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hypoxia inducible factor-1α mediates protective effects of ischemic preconditioning on ECV-304 endothelial cells

World Journal of Gastroenterology 2007年第16期13卷 2369-2373页

作者： Liu-Bin Shi Jian-Hua Huang Bao-San Han Department of Organ Transplantation Huashan Hospital Fudan University Shanghai 200040 China Institute of Integrative Medicine Huashan Hospital Fudan University Shanghai 200040 China Department of General Surgery Ruijin Hospital School of Medicine Shanghai Jiaotong University Shanghai 200025 China

AIM: To investigate whether hypoxia inducible factor-1α (HIF-1α) is linked to the protective effects of ischemic preconditioning (IP) on sinusoidal endothelial cells against ischemia/reperfusion injury. METHODS: Sinusoidal endothelial cell lines ECV-304 were cultured and divided into four groups: control group, cells were cultured in complete DMEM medium; cold anoxia/warm reoxygenation (A/R) group, cells were preserved in a 4℃ UW solution in a mixture of 95% N2 and 5% CO2 for 24 h; anoxia-preconditioning (APC) group, cells were treated with 4 cycles of short anoxia and reoxygenation before prolonged anoxia- preconditioning treatment; and anoxia-preconditioning and hypoxia inducible factor-1α (HIF-1α) inhibitor (I-HIF-1) group, cells were pretreated with 5 μm of HIF-1α inhibitor NS398 in DMEM medium before subjected to the same treatment as group APC. After the anoxia treatment, each group was reoxygenated in a mixture of 95% air and 5% CO2 incubator for 6 h. Cytoprotections were evaluated by cell viabilities from Trypan blue, lactate dehydrogenase (LDH) release rates, and intracellular cell adhesion molecule-1 (ICAM-1) expressions. Expressions of HIF-1α mRNA and HIF-1α protein from each group were determined by the RT-PCR method and Western blotting, respectively. RESULTS: Ischemia preconditioning increased cell viability, and reduced LDH release and ICAM-1 expressions. Ischemia preconditioning also upregulated the HIF-1α mRNA level and HIF-1α protein expression. However, all of these changes were reversed by HIF-1α inhibitor ***: Ischemia preconditioning effectively inhibited cold hypoxia/warm reoxygenation injury to endothelial cells, and the authors showed for the first time HIF-1α is causally linked to the protective effects of ischemic preconditioning on endothelial cells.

关键词： Preconditioning Anoxia/reoxygenation injury Reperfusion injury Endothelial cells hypoxia inducible factor-1α

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hypoxia inducible factor-1α related mechanism and TCM intervention in process of early fracture healing

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Chinese Herbal Medicines 2024年第1期16卷 56-69页

作者： Wenxian Zhang Fusen Yang Qikai Yan Jiahui Li Xiaogang Zhang Yiwei Jiang Jianye Dai Affiliated Hospital of Gansu University of Traditional Chinese Medicine Lanzhou 730000China School of Pharmacy Lanzhou UniversityLanzhou 730000China Xi’an Hospital of Traditional Chinese Medicine Xi’an 710021China

As a common clinical disease, fracture is often accompanied by pain, swelling, bleeding as well as other symptoms and has a high disability rate, even threatening life, seriously endangering patients’ physical and psychological health and quality of life. Medical practitioners take many strategies for the treatment of fracture healing, including Traditional Chinese Medicine(TCM). In the early stage of fracture healing,the local fracture is often in a state of hypoxia, accompanied by the expression of hypoxia inducible factor-1α(HIF-1α), which is beneficial to wound healing. Through literature mining, we thought that hypoxia, HIF-1α and downstream factors affected the mechanism of fracture healing, as well as dominated this process. Therefore, we reviewed the local characteristics and related signaling pathways involved in the fracture healing process and summarized the intervention of TCM on these mechanisms,in order to inspirit the new strategy for fracture healing, as well as elaborate on the possible principles of TCM in treating fractures based on the HIF molecular mechanism.

关键词： fracture healing hypoxia hypoxia inducible factor-1α traditional chinese medicine molecular mechanism

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hypoxia inducible factor-1αaccumulation in steatotic liver preservation:Role of nitric oxide

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World Journal of Gastroenterology 2010年第28期16卷 3499-3509页

作者： Mohamed Amine Zaouali Ismail Ben Mosbah Eleonora Boncompagni Hassen Ben Abdennebi Maria Teresa Mitjavila Ramon Bartrons Isabel Freitas Antoni Rimola Joan Roselló-Catafau Experimental Hepatic Ischemia Reperfusion Unit Institut of Biomedical Research of BarcelonaSpanish National Research Council08036BarcelonaSpain Liver Transplantation and Graft Viability Unit August Pi i Sunyer Biomedical Research Institut08036Barcelona Spain Animal Biology Department Pavia University27100PaviaItaly Laboratory of Human Physiology Faculty of PharmacyUniversity of Monastir5000Monastir Tunisia Department of Physiology Faculty of BiologyUniversity of Barcelona08028BarcelonaSpain Physiological Sciences Department Bellvitge CampusInstitut of Biomedical Research of Bellvitge-Barcelona University08907BarcelonaSpain

AIM:To examine the relevance of hypoxia inducible factor(HIF-1)and nitric oxide(NO)on the preservation of fatty liver against cold ischemia-reperfusion injury(IRI). METHODS:We used an isolated perfused rat liver model and we evaluated HIF-1αin steatotic and non-steatotic livers preserved for 24 h at 4℃in University of Wisconsin and IGL-1 solutions,and then subjected to 2 h of normothermic *** normoxic reperfusion,liver enzymes,bile production,bromosulfophthalein clearance,as well as HIF-1αand NO[endothelial NO synthase(eNOS)activity and nitrites/nitrates]were also *** factors associated with the higher susceptibility of steatotic livers to IRI,such as mitochondrial damage and vascular resistance were evaluated. RESULTS:A significant increase in HIF-1αwas found in steatotic and non-steatotic livers preserved in IGL-1 after cold *** preserved in IGL-1 showed a significant attenuation of liver injury and improvement in liver function *** benefits were enhanced by the addition of trimetazidine(an antiischemic drug),which induces NO and eNOS activation, to IGL-1 *** normoxic reperfusion,the presence of NO favors HIF-1αaccumulation,promoting also the activation of other cytoprotective genes,such as hemeoxygenase-1. CONCLUSION:We found evidence for the role of the HIF-1α/NO system in fatty liver preservation,especially when IGL-1 solution is used.

关键词： Fatty liver Tissue preservation hypoxia inducible factor-1α IGL-1 Nitric oxide Trimetazidine

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Sirolimus increases the anti-cancer effect of Huai Er by regulating hypoxia inducible factor-1α-mediated glycolysis in hepatocellular carcinoma

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World Journal of Gastroenterology 2022年第32期28卷 4600-4619页

作者： Lin Zhou Yang Zhao Li-Chao Pan Jing Wang Xian-Jie Shi Guo-Sheng Du Qiang He Department of Hepatobiliary and Pancreaticosplenic Surgery Beijing ChaoYang HospitalCapital Medical UniversityBeijing 100020China Faculty of Hepato-Pancreato-Biliary Surgery Chinese PLA General HospitalBeijing 100853China

BACKGROUND Glycolysis caused by hypoxia-induced abnormal activation of hypoxia inducible factor-1α(HIF-1α)in the immune microenvironment promotes the progression of hepatocellular carcinoma(HCC),leading to enhanced drug resistance in cancer ***,altering the immunosuppressive microenvironment by improving the hypoxic state is a new goal in improving cancer *** To analyse the role of HIF-1α,which is closely related to tumour proliferation,invasion,metastasis,and angiogenesis,in the proliferation and invasion of liver cancer,and to explore the HIF-1αpathway-mediated anti-cancer mechanism of sirolimus(SRL)combined with Huai *** Previous studies on HCC tissues identified the importance of HIF-1α,glucose transporter 1(GLUT1),and lactate dehydrogenase A(LDHA)*** this study,HepG2 and Huh7 cell lines were treated,under hypoxic and normoxic conditions,with a combination of SRL and Huai *** effects on proliferation,invasion,cell cycle,and apoptosis were *** and genomics techniques were used to analyze the HIF-1α-related signalling pathway during SRL combined with Huai Er treatment and its inhibition of the proliferation of HCC *** High levels of HIF-1α,LDHA,and GLUT-1 were found in poorly differentiated HCC,with lower patient survival *** promoted the proliferation of HepG2 and Huh7 cells and weakened the apoptosis and cell cycle blocking effects of the SRL/Huai Er *** was achieved by activation of HIF-1αand glycolysis in HCC,leading to the upregulation of LDHA,GLUT-1,Akt/mammalian target of rapamycin(mTOR),vascular endothelial growth factor(VEGF),and Forkhead box P3 and downregulation of phosphatase and tensin homolog deleted on chromosome ten(PTEN)and *** hypoxia-induced activation of HIF-1αshowed the greatest attenuation in the SRL/Huai Er(S50+H8)group compared to the drug treatments alone(P<0.001).The S50+H8 treatment significantly downregulated the expression of mTOR and HIF-1α,an

关键词： Hepatocellular carcinoma Sirolimus Huai Er Warburg effect hypoxia inducible factor-1α

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Expression and Implication of hypoxia inducible factor-1α in Prostate Neoplasm

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第6期24卷 593-595页

作者：平浩陈晓春耿怀振谷龙杰陈江鲁功成 Department of Urology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 China Department of Urology Heze Municipal Hospital Shandong 274031 China

Summary: To study the expression of hypoxia inducible factor-1α (HIF-1α) protein in prostate cancer (Pca) and its biological significance, the expression of HIF-1α was assayed by means of immunohistochemical technique in 42 prostate cancer, 12 prostatic intraepithelial neoplasm (PIN) and 9 normal prostate tissue (NP) specimens. Western blot was used to examine the expression of HIF-1α in prostate cancer cell line (PC-3M) induced by different oxygen tension. HIF-1α expression was positive in 33 Pca and 9 PIN specimens, and the positive rate of HIF-1α was higher in distant metastasis patients than in patients without metastasis of prostate cancer (P1α in NP. The level of HIF-1α in PC-3M significantly increased with the decrease of oxygen tension (P1). Overexpression of HIF-1α is the preliminary event of the formation of Pca, which may induce carcinoma into malignant phenotype. Thus it may serve as an early diagnosis marker and the novel target for Pca treatment.

关键词： prostatic neoplasms carcinoma hypoxia inducible factor-1α

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Expression of Nerve Growth factor and hypoxia inducible factor-1α and Its Correlation with Angiogenesis in Non-Small Cell Lung Cancer

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2014年第3期34卷 359-362页

作者：逯青丽刘建朱晓莉徐文佳 Department of Geriatrics Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Department of Internal Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology

Summary： In order to investigate the expression of nerve growth factor （NGF） and hypoxia inducible factor-1α （HIF-1α） and its correlation with angiogenesis in non-small cell lung cancer （NSCLC）, paraffin-embedded tissue blocks from 20 patients with NSCLC were examined. Twenty corresponding para-cancerous lung tissue specimens were obtained to serve as a control. The expression of NGF, HIF-1α, and vascular endothelial growth factor （VEGF） in the NSCLC tissues was detected by using immunohistochemistry. The microvascular density （MVD） was determined by CD31 staining. The resuits showed that the expression levels ofNGF, HIF-1α and VEGF in the NSCLC tissues were remarkably higher than those in the para-cancerous lung tissues （P〈0.05）. There was significant difference in the MVD between the NSCLC tissues （9.19±1.43） and para-cancerous lung tissues （2.23±1.19）（P〈0.05）. There were positive correlations between NGF and VEGF, between HIF-1α and VEGF, and between NGF and HIF-1α in NSCLC tissues, with the spearman correlation coefficient being 0.588, 0.519 and 0.588, respectively. In NSCLC tissues, the MVD had a positive correlation with the three factors （P〈0.05）. Theses results suggest that NGF and HIF-1α are synergically involved in the angiogenesis of NSCLC.

关键词： non-small cell lung cancer immunohistochemistry nerve growth factor hypoxia inducible factor-1α vascular endothelial growth factor CD31 microvascular density

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hypoxia Induces Transforming Growth factor-β1 Gene Expression in the Pulmonary Artery of Rats via hypoxia-inducible factor-1α

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Acta Biochimica et Biophysica Sinica 2007年第1期39卷 73-80页

作者： Yongliang JIANG Aiguo DAI Qifang LI and Ruicheng HU Depoptment of Respiratory Medicine,Hunan Institute of Gerontology,Hunan Province Geriatric Hospital,Changsha 410001,China Department of Respiratory Medicine Hunan Institute of Gerontology Hunan Province Geriatric HospitalChangsha 410001 China

The present study was undertaken to investigate the dynamic expression of hypoxia induciblefactor-1 α (HIF-1α) and transforming growth factor-β1 (TGF-β1) in hypoxia-induced pulmonary hypertensionof *** was found that mean pulmonary arterial pressure (mPAP) increased significantly after 7 d *** artery remodeling index and right ventricular hypertrophy became evident after 14 d ***-1α mRNA staining was less positive in the control,hypoxia for 3 d and hypoxia for 7 d,butbegan to enhance significantly after 14 d of hypoxia,then remained *** of HIF-1 α protein inthe control was less positive,but was up-regulated in pulmonary arterial tunica intima of all hypoxic ***-β1 mRNA expression in pulmonary arterial walls was increased significantly after 14 d of hypoxia, butshowed no obvious changes after 3 or 7 d of *** pulmonary tunica adventitia and tunica media,TGF-β1 protein staining was less positive in control rats,but was markedly enhanced after 3 d of hypoxia,reaching its peak after 7 d of hypoxia,and then weakening after 14 and 21 d of *** blottingshowed that HIF- 1α protein levels increased significantly after 7 d of hypoxia and then remained at a highlevel. TGF-β1 protein level was markedly enhanced after 3 d of hypoxia,reaching its peak after 7 d ofhypoxia,and then decreasing after 14 and 21 d of *** correlation analysis showed that HIF-1αmRNA, TGF-β1 mRNA, TGF-β1 protein were positively correlated with mPAP,vessel morphometry andright ventricular hypertrophy ***-β1 protein (tunica adventitia) was negatively correlated withHIF-lα *** together,our results suggest that changes in HIF-lα and TGF-β1 expression afterhypoxia play an important role in hypoxia-induced pulmonary hypertension of rats.

关键词： hypoxia inducible factor-1α transforming growth factor-β1 hypertension lung hypoxia

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hypoxia inducible factor-1alpha mediates protection of DL-3-n-butylphthalide in brain microvascular endothelial cells against oxygen glucose deprivation-induced injury

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Neural Regeneration Research 2012年第12期7卷 948-954页

作者： Weihong Yang Ling Li Ruxun Huang Zhong Pei Songjie Liao Jinsheng Zeng Department of Neurology First Affiliated Hospital of Sun Yat-Sen UniversityGuangzhou 510080Guangdong ProvinceChina

Studies have demonstrated that DL-3-n-butylphthalide can significantly alleviate oxygen glucose deprivation-induced injury of human umbilical vein endothelial cells at least partly associated with its enhancement on oxygen glucose deprivation-induced hypoxia inducible factor-1α *** this study,we hypothesized that DL-3-n-butylphthalide can protect against oxygen glucose deprivation-induced injury of newborn rat brain microvascular endothelial cells by means of upregulating hypoxia inducible factor-1α *** assay and Hoechst staining results showed that DL-3-n-butylphthalide protected brain microvascular endothelial cells against oxygen glucose deprivation-induced injury in a dose-dependent *** blot and immunofluorescent staining results further confirmed that the protective effect was related to upregulation of hypoxia inducible factor-1α.Real-time RT-PCR reaction results showed that DL-3-n-butylphthalide reduced apoptosis by inhibiting downregulation of pro-apoptotic gene caspase-3 mRNA expression and upregulation of apoptosis-executive protease bcl-2 mRNA expression;however,DL-3-n-butylphthalide had no protective effects on brain microvascular endothelial cells after knockdown of hypoxia inducible factor-1α by small interfering *** findings suggest that DL-3-n-butylphthalide can protect brain microvascular endothelial cells against oxygen glucose deprivation-induced injury by upregulating bcl-2 expression and downregulating caspase-3 expression though hypoxia inducible factor-1α pathway.

关键词： DL-3-n-butylphthalide apoptosis brain microvascular endothelial cells hypoxia inducible factor-1α

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Quantitative analysis of hepatic hypoxia-inducible factor-1α and its abnormal gene expression during the formation of hepatocellular carcinoma

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Hepatobiliary & Pancreatic Diseases International 2009年第4期8卷 407-413页

作者： Deng-Fu Yao,Hua Jiang,Min Yao,Yue-Ming Li,Wen-Jing Gu,Yu-Cheng Shen, Li-Wei Qiu,Wei Wu,Xin-Hua Wu and Wen-Li Sai Research Center of Clinical Molecular Biology,Department of Laboratory Science,and Department of Oncology,Affiliated Hospital of Nantong University,Nantong 226001, China Third Department of Medicine,Jiaonan People’s Hospital,Jiaonan 266400,China Research Center of Clinical Molecular Biology Affiliated Hospital of Nantong University Nantong 226001 China. yaodf@***

BACKGROUND:Hepatic hypoxia-inducible factor-1(HIF-1) is activated in the progression of hepatocellular carcinoma (HCC).This study aimed to investigate the dynamic alterations of HIF-1αand its gene expression so as to explore the relationship between HIF-1αexpression and hepatocarcinogenesis at the early stage of HCC. METHODS:A hepatoma model was made with 2-fluorenyl- acetamide(2-FAA)in male Sprague-Dawley *** changes of rat hepatocytes were assessed pathologically (HE staining).The dynamic expression of hepatic and circulating HIF-1αwas quantitatively analyzed by ELISA. The gene fragments of hepatic HIF-1αmRNA were amplified by RT-PCR and confirmed by *** cellular distribution of hepatic HIF-1αexpression was confirmed by immunohistochemistry. RESULTS:Histological examination confirmed granulelike degeneration to atypical hyperplasia and HCC development in rat hepatocytes and progressive increases in the levels of hepatic and circulating HIF-1αand its gene expression during the *** levels of HIF-1α expression in the liver and blood of rats with hepatoma were significantly higher than those in normal ratsand those with *** analysis confirmed the positive expression and hepatocyte distribution of HIF-1αin the development of rat hepatoma. A positive relationship was found between HIF-1α expression in the liver and blood(P<0.01). CONCLUSIONS:The above observations support the hypothesis that the overexpression of HIF-1αand its gene are closely associated with the malignant transformation of hepatocytes and play an important role at the stage of hepatocarcinogenesis.

关键词： hepatocellular carcinoma hypoxia inducible factor-1α early expression dynamic alteration

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Mechanism of piR-1245/PIWI-like protein-2 regulating Janus kinase-2/signal transducer and activator of transcription-3/vascular endothelial growth factor signaling pathway in retinal neovascularization

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Neural Regeneration Research 2023年第5期18卷 1132-1138页

作者： Yong Yu Li-Kun Xia Yu Di Qing-Zhu Nie Xiao-Long Chen Department of Ophthalmology Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina

Inhibiting retinal neovascularization is the optimal strategy for the treatment of retina-related diseases, but there is currently no effective treatment for retinal neovascularization. P-element-induced wimpy testis(PIWI)-interacting RNA(piRNA) is a type of small non-coding RNA implicated in a variety of diseases. In this study, we found that the expression of piR-1245 and the interacting protein PIWIL2 were remarkably increased in human retinal endothelial cells cultured in a hypoxic environment, and cell apoptosis, migration, tube formation and proliferation were remarkably enhanced in these cells. Knocking down piR-1245 inhibited the above phenomena. After intervention by a p-JAK2 activator, piR-1245 decreased the expression of hypoxia inducible factor-1α and vascular endothelial growth factor through the JAK2/STAT3 pathway. For in vivo analysis, 7-day-old newborn mice were raised in 75 ± 2% hyperoxia for 5 days and then piR-1245 in the retina was knocked down. In these mice, the number of newly formed vessels in the retina was decreased, the expressions of inflammationrelated proteins were reduced, the number of apoptotic cells in the retina was decreased, the JAK2/STAT3 pathway was inhibited, and the expressions of hypoxia inducible factor-1α and vascular endothelial growth factor were decreased. Injection of the JAK2 inhibitor JAK2/TYK2-IN-1 into the vitreous cavity inhibited retinal neovascularization in mice and reduced expression of hypoxia inducible factor-1α and vascular endothelial growth factor. These findings suggest that piR-1245 activates the JAK2/STAT3 pathway, regulates the expression of hypoxia inducible factor-1α and vascular endothelial growth factor, and promotes retinal neovascularization. Therefore, piR-1245 may be a new therapeutic target for retinal neovascularization.

关键词： angiogenesis human retinal endothelial cells hypoxia inducible factor-1α hypoxia interleukin-1β migration non-coding RNA oxygen-induced injury PIWI-interacting RNA retinopathy

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