Involvement of protein kinase in Δ12‐prostaglandin J2‐induced expression of rat heme oxygenase‐1 gene

Negishi, Manabu; Odani, Noriko; Koizumi, Toru; Takahashi, Shouji; Ichikawa, Atsushi

doi:10.1016/0014-5793(95)01001-u

Cited by 18 publications

(6 citation statements)

References 26 publications

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“…We demonstrated that the induction of HO-1 expression in HMEC-1 treated with 15d-PGJ 2 was mediated by the activation of HO-1 promoter, but not by the stabilization of HO-1 mRNA. The increased transcriptional activity of HO-1 promoter in response to another prostaglandin-J 2 derivative, 12d-PGJ 2 , was earlier observed in aortic endothelial cells and basophilic leukemia cells (25,34). Koizumi and colleagues showed that 12d-PGJ 2 induces the expression of the rat HO-1 gene through the phosphorylation of the nuclear proteins, which bind to the specific 12d-PGJ 2 responsive element located in HO-1 promoter (25,34).…”

Section: Discussionmentioning

confidence: 87%

Effect of Prostaglandin-J₂on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1

Józkowicz

Huk

Nigisch

et al. 2002

Antioxidants & Redox Signaling

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Heme oxygenase-1 (HO-1) is an inducible enzyme that degrades heme to carbon monoxide, iron ions, and biliverdin. Its expression can be induced by 15-deoxy-Delta(12,14)prostaglandin-J(2) (15d-PGJ(2)), a natural ligand of peroxisome proliferator-activated receptor-gamma transcription factor. In macrophages and vascular smooth muscle cells, 15d-PGJ(2) up-regulates the expression of vascular endothelial growth factor (VEGF), a fundamental regulator of angiogenesis. Here we investigated the involvement of HO-1 in the 15d-PGJ(2)-mediated regulation of VEGF production by human microvascular endothelial cells (HMEC-1). Resting HMEC-1 released approximately 20 pg/ml VEGF protein after 24 h of incubation. Treatment of cells with 15d-PGJ(2) (1-10 microM) significantly and dose-dependently increased the VEGF promoter activity, mRNA expression, and protein secretion. In the same cells, 15d-PGJ(2) potently induced the expression of HO-1 protein that correlated with HO-1 promoter activity. Activation of HO-1 with hemin or ectopic overexpression of HO-1 in HMEC-1 perfectly mimicked the effect of 15d-PGJ(2) and led to increased VEGF production. Importantly, the inhibition of the HO-1 pathway by tin protoporphyrin-IX significantly reduced the stimulatory effect of 15d-PGJ(2) on VEGF synthesis. Thus, we postulate that the up-regulation of VEGF expression in response to 15d-PGJ(2 )in HMEC-1 is mediated by the activation of HO-1.

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Section: Discussionmentioning

confidence: 87%

Effect of Prostaglandin-J₂on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1

Józkowicz

Huk

Nigisch

et al. 2002

Antioxidants & Redox Signaling

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“…A previous study failed to find changes in CO during histamine-induced bronchoconstriction, but this association only was explored in five patients (32). The increase of COex during histamine-induced bronchoconstriction could be due to the activation of OH-1 by prostaglandins released by mast cells (33) or by the changes in airway caliber. The increase of COex in subjects without response to histamine challenge could be justified by a subclinical bronchoconstriction, without change in FEV 1 , or by oxidative stress promoted by saline solution.…”

Section: Discussionmentioning

confidence: 94%

Relationship Between Exhaled Carbon Monoxide and Airway Hyperresponsiveness in Asthmatic Patients

et al. 2004

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The study objectives were to analyze the changes in exhaled carbon monoxide (COex) induced by histamine provocation challenge in asthmatic patients and to evaluate the relationship between COex and airway sensitivity and reactivity. Levels of COex were measured in 105 nonsmoking mildly asthmatic subjects before and after histamine provocation challenge. Dose-response curves were characterized by their sensitivity (PD20) and reactivity. Dose-response slope (DRS), continuous index of responsiveness (CIR), and bronchial reactivity index (BRI) were determined as reactivity indices. Bronchial challenge was positive for 47 subjects and negative for 58. The COex levels rose significantly after bronchial challenge in the positive response group (4.49 +/- 0.4 vs. 5.74 +/- 0.57 ppm, p = 0.025) and in the negative response group (2.84 +/- 0.25 vs. 4.00 +/- 0.41 ppm, p = 0.000). An inverse relation between basal COex and PD20 was found (r = -0.318, p = 0.030). In all subjects, a proportional direct relationship between COex and DRS (r = 0.214, p = 0.015), CIR (r = 0.401, p = 0.000), and BRI (r = 0.208, p = 0.012) was observed. On stepwise multiple linear regression analysis, COex only significantly correlated with CIR (multiple r2 = 0.174, p = 0.000). In conclusion, exhaled CO determination is a noninvasive inflammatory marker of the respiratory tract, which shows an acceptable association with airway hyperresponsiveness.

