Role of Akt/HO-1 pathway in estrogen-mediated attenuation of trauma-hemorrhage-induced lung injury

Yeh, Huei-Chung; Chen, Tsung‐Hsing; Kuo, Chia‐Jung; Lin, Chun-Jun; Chiang, Kun‐Chun; Yeh, Ta‐Sen; Hwang, Tsann‐Long; Chaudry, Irshad I.

doi:10.1016/j.jss.2012.10.926

Cited by 19 publications

(16 citation statements)

References 46 publications

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“…13,14 HO-1 plays a pivotal role in the defense against oxidative and inflammatory processes in the lung. 15 Activating HO-1 has been shown to attenuate hyperoxic lung injury in rats, 16 cecal ligation and puncture-induced ALI in mice, 17 trauma-hemorrhage-induced lung injury in rats, 18 and ventilator-induced ALI in rabbits. 19 HO-1 is expressed in lung endothelial [20][21][22] and epithelial cells, 23,24 monocytes, 25 and neutrophils.…”

Section: Introductionmentioning

confidence: 99%

Tissue heme oxygenase-1 exerts anti-inflammatory effects on LPS-induced pulmonary inflammation

et al. 2016

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Heme oxygenase-1 (HO-1) has been shown to display anti-inflammatory properties in models of acute pulmonary inflammation. For the first time, we investigated the role of leukocytic HO-1 using a model of HO-1(flox/flox) mice lacking leukocytic HO-1 that were subjected to lipopolysaccharide (LPS)-induced acute pulmonary inflammation. Immunohistology and flow cytometry demonstrated that activation of HO-1 using hemin decreased migration of polymorphonuclear leukocytes (PMNs) to the lung interstitium and bronchoalveolar lavage (BAL) in the wild-type and, surprisingly, also in HO-1(flox/flox) mice, emphasizing the anti-inflammatory potential of nonmyeloid HO-1. Nevertheless, hemin reduced the CXCL1, CXCL2/3, tumor necrosis factor-α (TNFα), and interleukin 6 (IL6) levels in both animal strains. Microvascular permeability was attenuated by hemin in wild-type and HO-1(flox/flox) mice, indicating a crucial role of non-myeloid HO-1 in endothelial integrity. The determination of the activity of HO-1 in mouse lungs revealed no compensatory increase in the HO-1(flox/flox) mice. Topical administration of hemin via inhalation reduced the dose required to attenuate PMN migration and microvascular permeability by a factor of 40, emphasizing its clinical potential. In addition, HO-1 stimulation was protective against pulmonary inflammation when initiated after the inflammatory stimulus. In conclusion, nonmyeloid HO-1 is crucial for the anti-inflammatory effect of this enzyme on PMN migration to different compartments of the lung and on microvascular permeability.

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Section: Introductionmentioning

confidence: 99%

Tissue heme oxygenase-1 exerts anti-inflammatory effects on LPS-induced pulmonary inflammation

et al. 2016

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“…Moreover, E2 also served to induce activation of HIF‐1 on the precondition that the phosphatidylinositol 3‐kinase/Akt pathway was activated, and HIF‐1 activation might also be initiated via ER‐related PI3K/Akt and MAPK1 pathways . Ultimately, HO‐1 was involved in the attenuation of lung injury mediated by E2 …”

Section: Introductionmentioning

confidence: 99%

“…17 Ultimately, HO-1 was involved in the attenuation of lung injury mediated by E2. 18 In view of the complicated relationships among E2, the MAPK1/ HIF-1/HO-1 signaling pathway, and potential risk of CAD, we intended to discover whether SNPs within MAPK1, HIF-1, and HO-1 could explain the high risk of perimenopausal CAD. gram, which was very robust.…”

Section: Introductionmentioning

confidence: 99%

Correlation between genetic polymorphisms within the MAPK1/HIF‐1/HO‐1 signaling pathway and risk or prognosis of perimenopausal coronary artery disease

