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6. Epithelial Interleukin-25 Is a Key Mediator in Th2-High, Corticosteroid-Responsive Asthma

Author

Cheng, Dan, Xue, Zheng, Yi, Lingling, Shi, Huimin, Zhang, Kan, Huo, Xiaorong, Bonser, Luke R, Zhao, Jianping, Xu, Yongjian, Erle, David J, and Zhen, Guohua

Subjects
Lung, Clinical Research, Asthma, 2.1 Biological and endogenous factors, Aetiology, Respiratory, Adrenal Cortex Hormones, Adult, Anti-Asthmatic Agents, Cytokines, Epithelial Cells, Female, Humans, Interleukin-17, Interleukin-33, Interleukins, Male, Middle Aged, Th2 Cells, IL-25, asthma, phenotype, Thymic Stromal Lymphopoietin, Medical and Health Sciences, Respiratory System
Abstract

RationaleActivation of type 2 cytokine pathways plays a central role in a large subset of subjects with asthma. Th2-high and Th2-low asthma have distinct clinical, pathologic, and molecular phenotypes and respond differently to therapy. The factors that initiate type 2 responses in some subjects with asthma are unknown.ObjectivesTo determine whether expression of epithelial cytokines IL-25, IL-33, and thymic stromal lymphopoietin are associated with type 2 responses and predict response to inhaled corticosteroid (ICS) in asthma.MethodsWe analyzed pulmonary function tests, blood, and bronchoscopic biopsies from 21 healthy control subjects and 43 subjects with asthma. Subjects with asthma underwent an 8-week treatment with inhaled budesonide.Measurements and main resultsEpithelial expression of IL-25, but not IL-33 or thymic stromal lymphopoietin, was increased in a subset of subjects with asthma. The IL-25-high subset had greater airway hyperresponsiveness, more airway and blood eosinophils, higher serum IgE, more subepithelial thickening, and higher expression of Th2 signature genes. ICS improved FEV1 and hyperresponsiveness in the IL-25-high but not the IL-25-low subset. Plasma IL-25 levels correlated with epithelial IL-25 expression, airway eosinophilia, and beneficial responses to ICS treatment.ConclusionsIL-25 measurements identify two subsets of subjects with distinct asthma phenotypes and different responses to ICS. Because IL-25 has a major role in triggering type 2 responses, bronchial epithelial IL-25 expression is likely a key determinant of type 2 response activation in asthma. Plasma IL-25 level reflects airway IL-25/type 2 response activation and may be useful for predicting responses to asthma therapy.

Published
2014

8. The value of metagenomic next-generation sequencing for the diagnosis of pulmonary tuberculosis using bronchoalveolar lavage fluid.

Author

Gao, Jiali, Zhao, Lu, Chen, Gongqi, Huang, Chunli, Kong, Weiqiang, Feng, Yuchen, and Zhen, Guohua

Subjects
TUBERCULOSIS microbiology, TUBERCULOSIS diagnosis, HOSPITALS, SEQUENCE analysis, BRONCHOALVEOLAR lavage, STAINS & staining (Microscopy), CONFIDENCE intervals, MICROBIAL genetics, RETROSPECTIVE studies, ACQUISITION of data, COMPARATIVE studies, MYCOBACTERIUM tuberculosis, DESCRIPTIVE statistics, MEDICAL records, RESEARCH funding, GENOMICS, SENSITIVITY & specificity (Statistics), RECEIVER operating characteristic curves, DATA analysis software, DATA analysis, MICROBIAL sensitivity tests, EVALUATION
Abstract