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“…The activation of HO-1 by prostaglandins [30] released by mast cells during the early asthmatic reaction [3,31] may explain the elevated levels of exhaled CO during this phase. The absence of significant changes in exhaled NO levels is possibly due to the inability of prostaglandins and other compounds released during the early reaction, such as leukotrienes and histamine, to activate iNOS.…”

Section: Discussionmentioning

confidence: 99%

Changes in exhaled carbon monoxide and nitric oxide levels following allergen challenge in patients with asthma

et al. 1999

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Carbon monoxide is a product of haem degradation by haem oxygenase (HO), activated by inflammatory cytokines and oxidants. This study examined whether allergen challenge can increase exhaled CO levels, as a reflection of HO activation.Exhaled CO and nitric oxide, an expired gas also thought to reflect cytokine-induced airway inflammation, were measured in 15 atopic steroid-naive nonsmoking patients with asthma (13 males, aged 3062 yrs) before and for up to 20 h after allergen challenge.Baseline CO (4.40.3 parts per million (ppm)) and NO (20.661.2 parts per billion (ppb)) levels were elevated in asthmatic as compared with nonsmoking normal volunteers (n=37, 2.10.2 ppm and 7.00.1 ppb, respectively, p<0.05). In 10 patients with a dual response in the forced expiratory volume in one second (FEV1) there was a maximal increase in exhaled CO at 1 h (34.37.1%) and at 6 h (6912%, p<0.01), followed by a maximal fall in FEV1 (289%, p<0.05) at 9 h, whereas the maximal NO increase was observed at 10 h (50.211.8%). The maximal increase in exhaled CO in single response patients (n=5) was 302% during the early asthmatic reaction and 46.3 9.2% between 4 and 10 h, followed by a fall in FEV1 (93%, p>0.05) at 9 h, whereas exhaled NO was not significantly changed. In five patients exhaled CO was not attenuated by inhalation of increasing concentrations of histamine causing a 20% fall in FEV1 (PC20) or its subsequent relief by b 2 -agonists.In conclusion, exhaled carbon monoxide is increased during the early and late asthmatic reactions independently of the change in airway calibre, while exhaled nitric oxide is increased only during the late reaction and follows the increase in carbon monoxide and fall in the forced expiratory volume in one second in time. Eur Respir J 1999; 13: 48±52. There is considerable evidence for airway inflammation and oxidative stress in patients with asthma, even when the disease is mild [1,2]. Bronchoalveolar lavage (BAL) and bronchial biopsy studies have demonstrated the infiltration of activated inflammatory cells in the airway mucosa and there is a broad relationship between the intensity of inflammation and the clinical severity of asthma. Inhalation of allergen provides a model of asthmatic inflammation, as it provokes an early fall in forced expiratory volume in one second (FEV1) owing to the release of bronchoconstrictor mediators, such as histamine, leukotrienes and prostaglandins [3], and a late asthmatic response which is associated with a prolonged bronchoconstriction, influx of inflammatory cells [4] and mediators [5±7] and an increase in the oxidative stress in the airway.It is becoming clear that some oxidant-induced mediators and enzymes, such as haem oxygenase (HO), may also play a vital role in the airway protective response to oxidative stress. Two isoforms of HO have been described: the constitutive HO-2, which is highly expressed in the brain and testes, and the inducible HO-1, which is ubiquitously distributed. The latter is activated by a variety of pro-inflammatory cytoki...

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Involvement of protein kinase in Δ¹²‐prostaglandin J₂‐induced expression of rat heme oxygenase‐1 gene

Cited by 18 publications

References 26 publications

Effect of Prostaglandin-J₂on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1

Effect of Prostaglandin-J₂on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1

Relationship Between Exhaled Carbon Monoxide and Airway Hyperresponsiveness in Asthmatic Patients

Changes in exhaled carbon monoxide and nitric oxide levels following allergen challenge in patients with asthma

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Involvement of protein kinase in Δ12‐prostaglandin J2‐induced expression of rat heme oxygenase‐1 gene

Cited by 18 publications

References 26 publications

Effect of Prostaglandin-J2on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1

Effect of Prostaglandin-J2on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1

Relationship Between Exhaled Carbon Monoxide and Airway Hyperresponsiveness in Asthmatic Patients

Changes in exhaled carbon monoxide and nitric oxide levels following allergen challenge in patients with asthma

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Involvement of protein kinase in Δ¹²‐prostaglandin J₂‐induced expression of rat heme oxygenase‐1 gene

Effect of Prostaglandin-J₂on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1

Effect of Prostaglandin-J₂on VEGF Synthesis Depends on the Induction of Heme Oxygenase-1