Guo

Zhang

Yan

et al. 2017

Clinical Cardiology

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Background Mitogen‐activated protein kinase‐1 (MAPK1), as well as its downstream factors of hypoxia‐inducible factor‐1 (HIF‐1) and heme oxygenase‐1 (HO‐1), have been documented to be involved in modulating development of coronary artery disease (CAD). Hypothesis Genetic mutations within the MAPK1/HIF‐1/HO‐1 signaling pathway could alter the risk of perimenopausal CAD in Chinese patients. Methods Peripheral blood samples were gathered from 589 CAD patients and 860 healthy controls, and 12 potential single‐nucleotide polymorphisms (SNPs) were obtained from HapMap database and previously published studies. Genotyping of SNPs was implemented with the TaqMan SNP Genotyping Assays. Odds ratios (OR) and 95% confidence intervals (CI) were utilized to evaluate the correlations between SNPs and CAD risk. Results Regarding MAPK1 , rs6928 (OR: 1.71, 95% CI: 1.47‐1.98, P < 0.05), rs9340 (OR: 0.85, 95% CI: 0.73‐0.99, P < 0.05), and rs11913721 (OR: 0.70, 95% CI: 0.52‐0.95, P < 0.05) were remarkably associated with susceptibility to perimenopausal CAD. Of these, rs9340 and rs11913721 were also regarded as protective factors for perimenopausal CAD patients. Moreover, results of HIF‐1 indicated noticeable correlations between combined SNPs of rs1087314 and rs2057482 and risk of perimenopausal CAD (OR: 1.24, 95% CI: 1.01‐1.53, P < 0.05; and OR: 0.71, 95% CI: 0.55‐0.91, P < 0.05, respectively). Nonetheless, rs2071746 in HO‐1 was found to be only associated with perimenopausal CAD risk (OR: 0.67, 95% CI: 0.58‐0.78, P < 0.05). Conclusions The genetic mutations within MAPK1 (rs6928, rs9340, rs11913721), HIF‐1 (rs1087314, rs2057482), and HO‐1 (rs2071746) could alter susceptibility to perimenopausal CAD in this Chinese population.

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“…Animals were fasted for 8 h before the experiment but had free access to water ad libitum. A nonheparinized model of trauma-hemorrhagic shock was used as described previously (11,12). At the time of the experiment, the rats were breathing in 100% O 2 and anesthetized by isoflurane inhalation (1.2%) using anesthesia vaporizer (VIP-3000, Paragon Medical, Coral Springs, FL) before the induction of soft-tissue trauma via only 5-cm midline laparotomy.…”

Section: Methodsmentioning

confidence: 99%

Role of p38 MAPK pathway in 17β-estradiol-mediated attenuation of hemorrhagic shock-induced hepatic injury

Chen

Chiang

Kuo

et al. 2015

Journal of Applied Physiology

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Although 17β-estradiol (E2) treatment following hemorrhagic shock or ischemic reperfusion prevents organs from dysfunction and injury, the precise mechanism remains unknown. We hypothesize that the E2-mediated attenuation of liver injury following hemorrhagic shock and fluid resuscitation occurs via the p38 mitogen-activated protein kinase (MAPK)-dependent heme oxygenase (HO)-1 pathway. After a 5-cm midline laparotomy, male rats underwent hemorrhagic shock (mean blood pressure ∼40 mmHg for 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were treated with vehicle, E2 (1 mg/kg) alone, or E2 plus p38 MAPK inhibitor SB-203580 (2 mg/kg), HO-1 inhibitor chromium mesoporphyrin-IX chloride (2.5 mg/kg) or estrogen receptor antagonist ICI 182,780 (3 mg/kg). At 2 h after hemorrhagic shock and fluid resuscitation, the liver injury markers were significantly increased compared with sham-operated control. Hemorrhagic shock resulted in a significant decrease in p38 MAPK phosphorylation compared with the shams. Administration of E2 following hemorrhagic shock normalized liver p38 MAPK phosphorylation, further increased HO-1 expression, and reduced cleaved caspase-3 levels. Coadministration of SB-203580 abolished the E2-mediated attenuation of the shock-induced liver injury markers. In addition, administration of chromium mesoporphyrin-IX chloride or ICI 182,780 abolished E2-mediated increases in liver HO-1 expression or p38 MAPK activation following hemorrhagic shock. Our results collectively suggest that the salutary effects of E2 on hepatic injury following hemorrhagic shock and resuscitation are in part mediated through an estrogen-receptor-related p38 MAPK-dependent HO-1 upregulation.

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Role of Akt/HO-1 pathway in estrogen-mediated attenuation of trauma-hemorrhage-induced lung injury

Cited by 19 publications

References 46 publications

Tissue heme oxygenase-1 exerts anti-inflammatory effects on LPS-induced pulmonary inflammation

Tissue heme oxygenase-1 exerts anti-inflammatory effects on LPS-induced pulmonary inflammation

Correlation between genetic polymorphisms within the MAPK1/HIF‐1/HO‐1 signaling pathway and risk or prognosis of perimenopausal coronary artery disease

Role of p38 MAPK pathway in 17β-estradiol-mediated attenuation of hemorrhagic shock-induced hepatic injury

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