insulin-induced HOX-1 up-regulation was verified, with ERK1/2, Src, and c-Jun terminal kinases 1 and 2 mediating p65-nuclear factor-B subunit phosphorylation. Overall, our novel findings highlight for the first time the transduction mechanisms mediating HOX-1 induction in insulin-treated C2 myoblasts. This effect was established to be cell type specific because insulin failed to promote HOX-1 expression in HepG2 hepatoma cells. Deciphering the signaling networks involved in insulin-stimulated HOX-1 up-regulation is of prominent significance because it may potentially contribute to elucidation of the mechanisms involved in associated metabolic pathologies. (Endocrinology 152: 1274 -1283, 2011)

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Cigarette smoke extract induces HO‐1 expression in mouse cerebral vascular endothelial cells: Involvement of c‐Src/NADPH oxidase/PDGFR/JAK2/STAT3 pathway

Cited by 28 publications

References 42 publications

Stimulation of Alpha7 Nicotinic Acetylcholine Receptor by Nicotine Attenuates Inflammatory Response in Macrophages and Improves Survival in Experimental Model of Sepsis Through Heme Oxygenase-1 Induction

Stimulation of Alpha7 Nicotinic Acetylcholine Receptor by Nicotine Attenuates Inflammatory Response in Macrophages and Improves Survival in Experimental Model of Sepsis Through Heme Oxygenase-1 Induction

Nrf2-dependent and Nrf2-independent induction of phase 2 detoxifying and antioxidant enzymes during keratinocyte differentiation

Insulin-Induced Oxidative Stress Up-Regulates Heme Oxygenase-1 via Diverse Signaling Cascades in the C2 Skeletal Myoblast Cell Line

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