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3. Krüppel-Like Factor 4 Regulation of Cholesterol-25-Hydroxylase and Liver X Receptor Mitigates Atherosclerosis Susceptibility

Author

Li, Zhao, Martin, Marcy, Zhang, Jin, Huang, Hsi-Yuan, Bai, Liang, Zhang, Jiao, Kang, Jian, He, Ming, Li, Jie, Maurya, Mano R, Gupta, Shakti, Zhou, Guangjin, Sangwung, Panjamaporn, Xu, Yong-Jiang, Lei, Ting, Huang, Hsien-Da, Jain, Mohit, Jain, Mukesh K, Subramaniam, Shankar, and Shyy, John Y-J

Subjects
Digestive Diseases, Cardiovascular, Atherosclerosis, Liver Disease, 2.1 Biological and endogenous factors, Aetiology, Animals, Gene Expression, Humans, Hydroxycholesterols, Kruppel-Like Factor 4, Kruppel-Like Transcription Factors, Liver X Receptors, Male, Mice, atherosclerosis, cholesterol, endothelial cells, inflammation, macrophages, shear stress, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Public Health and Health Services, Cardiovascular System & Hematology
Abstract

BackgroundAtherosclerosis is a multifaceted inflammatory disease involving cells in the vascular wall (eg, endothelial cells [ECs]), as well as circulating and resident immunogenic cells (eg, monocytes/macrophages). Acting as a ligand for liver X receptor (LXR), but an inhibitor of SREBP2 (sterol regulatory element-binding protein 2), 25-hydroxycholesterol, and its catalyzing enzyme cholesterol-25-hydroxylase (Ch25h) are important in regulating cellular inflammatory status and cholesterol biosynthesis in both ECs and monocytes/macrophages.MethodsBioinformatic analyses were used to investigate RNA-sequencing data to identify cholesterol oxidation and efflux genes regulated by Krüppel-like factor 4 (KLF4). In vitro experiments involving cultured ECs and macrophages and in vivo methods involving mice with Ch25h ablation were then used to explore the atheroprotective role of KLF4-Ch25h/LXR.ResultsVasoprotective stimuli increased the expression of Ch25h and LXR via KLF4. The KLF4-Ch25h/LXR homeostatic axis functions through suppressing inflammation, evidenced by the reduction of inflammasome activity in ECs and the promotion of M1 to M2 phenotypic transition in macrophages. The increased atherosclerosis in apolipoprotein E-/-/Ch25h-/- mice further demonstrates the beneficial role of the KLF4-Ch25h/LXR axis in vascular function and disease.ConclusionsKLF4 transactivates Ch25h and LXR, thereby promoting the synergistic effects between ECs and macrophages to protect against atherosclerosis susceptibility.

Published
2017

7. Abstract 10096: Genetic Control of Lysosomal Dysfunction Reprograms Sterol Metabolism in Pulmonary Arterial Hypertension

Author

Harvey, Lloyd D, Kim, Hee-Jung J, Alotaibi, Mona, Tai, Yi-Yin, Tang, Ying, Arshad, Sanya, Sun, Wei, Wu, Haodi, Zhao, Jingsi, Kirillova, Anna, Woodcock, Chen-shan J, Handen, Adam, Al Aaraj, Yassmin, Culley, Miranda K, Hafeez, Neha, Watson, Annie, Wallace, Callen, Wu, Haodi, Sullivan, Mara G, St. Croix, Claudette M, Stolz, Donna, Li, Gang, Corley, Chase, McDonald, Jeffrey G, Nouraie, Mehdi, Schwantes-An, Tae-Hwi, Desai, Ankit A, Pauciulo, Michael, Nichols, Bill, Lafyatis, Robert, Benza, Raymond L, Bertero, Thomas, Jain, Mohit, and Chan, Stephen Y

Published
2022
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12. Abstract P330: Effect of Randomized Omega-3 Treatment on Downstream Bioactive Lipids and Their Association With Incident Cardiovascular Disease Events: Metabolomic Studies of the Vital and Jupiter Trials

Author

Demler, Olga, primary, Liu, Yanyan, additional, Alotaibi, Mona, additional, Hoshi, Rosangela, additional, Giulianini, Franco, additional, Gibson, Heike, additional, Watrous, Jeramie, additional, Cook, Nancy R, additional, Costenbader, Karen, additional, Okereke, Olivia, additional, Glynn, Robert, additional, Ridker, Paul M, additional, Manson, Joann E, additional, Cheng, Susan, additional, Chasman, Daniel, additional, Jain, Mohit, additional, and Mora, Samia, additional

Published
2023
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15. Abstract 9784: Association of Physical Activity with Bioactive Lipids, BMI, and Risk of Future Cardiovascular Events - Mediation Analysis from the Vitamin D and Omega-3 Trial (Vital) and Jupiter Studies

Author

Hoshi, Rosangela, primary, Liu, Yanyan, additional, Guo, Yanjun, additional, Tiwari, Saumya, additional, Gibson, Heike, additional, Andres, Allen M, additional, Watrous, Jeramie, additional, Cook, Nancy R, additional, Copeland, Trisha, additional, Costenbader, Karen, additional, Okereke, Olivia, additional, Ridker, Paul M, additional, Manson, Joann, additional, Lee, I-min M, additional, Cheng, Susan, additional, Jain, Mohit, additional, Demler, Olga, additional, and Mora, Samia, additional

Published
2021
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17. A Novel Role for Tumor Necrosis Factor–Like Weak Inducer of Apoptosis (TWEAK) in the Development of Cardiac Dysfunction and Failure

Author

Jain, Mohit, primary, Jakubowski, Aniela, additional, Cui, Lei, additional, Shi, Jianru, additional, Su, Lihe, additional, Bauer, Michael, additional, Guan, Jian, additional, Lim, Chee Chew, additional, Naito, Yoshiro, additional, Thompson, Jeffrey S., additional, Sam, Flora, additional, Ambrose, Christine, additional, Parr, Michael, additional, Crowell, Thomas, additional, Lincecum, John M., additional, Wang, Monica Z., additional, Hsu, Yen-Ming, additional, Zheng, Timothy S., additional, Michaelson, Jennifer S., additional, Liao, Ronglih, additional, and Burkly, Linda C., additional

Published
2009
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22. Cell Therapy Attenuates Deleterious Ventricular Remodeling and Improves Cardiac Performance After Myocardial Infarction

Author

Jain, Mohit, primary, DerSimonian, Harout, additional, Brenner, Daniel A., additional, Ngoy, Soeun, additional, Teller, Paige, additional, Edge, Albert S. B., additional, Zawadzka, Agatha, additional, Wetzel, Kristie, additional, Sawyer, Douglas B., additional, Colucci, Wilson S., additional, Apstein, Carl S., additional, and Liao, Ronglih, additional

Published
2001
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24. Increased myocardial dysfunction after ischemia-reperfusion in mice lacking glucose-6-phosphate dehydrogenase.

Author

Jain M, Cui L, Brenner DA, Wang B, Handy DE, Leopold JA, Loscalzo J, Apstein CS, and Liao R

Subjects
Animals, Antioxidants pharmacology, Antioxidants therapeutic use, Female, Genotype, Glucosephosphate Dehydrogenase genetics, Glutathione metabolism, Male, Metalloporphyrins pharmacology, Metalloporphyrins therapeutic use, Mice, Mice, Knockout, Myocardial Contraction drug effects, Myocardial Ischemia enzymology, Myocardial Ischemia physiopathology, Myocardial Reperfusion Injury enzymology, Myocardial Reperfusion Injury physiopathology, NADP physiology, Oxidation-Reduction, Ribose deficiency, Ribose pharmacology, Glucosephosphate Dehydrogenase physiology, Glucosephosphate Dehydrogenase Deficiency complications, Myocardial Contraction physiology, Myocardial Ischemia genetics, Myocardial Reperfusion Injury genetics
Abstract

Background: Free radical injury contributes to cardiac dysfunction during ischemia-reperfusion. Detoxification of free radicals requires maintenance of reduced glutathione (GSH) by NADPH. The principal mechanism responsible for generating NADPH and maintaining GSH during periods of myocardial ischemia-reperfusion remains unknown. Glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme in the pentose phosphate pathway, generates NADPH in a reaction linked to the de novo production of ribose. We therefore hypothesized that G6PD is essential for maintaining GSH levels and protecting the heart during ischemia-reperfusion injury., Methods and Results: Susceptibility to myocardial ischemia-reperfusion injury was determined in Langendorff-perfused hearts isolated from wild-type mice (WT) and mice lacking G6PD (G6PD(def)) (20% of WT myocardial G6PD activity). During global zero-flow ischemia, cardiac function was similar between WT and G6PD(def) hearts. On reperfusion, however, cardiac relaxation and contractile performance were greatly impaired in G6PD(def) myocardium, as demonstrated by elevated end-diastolic pressures and decreased percent recovery of developed pressure relative to WT hearts. Contractile dysfunction in G6PD(def) hearts was associated with depletion of total glutathione stores and impaired generation of GSH from its oxidized form. Increased ischemia-reperfusion injury in G6PD(def) hearts was reversed by treatment with the antioxidant MnTMPyP but unaffected by supplementation of ribose stores., Conclusions: These results demonstrate that G6PD is an essential myocardial antioxidant enzyme, required for maintaining cellular glutathione levels and protecting against oxidative stress-induced cardiac dysfunction during ischemia-reperfusion.

Published
2004
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