Objective The aim of this study was to compare metagenomic next-generation sequencing (mNGS) with other methods, including Xpert MTB/RIF, Mycobacterium tuberculosis (MTB) culture, and acid-fast bacillus (AFB) staining in the diagnosis of pulmonary tuberculosis (PTB) using bronchoalveolar lavage fluid (BALF). Methods The data of 186 patients with suspected PTB were retrospectively collected from January 2020 to May 2021 at Tongji Hospital. BALF samples were collected from all patients and analyzed using AFB staining, MTB culture, Xpert MTB/RIF, and mNGS. Results Of the 186 patients, 38 patients were ultimately diagnosed as PTB. Metagenomic next-generation sequencing exhibited a sensitivity of 78.95%, which was higher than AFB staining (27.59%) and MTB culture (44.12%) but similar to Xpert MTB/RIF (72.73%). Utilization of combined methods demonstrates improvement for PTB diagnosis. In support of this, the area under the receiver operating characteristic curve for the combination of mNGS and MTB culture (0.933, 95% CI: 0.871, 0.995) was larger than those of mNGS, Xpert MTB/RIF, MTB culture, and the combination of Xpert MTB/RIF and MTB culture. Conclusion The sensitivity of mNGS in the diagnosis of PTB using BALF specimen is similar to Xpert MTB/RIF. Metagenomic next-generation sequencing in combination with MTB culture may further improve the diagnosis of pulmonary tuberculosis. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Prevalence, Risk Factor and Clinical Characteristics of Venous Thrombus Embolism in Patients with Acute Exacerbation of COPD: A Prospective Multicenter Study

Author

Liu,Xia, Jiao,Xiaojing, Gong,Xiaowei, Nie,Qingrong, Li,Yang, Zhen,Guohua, Cheng,Mengyu, He,Jianguo, Yuan,Yadong, Yang,Yuanhua, Liu,Xia, Jiao,Xiaojing, Gong,Xiaowei, Nie,Qingrong, Li,Yang, Zhen,Guohua, Cheng,Mengyu, He,Jianguo, Yuan,Yadong, and Yang,Yuanhua

Abstract

Xia Liu,1,2,* Xiaojing Jiao,1,* Xiaowei Gong,3 Qingrong Nie,4 Yang Li,2 Guohua Zhen,5 Mengyu Cheng,6 Jianguo He,7 Yadong Yuan,3 Yuanhua Yang1 1Department of Respiratory and Critical Care Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of Respiratory and Critical Care Medicine, Capital Medical University Daxing Teaching Hospital, Capital Medical University, Beijing, People’s Republic of China; 3Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China; 4Department of Respiratory and Critical Care Medicine, Beijing Fangshan District Liangxiang Hospital, Beijing, People’s Republic of China; 5Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 6Department of Respiratory and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, People’s Republic of China; 7Department of Cardiovascular Medicine, Fuwai Hospital, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yuanhua Yang, Department of Respiratory and Critical Care Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, People’s Republic of China, Email yyh1031@sina.com Yadong Yuan, The Second Hospital of Hebei Medical University, Hebei, 050004, People’s Republic of China, Email yyd1108@163.comBackground and Objective: The prevalence of venous thrombus embolism (VTE) in patients with chronic obstructive pulmonary disease (COPD) is higher than in patients without COPD. Owing to the similarity of clinical symptoms between PE and acute exacerbation COPD (AECOPD), PE is likely to be overloo

Published
2023

13. Additional file 1 of Epithelial microRNA-30a-3p targets RUNX2/HMGB1 axis to suppress airway eosinophilic inflammation in asthma

Author

Wu, Wenliang, Gao, Jiali, Chen, Dian, Chen, Gongqi, Feng, Yuchen, Chang, Chenli, Chen, Shengchong, Yi, Lingling, and Zhen, Guohua

Subjects
respiratory system
Abstract

Additional file 1: Table S1. Primers for quantitative PCR. Table S2. Candidate targets of miR-30a-3p predicted by online algorithms miRanda and TargetScan. Figure S1. Inhibition of miR-30a-3p enhances the expression of HMGB1. Figure S2. Mmu-miR-30a-3p agomir is sufficient to abrogate the decrease of the expression of mmu-miR-30a-3p in OVA-challenge mice. Figure S3. Mmu-miR-30a-3p overexpression did not affect Ccl11 and Ccl24 expression in mouse lung tissue. Figure S4. Mmu-miR-30a-3p overexpression decreased the mucus production in OVA sensitized and challenged mice. Figure S5. The expression of miR-30a-3p, RUNX2, HMGB1, and the correlation between miR-30a-3p and airway eosinophilia in 16 asthma patients randomly selected from the cohort of 51 asthma patients.

Published
2022
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22. Intelectin is required for IL-13-induced monocyte chemotactic protein-1 and -3 expression in lung epithelial cells and promotes allergic airway inflammation

Author

Gu, Naibing, Kang, Guannan, Jin, Chang'E, Xu, Yongjian, Zhang, Zhenxiang, Erle, David J., and Zhen, Guohua

Subjects
Asthma -- Risk factors, Asthma -- Research, Cellular proteins -- Health aspects, Cellular proteins -- Research, Epithelial cells -- Physiological aspects, Epithelial cells -- Research, Interleukin-13 -- Health aspects, Interleukin-13 -- Research, Biological sciences
Abstract

Asthma is characterized by airway inflammation, mucus overproduction, airway hyperreactivity, and peribronchial fibrosis. Intelectin has been shown to be increased in airway epithelium of asthmatics. However, the role of intelectin in the pathogenesis of asthma is unknown. Airway epithelial cells can secrete chemokines such as monocyte chemotactic protein (MCP)-1 and -3 that play crucial roles in asthmatic airway inflammation. We hypothesized that intelectin plays a role in allergic airway inflammation by regulating chemokine expression. In a mouse allergic asthma model, we found that mRNA expression of intelectin-2 as well as MCP-1 and -3 in mouse lung was increased very early (within 2 h) after allergen challenge. Expression of intelectin protein was localized to mucous cells in airway epithelium. Treatment of MLE12 mouse lung epithelial cells with interleukin IL-13, a critical mediator of allergic airway disease, induced expression of intelectin-1 and -2 as well as MCP-1 and -3. When IL-13-induced intelectin-1 and -2 expression was inhibited by RNA interference, IL-13-induced extracellular signal-regulated kinase 1/2 phosphorylation and MCP-1 and -3 production by MLE12 cells was inhibited. Furthermore, inhibition of intelectin expression by airway transfection with shRNA targeting intelectin-1 and -2 attenuated allergen-induced airway inflammation. We conclude that intelectin, a molecule expressed by airway epithelial cells and upregulated in asthma, is required for IL-13-induced MCP-1 and -3 production in mouse lung epithelial cells and contributes to allergic airway inflammation. lectin; chemokine; asthma doi:10.1152/ajplung.90612.2008.

Published
2010

24. Defective STING expression potentiates IL-13 signaling in epithelial cells in eosinophilic chronic rhinosinusitis with nasal polyps

Author

Wang, Hai, primary, Hu, Dan-Qing, additional, Xiao, Qiao, additional, Liu, Yi-Bo, additional, Song, Jia, additional, Liang, Yuxia, additional, Ruan, Jian-Wen, additional, Wang, Zhe-Zheng, additional, Li, Jing-Xian, additional, Pan, Li, additional, Wang, Meng-Chen, additional, Zeng, Ming, additional, Shi, Li-Li, additional, Xu, Kai, additional, Ning, Qin, additional, Zhen, Guohua, additional, Yu, Di, additional, Wang, De-Yun, additional, Wenzel, Sally E., additional, and Liu, Zheng, additional

Published
2021
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27. ATP6V0d2 Suppresses Alveoli Macrophage Alternative Polarization and Allergic Asthma via Degradation of PU.1

Author

Liu, Na, primary, Feng, Yuchen, additional, Liu, Huicheng, additional, Wu, Wenliang, additional, Liang, Yuxia, additional, Li, Pingfei, additional, Wei, Zhengping, additional, Wu, Min, additional, Tang, Zhao-Hui, additional, Han, Junyan, additional, Cheng, Xiang, additional, Liu, Zheng, additional, Laurence, Arian, additional, Li, Huabin, additional, Zhen, Guohua, additional, and Yang, Xiang-Ping, additional

Published
2021
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38. Decreased eosinophil counts and elevated lactate dehydrogenase predict severe COVID-19 in patients with underlying chronic airway diseases

Author

Chen, Dian, Zhang, Shuchen, Feng, Yuchen, Wu, Wenliang, Chang, Chenli, Chen, Shengchong, Zhen, Guohua, and Yi, Lingling

Abstract

BackgroundSeveral predictors of COVID-19 severity have been reported. However, chronic airway inflammation characterised by accumulated lymphocytes or eosinophils may affect the pathogenesis of COVID-19.MethodsIn this retrospective cohort study, we reviewed the medical records of all patients with laboratory-confirmed COVID-19 with chronic bronchitis, chronic obstructive pulmonary disease (COPD) and asthma admitted to the Sino-French New City Branch of Tongji Hospital, a large regional hospital in Wuhan, China, from 26 January to 3 April. The Tongji Hospital Ethics Committee approved this study.ResultsThere were 59 patients with chronic bronchitis, COPD and asthma. When compared with non-severe patients, severe patients were more likely to have decreased lymphocyte counts (0.6×10/L vs 1.1×10/L, p<0.001), eosinopaenia (<0.02×10/L; 73% vs 24%, p<0.001), increased lactate dehydrogenase (LDH) (471.0 U/L vs 230.0 U/L, p<0.001) and elevated interleukin 6 level (47.4 pg/mL vs 5.7 pg/mL, p=0.002) on admission. Eosinopaenia and elevated LDH were significantly associated with disease severity in both univariate and multivariate regression models including the above variables. Moreover, eosinophil count and LDH level tended to return to normal range over time in both groups after treatment and severe patients recovered slower than non-severe patients, especially in eosinophil count.ConclusionsEosinopaenia and elevated LDH are potential predictors of disease severity in patients with COVID-19 with underlying chronic airway diseases. In addition, they could indicate disease progression and treatment effectiveness.

Published
2022
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39. microRNA‐218‐5p plays a protective role in eosinophilic airway inflammation via targeting δ‐catenin, a novel catenin in asthma.

Author

Liang, Yuxia, Feng, Yuchen, Wu, Wenliang, Chang, Chenli, Chen, Dian, Chen, Shengchong, and Zhen, Guohua

Subjects
ASTHMA, INFLAMMATION, ASTHMATICS, CELL culture, EOSINOPHILIA
Abstract

Background: microRNA (miR)‐218‐5p is involved in cigarette smoke‐induced airway inflammation. In our earlier asthma epithelial miRNA profiling data, miR‐218‐5p was the top 2 down‐regulated miRNA. We hypothesize that miR‐218‐5p plays a role in asthma airway inflammation. Objective: To unveil the role of miR‐218‐5p and its target gene in asthma airway inflammation. Methods: We measured miR‐218‐5p expression in bronchial brushings of asthma patients (n = 50) and healthy controls (n = 15), and analysed the correlations between miR‐218‐5p expression and airway eosinophilia. We examined whether CTNND2 was a target of miR‐218‐5p, and the expression of 12 catenin family members in bronchial brushings, in cultured human bronchial epithelial (HBE) cells and BEAS‐2B cells. We explored the role of miR‐218‐5p‐CTNND2 pathway using a murine model of allergic airway inflammation. Results: Epithelial miR‐218‐5p expression was significantly decreased and negatively correlated with eosinophils in induced sputum and bronchial biopsies, and other type 2 biomarkers in asthma patients. We verified that CTNND2 (encoding δ‐catenin) was a target of miR‐218‐5p. Remarkably, CTNND2 was the most significantly up‐regulated catenin compared with the other 11 catenin family members in bronchial brushings of asthma patients, IL‐13‐stimulated HBE and BEAS‐2B cells. Moreover, epithelial CTNND2 expression positively correlated with airway eosinophilia in asthma. Airway mmu‐miR‐218‐5p expression was also decreased, and Ctnnd2 expression was increased in a murine model of allergic airway inflammation. Intriguingly, mmu‐miR‐218‐5p overexpression suppressed airway hyperresponsiveness, eosinophilic airway inflammation and Ctnnd2 up‐regulation in the mouse model. Finally, perturbation of miR‐218‐5p or CTNND2 expression significantly altered chemokine CCL26 expression in the cell cultures and the mouse model. Conclusions and Clinical Relevance: Epithelial miR‐218‐5p plays a protective role in eosinophilic airway inflammation via targeting CTNND2, a novel catenin in asthma, and suppressing chemokine CCL26 expression. [ABSTRACT FROM AUTHOR]

Published
2020
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41. Association between ORMDL3 polymorphism and susceptibility to asthma: a meta-analysis

Author

Shi, Huimin, Cheng, Dan, Yi, Lingling, Huo, Xiaorong, Zhang, Kan, and Zhen, Guohua

