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25 results on '"Zhao, Huishou"'

4. Cardiomyocyte βII spectrin plays a critical role in maintaining cardiac function by regulating mitochondrial respiratory function

Author

Yang, Rongjin, primary, Ruan, Banjun, additional, Wang, Rutao, additional, Zhang, Xiaomeng, additional, Xing, Pingping, additional, Li, Congye, additional, Zhang, Yunyun, additional, Chang, Xiaoqian, additional, Song, Haifeng, additional, Zhang, Shun, additional, Zhao, Huishou, additional, Zhang, Feiyu, additional, Yin, Tao, additional, Qi, Tingting, additional, Yan, Wenjun, additional, Zhang, Fuyang, additional, Hu, Guangyu, additional, Wang, Shan, additional, and Tao, Ling, additional

Published
2024
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6. CSF2RB overexpression promotes the protective effects of mesenchymal stromal cells against ischemic heart injury

Author

Qi, Tingting, primary, Xu, Xiaoming, additional, Guo, Yongzhen, additional, Xia, Yunlong, additional, Peng, Lu, additional, Li, Congye, additional, Ding, Fengyue, additional, Gao, Chao, additional, Fan, Miaomiao, additional, Yu, Min, additional, Zhao, Huishou, additional, He, Yuan, additional, Li, Wenli, additional, Hai, Chunxu, additional, Gao, Erhe, additional, Zhang, Xing, additional, Gao, Feng, additional, Fan, Yanhong, additional, Yan, Wenjun, additional, and Tao, Ling, additional

Published
2023
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8. Branched-Chain Amino Acids Exacerbate Obesity-Related Hepatic Glucose and Lipid Metabolic Disorders via Attenuating Akt2 Signaling

Author

Admin, Ada, primary, Zhao, Huishou, primary, Zhang, Fuyang, primary, Sun, Dan, primary, Wang, Xiong, primary, Zhang, Xiaomeng, primary, Zhang, Jinglong, primary, Yan, Feng, primary, Huang, Chong, primary, Xie, Huaning, primary, Lin, Chen, primary, Liu, Yi, primary, Fan, Miaomiao, primary, Yan, Wenjun, primary, Chen, Youhu, primary, Lian, Kun, primary, Li, Yueyang, primary, Zhang, Ling, primary, Wang, Shan, primary, and Tao, Ling, primary

Published
2020
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9. Branched-Chain Amino Acids Exacerbate Obesity-Related Hepatic Glucose and Lipid Metabolic Disorders via Attenuating Akt2 Signaling

Author

Zhao, Huishou, primary, Zhang, Fuyang, additional, Sun, Dan, additional, Wang, Xiong, additional, Zhang, Xiaomeng, additional, Zhang, Jinglong, additional, Yan, Feng, additional, Huang, Chong, additional, Xie, Huaning, additional, Lin, Chen, additional, Liu, Yi, additional, Fan, Miaomiao, additional, Yan, Wenjun, additional, Chen, Youhu, additional, Lian, Kun, additional, Li, Yueyang, additional, Zhang, Ling, additional, Wang, Shan, additional, and Tao, Ling, additional

Published
2020
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10. Branched chain amino acids exacerbate myocardial ischemia/reperfusion vulnerability via enhancing GCN2/ATF6/PPAR-α pathway-dependent fatty acid oxidation

Author

Li, Yueyang, primary, Xiong, Zhenyu, additional, Yan, Wenjun, additional, Gao, Erhe, additional, Cheng, Hexiang, additional, Wu, Guiling, additional, Liu, Yi, additional, Zhang, Ling, additional, Li, Congye, additional, Wang, Shan, additional, Fan, Miaomiao, additional, Zhao, Huishou, additional, Zhang, Fuyang, additional, and Tao, Ling, additional

Published
2020
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11. Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP‑PKG signaling

Author

Chang, Pan, primary, Zhang, Xiaomeng, additional, Zhang, Mingyang, additional, Li, Guohua, additional, Hu, Lang, additional, Zhao, Huishou, additional, Zhu, Xiaoxing, additional, Wu, Juan, additional, Wang, Xihui, additional, Wang, Kaiyan, additional, Zhang, Jing, additional, Ren, Minggang, additional, Chen, Baoying, additional, Zhu, Xiaoling, additional, Zhu, Miaozhang, additional, and Yu, Jun, additional

Published
2019
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14. Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP-PKG signaling.

Author

Chang, