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5. Endothelial Aryl Hydrocarbon Receptor Nuclear Translocator Mediates the Angiogenic Response to Peripheral Ischemia in Mice with Type 2 Diabetes Mellitus

Author

Nguyen, Tu, primary, Zheng, Mei, additional, Knapp, Maura, additional, Sladojevic, Nikola, additional, Zhang, Qin, additional, Ai, Lizhuo, additional, Harrison, Devin, additional, Chen, Anna, additional, Sitikov, Albert, additional, Shen, Le, additional, Gonzalez, Frank J, additional, Zhao, Qiong, additional, Fang, Yun, additional, Liao, James JK, additional, and Wu, Rongxue, additional

Published
2022
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7. SIRT2 inhibition protects against cardiac hypertrophy and ischemic injury

Author

Yang, Xiaoyan, primary, Chang, Hsiang-Chun, additional, Tatekoshi, Yuki, additional, Mahmoodzadeh, Amir, additional, Balibegloo, Maryam, additional, Najafi, Zeinab, additional, Wu, Rongxue, additional, Chen, Chunlei, additional, Sato, Tatsuya, additional, Shapiro, Jason Solomon, additional, and Ardehali, Hossein, additional

Published
2023
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9. Abstract P2127: A Novel Arnt Dependent Hif2a Singling In Protecting Against Cardiac Microvascular Endothelial Barrier Dysfunction Following Myocardial Infarction

Author

Karim Ullah, Karim, primary, Ai, Lizhuo, additional, Li, Yan, additional, Liu, Lifeng, additional, Pan, Kaichao, additional, Humayun, Zainab, additional, Sitikov, Albert, additional, Su, Qiaozhu, additional, Zhao, Qiong, additional, Sharp, Willard W, additional, Fang, Yun, additional, Wu, David, additional, Liao, James K, additional, and Wu, Rongxue R, additional

Published
2023
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12. Polymorphisms of fat mass and obesity-associated gene in the pathogenesis of child and adolescent metabolic syndrome

Author

Song, Yongyan, Wade, Henry, Zhang, Bingrui, Xu, Wenhao, Wu, Rongxue, Li , Shujin, and Su, Qiaozhu

Subjects
SDG 3 - Good Health and Well-being
Abstract

Childhood metabolic syndrome (MetS) is prevalent around the world and is associated with a high likelihood of suffering from severe diseases such as cardiovascular disease later in adulthood. MetS is associated with genetic susceptibility that involves gene polymorphisms. The fat mass and obesity-associated gene (FTO) encodes an RNA N6-methyladenosine demethylase that regulates RNA stability and molecular functions. Human FTO contains genetic variants that significantly contribute to the early onset of MetS in children and adolescents. Emerging evidence has also uncovered that FTO polymorphisms in intron 1, such as rs9939609 and rs9930506 polymorphisms, are significantly associated with the development of MetS in children and adolescents. Mechanistic studies reported that FTO polymorphisms lead to aberrant expressions of FTO and the adjacent genes that promote adipogenesis and appetite and reduce steatolysis, satiety, and energy expenditure in the carriers. The present review highlights the recent observations on the key FTO polymorphisms that are associated with child and adolescent MetS with an exploration of the molecular mechanisms underlying the development of increased waist circumference, hypertension, and hyperlipidemia in child and adolescent MetS.

Published
2023

14. A Novel HIF-2α/ARNT Signaling Pathway Protects Against Microvascular Dysfunction and heart failure After Myocardial Infarction

Author

Ullah, Karim, primary, Ai, Lizhuo, additional, Li, Yan, additional, Liu, Lifeng, additional, Zhang, Qin, additional, Pan, Kaichao, additional, Humayun, Zainab, additional, Sitikov, Albert, additional, Su, Qiaozhu, additional, Zhao, Qiong, additional, Sharp, Willard W, additional, Fang, Yun, additional, Wu, David, additional, Liao, James K, additional, and Wu, Rongxue, additional

Published
2023
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17. Role of MMP3 in cardiac microvascular barrier dysfunction and heart failure during sepsis

Author

Wu, Rongxue

Abstract

Sepsis is a life-threatening multiorgan dysfunction syndrome caused by a dysregulated body response to infection. Heart failure occurs in critically ill patients with sepsis, leading to a mortality rate of up to 70%. Despite intensive study in the past 40 years, there is still no effective clinical treatment for sepsis-induced cardiac dysfunction, primarily because the mechanisms why sepsis develops heart failure are not fully understood. Recent data from our study suggested that an exaggerated increase in microvascular permeability in sepsis is a significant predictor of severity and mortality. Therefore, protecting microvascular integrity and reducing cardiac edema (defined as excess accumulation of fluid in the myocardial interstitial) may improve the survival of patients with sepsis. Interestingly, we found drastically increased mmp3 serum levels in a septic animal model, consistent with a most recent clinical report in patients. Our data collected from septic patients also suggested a robust diagnosis value of serum MMP3 on sepsis, which was much greater than any other septic markers tested in our studies. However, what is the role of MMP3 in sepsis is not well elucidated. In our pilot study, MMP3-knock out (KO) mice displayed: 1) less microvascular leakage and fluid accumulation in the heart; 2) significantly improved cardiac function, maintained normal blood pressure and markedly increased survival rate; 3) repressed pro-inflammatory cytokines (i.e. iNOS, IL-6) under sepsis conditions. MMP3 is predominantly expressed in endothelial cells, Mice with CRISPR/Cas9 genome editing of MMP3 selectively in endothelial cells exhibited greater survival than control mice following sepsis challenge. Our supporting data also show that B1R inhibitor treatment in WT mice markedly attenuated the serum level of MMP3 and reduced cardiac microvascular leakage under sepsis conditions. Thus, we hypothesize that upregulation of endothelial MMP3 via a B1R-dependent pathway following sepsis challenge plays a critical role in inducing cardiac microvascular barrier dysfunction which leads to the development of sepsis-induced heart failure. We propose the following three specie aims. Studies in Aim1 will delineate the fundamental role of endothelial MMP3 in regulating cardiac microvascular permeability and cardiac function during sepsis and, thus, developing SICM. Aim 2 will define the molecular mechanism of sepsis-induced MMP3 in endothelial cells via B1R signaling. Aim 3 will explore the therapeutic potential of MMP3 inhibition in preventing/inhibiting sepsis-induced cardiomyopathy. Upon completion, we expect the results from our studies to have a comprehensive understanding of the mechanism of sepsis-induced heart failure and identified novel therapeutic targets and strategies for improving patient outcomes by reducing cardiac edema during the early stages of recovery from sepsis and preventing/inhibiting the progression of heart failure.

Published
2023
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18. Targeting Endothelial HIF2α/ARNT Expression for Ischemic Heart Disease Therapy.

Author

Ullah, Karim, Ai, Lizhuo, Humayun, Zainab, and Wu, Rongxue

Subjects
MYOCARDIAL ischemia, CORONARY disease, ENDOTHELIAL cells, VASCULAR endothelial cells, CARDIOVASCULAR system, ENDOTHELIUM diseases, CARDIOVASCULAR development
Abstract

Simple Summary: In this review paper, we discuss potential new therapies for ischemic heart disease (IHD), a leading cause of death and disability around the world. IHD results from a lack of oxygen supply to the heart muscle, often due to blocked or narrowed blood vessels. One key factor in IHD is the dysfunction of cells lining blood vessels, called endothelial cells. In response to low oxygen levels, these cells activate proteins called hypoxia-inducible factors (HIFs), which help regulate various processes related to cardiovascular diseases. In particular, we focus on HIF2α, which is mainly found in endothelial cells, and its partner ARNT, both of which play crucial roles in IHD development. Our review provides an overview of the current understanding of HIF2α and ARNT signaling in endothelial cells, their roles in inflammation and maintaining blood vessel integrity, and their involvement in IHD. We explore how these proteins work together and how their activity can be controlled using drugs. In conclusion, targeting HIF2α and ARNT in endothelial cells could offer promising new approaches for treating IHD, ultimately helping to improve the quality of life for millions of people affected by this debilitating condition. Ischemic heart disease (IHD) is a major cause of mortality and morbidity worldwide, with novel therapeutic strategies urgently needed. Endothelial dysfunction is a hallmark of IHD, contributing to its development and progression. Hypoxia-inducible factors (HIFs) are transcription factors activated in response to low oxygen levels, playing crucial roles in various pathophysiological processes related to cardiovascular diseases. Among the HIF isoforms, HIF2α is predominantly expressed in cardiac vascular endothelial cells and has a key role in cardiovascular diseases. HIFβ, also known as ARNT, is the obligate binding partner of HIFα subunits and is necessary for HIFα's transcriptional activity. ARNT itself plays an essential role in the development of the cardiovascular system, regulating angiogenesis, limiting inflammatory cytokine production, and protecting against cardiomyopathy. This review provides an overview of the current understanding of HIF2α and ARNT signaling in endothelial cell function and dysfunction and their involvement in IHD pathogenesis. We highlight their roles in inflammation and maintaining the integrity of the endothelial barrier, as well as their potential as therapeutic targets for IHD. [ABSTRACT FROM AUTHOR]

Published
2023
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25. Decreased Tissue Kallikrein Levels and the Risk of Ischemic Stroke: A Community-Based Cross-Sectional Study in China

Author

Ran,Xiao, Wang,Dao Wen, Yu,Zhen, Wu,Rongxue, Zhang,Qin, Ran,Xiao, Wang,Dao Wen, Yu,Zhen, Wu,Rongxue, and Zhang,Qin

Abstract

Xiao Ran,1 Dao Wen Wang,2 Zhen Yu,1 Rongxue Wu,3 Qin Zhang4 1Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of China; 2The Institute of Hypertension and Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of China; 3Department of Biological Sciences Division/ Cardiology, University of Chicago, Chicago, IL, 60637, USA; 4Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of ChinaCorrespondence: Qin Zhang Email qzhang8@tjh.tjmu.cnAim: Tissue kallikrein (TK) exerts protective effects on cardiac cerebrovascular diseases (CCVDs). Changes in TK level in plasma are associated with ischemic stroke and coronary artery disease (CAD); however, a causal correlation could not be established. Therefore, we investigated the association between TK levels and CCVDs in a community-based cross-sectional study in China.Methods: A total of 6043 subjects (4242 men and 1801 women) were enrolled in this community-based cross-sectional study. Then, TK levels were measured using an enzyme-linked immunosorbent assay kit. Multivariate linear regression model and logistic regression were used to assess the correlations between TK levels and CCVDs. Subsequently, the receiver operating characteristic (ROC) curve was drawn to assess the value of TK level in evaluating the risk of ischemic stroke. Finally, the influence of various medications was evaluated on TK levels.Results: The TK level was significantly lower in subjects with ischemic stroke (P < 0.001) and hypertension (P < 0.001) and negatively associated with ischemic stroke (P < 0.001) but not associated with hypertension, coronary heart disease, and diabetes compared to the traditional risk factors. The diagn

Published
2022

29. Cardiac-specific ablation of ARNT leads to lipotoxicity and cardiomyopathy

Author

Wu, Rongxue, Chang, Hsiang-Chun, Khechaduri, Arineh, Chawla, Kusum, Tran, Minh, Chai, Xiaomeng, Wagg, Cory, Ghanefar, Mohsen, Jiang, Xinghang, Bayeva, Marina, Gonzalez, Frank, Lopaschuk, Gary, and Ardehali, Hossein

Subjects
Heart diseases -- Risk factors -- Research -- Genetic aspects, Genes -- Physiological aspects -- Research, Metabolic diseases -- Risk factors -- Research -- Genetic aspects, Cardiomyopathy -- Risk factors -- Research -- Genetic aspects, Health care industry
Abstract

Patients with type 2 diabetes often present with cardiovascular complications; however, it is not clear how diabetes promotes cardiac dysfunction. In murine models, deletion of the gene encoding aryl hydrocarbon nuclear translocator (ARNT, also known as HIF1β) in the liver or pancreas leads to a diabetic phenotype; however, the role of ARNT in cardiac metabolism is unknown. Here, we determined that cardiac-specific deletion of Arnt in adult mice results in rapid development of cardiomyopathy (CM) that is characterized by accumulation of lipid droplets. Compared with hearts from ARNT-expressing mice, ex vivo analysis of ARNT-deficient hearts revealed a 2-fold increase in fatty acid (FA) oxidation as well as a substantial increase in the expression of PPARa and its target genes. Furthermore, deletion of both Arnt and Ppara preserved cardiac function, improved survival, and completely reversed the FA accumulation phenotype, indicating that PPARα mediates the detrimental effects of Arnt deletion in the heart. Finally, we determined that ARNT directly regulates Ppara expression by binding to its promoter and forming a complex with HIF2α. Together, these findings suggest that ARNT is a critical regulator of myocardial FA metabolism and that its deletion leads to CM and an increase in triglyceride accumulation through PPARα., Introduction Diabetes mellitus is a common disorder, with approximately 300 million people worldwide believed to be affected (1). Type 2 diabetes is associated with cardiovascular complications, including an increased incidence [...]

Published
2014
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30. Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation

Author

Ichikawa, Yoshihiko, Ghanefar, Mohsen, Bayeva, Marina, Wu, Rongxue, Khechaduri, Arineh, Prasad, Sathyamangla V. Naga, Mutharasan, R. Kannan, Naik, Tejaswitha Jairaj, and Ardehali, Hossein

Subjects
Iron in the body -- Research, Heart cells -- Physiological aspects -- Research, Cell-mediated cytotoxicity -- Research, Doxorubicin -- Complications and side effects -- Research, Health care industry
Abstract

Doxorubicin is an effective anticancer drug with known cardiotoxic side effects. It has been hypothesized that doxorubicin-dependent cardiotoxicity occurs through ROS production and possibly cellular iron accumulation. Here, we found that cardiotoxicity develops through the preferential accumulation of iron inside the mitochondria following doxorubicin treatment. In isolated cardiomyocytes, doxorubicin became concentrated in the mitochondria and increased both mitochondrial iron and cellular ROS levels. Overexpression of ABCB8, a mitochondrial protein that facilitates iron export, in vitro and in the hearts of transgenic mice decreased mitochondrial iron and cellular ROS and protected against doxorubicin-induced cardiomyopathy. Dexrazoxane, a drug that attenuates doxorubicin-induced cardiotoxicity, decreased mitochondrial iron levels and reversed doxorubicin-induced cardiac damage. Finally, hearts from patients with doxorubicin-induced cardiomyopathy had markedly higher mitochondrial iron levels than hearts from patients with other types of cardiomyopathies or normal cardiac function. These results suggest that the cardiotoxic effects of doxorubicin develop from mitochondrial iron accumulation and that reducing mitochondrial iron levels protects against doxorubicin-induced cardiomyopathy., Introduction Doxorubicin (DOX) is one of the most widely used antineoplastic drugs. The anticancer effects of DOX are believed to occur through the inhibition of topoisomerase enzyme and subsequent blockage [...]

Published
2014
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37. Endothelial Aryl Hydrocarbon Receptor Nuclear Translocator Mediates the Angiogenic Response to Peripheral Ischemia in Mice With Type 2 Diabetes Mellitus

Author

Nguyen, Tu, primary, Zheng, Mei, additional, Knapp, Maura, additional, Sladojevic, Nikola, additional, Zhang, Qin, additional, Ai, Lizhuo, additional, Harrison, Devin, additional, Chen, Anna, additional, Sitikov, Albert, additional, Shen, Le, additional, Gonzalez, Frank J., additional, Zhao, Qiong, additional, Fang, Yun, additional, Liao, James J. K., additional, and Wu, Rongxue, additional

Published
2021
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40. Increase in Blood–Brain Barrier Permeability is Modulated by Tissue Kallikrein via Activation of Bradykinin B1 and B2 Receptor-Mediated Signaling

Author

Zhang,Qin, Tan,Juan, Wan,Li, Chen,Chao, Wu,Bin, Ke,Xijian, Wu,Rongxue, Ran,Xiao, Zhang,Qin, Tan,Juan, Wan,Li, Chen,Chao, Wu,Bin, Ke,Xijian, Wu,Rongxue, and Ran,Xiao

Abstract

Qin Zhang,1 Juan Tan,1 Li Wan,1 Chao Chen,1 Bin Wu,2 Xijian Ke,1 Rongxue Wu,3 Xiao Ran4 1Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of China; 2Laboratory of Platelet and Endothelium Biology, Department of Transfusion Medicine, Wuhan Hospital of Traditional Chinese and Western Medicine (Wuhan No.1 Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of China; 3Department of Biological Sciences Division/ Cardiology, University of Chicago, Chicago, IL, 60637, USA; 4Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of ChinaCorrespondence: Xiao Ran Email ranxiao1001@tjh.tjmu.edu.cnAim: Disruption of the blood–brain barrier (BBB) is a critical pathological feature after stroke. Although tissue kallikrein (TK) has used in the treatment of stroke in China, the role of TK in modulating BBB permeability is not clear.Methods: We investigated the effect of different doses of TK on BBB by in vivo assessments of Evans blue (EB) and sodium-fluorescein isothiocyanate (FITC) leakage and in vitro assessments of the integrity of BBB and monolayers of microvascular endothelial cells (BMVECs). The expression of zonula occludens-1 (ZO-1) and bradykinin receptor-mediated signaling in BMVECs was detected.Results: A significant increase in BBB permeability was observed in the mice treated with high dose of TK. However, standard and medium doses of TK could only enable sodium-FITC to enter the brain. The result of in vitro study indicated that high-doses of TK, but not standard and medium-dose of TK, reduced normal BBB integrity accompanied by a decreased expression of zonula occludens-1 (ZO-1), upregulated the mRNA levels of bradykinin 2 receptor (B2R) and endothelial nitric oxide synthase (eNOS) and

Published
2021

41. Tissue Kallikrein Exacerbating Sepsis-Induced Endothelial Hyperpermeability is Highly Predictive of Severity and Mortality in Sepsis

Author

Ran,Xiao, Zhang,Qin, Li,Shaoping, Yu,Zhen, Wan,Li, Wu,Bin, Wu,Rongxue, Li,Shusheng, Ran,Xiao, Zhang,Qin, Li,Shaoping, Yu,Zhen, Wan,Li, Wu,Bin, Wu,Rongxue, and Li,Shusheng

Abstract

Xiao Ran,1 Qin Zhang,2 Shaoping Li,1 Zhen Yu,1 Li Wan,2 Bin Wu,3 Rongxue Wu,4 Shusheng Li1 1Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of China; 2Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of China; 3Laboratory of Platelet and Endothelium Biology, Department of Transfusion Medicine, Wuhan Hospital of Traditional Chinese and Western Medicine (Wuhan No.1 Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, People’s Republic of China; 4Department of Biological Sciences Division/Cardiology, University of Chicago, Chicago, IL, 60637, USACorrespondence: Qin Zhang Email qzhang8@tjh.tjmu.cnShusheng Li Email Shushengli16@sina.comAim: Sepsis, an acute, life-threatening dysregulated response to infection, affects practically all aspects of endothelial function. Tissue kallikrein (TK) is a key enzyme in the kallikrein–kinin system (KKS) which has been implicated in endothelial permeability. Thus, we aimed to establish a potentially novel association among TK, endothelial permeability, and sepsis demonstrated by clinical investigation and in vitro studies.Methods: We performed a clinical investigation with the participation of a total of 76 controls, 42 systemic inflammatory response syndrome (SIRS) patients, and 150 patients with sepsis, who were followed-up for 28 days. Circulating TK levels were measured with an enzyme-linked immunosorbent assay. Then, the effect of TK on sepsis-induced endothelial hyperpermeability was evaluated by in vitro study.Results: Data showed a gradual increase in TK level among controls and the patients with SIRS, sepsis, and septic shock (0.288± 0.097 mg/l vs 0.335± 0.149 vs 0.495± 0.170 vs 0.531± 0.188 mg/l, respectively, P < 0.001). Further analysis revealed th

Published
2021

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