Subjects
Original Article
Abstract

The aim of this study was to determine whether orosomucoid1- like 3 (ORMDL3) single nucleotide polymorphisms rs7216389, rs11650680, rs12603332 are associated with susceptibility to asthma. We performed a meta-analysis by searching PubMed, EMBASE, Elsevier and Wanfang Databases. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the strength of associations. We examined the association between the three SNPs and asthma risk in four genetic models (TT + TC vs. CC, TC vs. CC, TT vs. CC, TT vs. TC + CC). Thirteen published case-control studies involving 6462 cases and 7357 controls were included. Our meta-analysis indicated that rs7216389 was significantly associated with increased asthma risk in overall population. Subgroup analysis by age indicated significant association between the rs7216389 and asthma in children. Moreover, ORMDL3 rs11650680 was significantly associated with decreased asthma risk in dominant model (TT + TC vs. CC), and rs12603332 was significantly associated with decreased asthma risk in 3 models (TT + TC vs. CC, TC vs. CC and TT vs. CC). To Conclude, ORMDL3 rs7216389 polymorphism is associated with susceptibility to asthma. Children with variant T allele (TT or TC) and adults with TT homozygote in rs7216389 are at high risks to suffer from asthma. However, people with T allele in rs11650680 or rs12603332 are protected from asthma.

Published
2015

42. Association between angiotensin I-converting enzyme gene polymorphism and susceptibility to cancer: a meta analysis

Author

Zhang, Kan, Cheng, Dan, Yi, Lingling, Shi, Huimin, and Zhen, Guohua

Subjects
Chi-Square Distribution, Polymorphism, Genetic, Peptidyl-Dipeptidase A, Risk Assessment, White People, Phenotype, Gene Frequency, Risk Factors, Case-Control Studies, Neoplasms, Odds Ratio, Humans, Original Article, Genetic Predisposition to Disease
Abstract

Background: Angiotensin I-converting enzyme (ACE) gene plays an important role in the pathogenesis of cancers. The association between ACE insertion/deletion (I/D) polymorphism and the risk of various cancers has been studied. However, the results of these studies remain conflicting. Therefore, we performed a meta-analysis to evaluate the association between ACE I/D polymorphism and the risk of cancers. Methods: PubMed, Embase, ScienceDirect, Springer, CNKI, Wanfang, Weipu, CBM databases and Google Scholar were searched for case-control studies on ACE I/D polymorphism and the risk of cancers, published up to Dec 31, 2013. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association between ACE I/D polymorphism and cancer risk. Results: Thirty-five published studies with 5007 cases and 8173 controls were included. Overall, there were no significant association between ACE I/D polymorphism and the risk of cancers (II vs. ID+DD OR = 1.05, 95% CI = 0.89-1.23, I vs. D OR = 1.00, 95% CI = 0.89-1.13). However, when stratified by ethnicity, we found a significant association between this polymorphism and cancer risk in Caucasians (II vs. ID+DD: OR = 1.43, 95% CI = 1.02-2.00, I vs. D: OR = 1.23, 95% CI 1.01-1.49). Conclusion: ACE I/D polymorphism is associated with the cancer risk in Caucasians.

Published
2014

43. Pulmonary epithelioid hemangioendothelioma coexisting with pulmonary nodular amyloidosis: case discussion and review of the literature

Author

Yi, Lingling, Cheng, Dan, Shi, Huimin, Zhang, Kan, Liao, Yongde, Ao, Qilin, and Zhen, Guohua

Subjects
Case Report
Abstract

A 38-year-old female was found to have multiple bilateral lung nodules in a routine chest X-ray examination. Thoracoscopy was performed with biopsy of three nodules from the right lower lobe and Congo red staining showed typical amyloid pattern. Initial diagnosis of pulmonary nodular amyloidosis was made. However, one nodule in the right upper lobe enlarged as detected by follow-up CT scan. The patient underwent F-18 fluorodeoxyglucose positron emission tomography (18F-FDG-PET)/CT and a significant high FDG uptake in the largest nodule in right upper lobe was observed while the uptake was normal or mildly increased in the other nodules. Meanwhile, right hilar and mediastinal lymph nodes adenopathy was noted. Right upper lobe was resected by thoracotomy. Surprisingly, histopathological findings showed pulmonary epithelioid hemangioendothelioma (PEH) with metastasis of hilar and mediastinal lymph nodes. To our knowledge, this is the first described case of PEH coexisting with pulmonary nodular amyloidosis.

Published
2014

46. Expression of heme oxygenase-1 in the peripheral blood mononuclear cells from asthmatic patients

Author

Liu Xian-sheng, Mo Biwen, Zhang Zhenxiang, Xiong Weining, XU Yong-jian, and Zhen Guohua

Subjects
Adult, Male, medicine.medical_specialty, Biomedical Engineering, Biochemistry, Peripheral blood mononuclear cell, Biomaterials, Pathogenesis, chemistry.chemical_compound, Internal medicine, Genetics, medicine, Asthmatic patient, Humans, RNA, Messenger, Heme, Earth-Surface Processes, Asthma, Messenger RNA, Carbon Monoxide, business.industry, Immunoglobulin E, Middle Aged, medicine.disease, Heme oxygenase, Endocrinology, chemistry, Immunology, Leukocytes, Mononuclear, Immunohistochemistry, Female, business, Heme Oxygenase-1
Abstract

To explore the expression of heme oxygenase-1 (HO-1) in the peripheral blood mononuclear cells (PBMCs) and its relationship with pulmonary ventilation function in asthmatic patients, 18 asthmatic patients and 18 healthy subjects were selected. HO-1 protein and mRNA levels in PBMCs were measured by immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Blood carbon monoxide Hb (COHb), serum total IgE and pulmonary ventilatory function were observed. Our results showed that the percentage of cells positive for immunohistochemical staining of HO-1 were significantly higher in asthmatic patients (41.72 +/- 7.44) % than that in with healthy subjects (10.45 +/- 4.36) % (P0.001) and the optical density of PBMC HO-1 mRNA was higher in asthmatic patients (26.05 +/- 4.14) than that in healthy subjects (10. 82 +/- 4.26) (P0.001). The relation analysis showed that PBMC HO-1 protein and mRNA levels had significantly negative relation with FEV1%, PEFR, MEFR50%, respectively (r = -0.51-0.89, P0.05-0.001, respectively) and a positive relation with COHb and serum total IgE (r = 0.48-0. 85, 0.05-0.001, respectively). It is concluded that the expression of PBMC HO-1 protein and mRNA increased significantly in asthmatic patients, and HO-1 may play a significant role in the pathogenesis of asthma. The expression of HO-1 may bear a relation with severity of asthma.

Published
2005

47. The role of endogenous carbon monoxide in the hypoxic vascular remodeling of rat model of hypoxic pulmonary hypertension

Author

Zhang Zhenxiang, XU Yong-jian, and Zhen Guohua

Subjects
medicine.medical_specialty, Hypertension, Pulmonary, Myocytes, Smooth Muscle, Biomedical Engineering, Endogeny, Pulmonary Artery, Biochemistry, Biomaterials, chemistry.chemical_compound, Internal medicine, Genetics, Medicine, Animals, RNA, Messenger, Hypoxia, Lung, Earth-Surface Processes, Carbon Monoxide, business.industry, Hypoxia (medical), medicine.disease, Pulmonary hypertension, Rats, Heme oxygenase, medicine.anatomical_structure, Endocrinology, chemistry, Heme Oxygenase (Decyclizing), Ventricular pressure, Cardiology, Arterial blood, medicine.symptom, business, Heme Oxygenase-1, Hemin
Abstract

We investigated the expression of heme oxygenase-1 (HO-1) gene and production of endogenous carbon monoxide (CO) in the rat lung tissue at different time points of chronic hypoxic pulmonary hypertension and the effect of hemin on the expression of HO-1 gene and pulmonary hypertension. A rat model of hypoxic pulmonary hypertension was recreated by exposure to intermittent normobaric hypoxic environment (10% O2). Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to determine the level of HO-1 mRNA in the rat lung tissue and double wave length spectrophotometry was used to evaluate the quantity of COHb in arterial blood. Cardiac catheterization was employed to measure the right ventricular systolic pressure (RVSP) and HE staining was performed in dissected lung tissue to observe the pathological changes of the intra-acinar pulmonary arteries (IAPA). It was found that (1) There was a low level of HO-1 mRNA in normal rat lung tissue, but the level of HO-1 mRNA increased by 2–4 times in the lung tissue of hypoxic rats (P

Published
2004

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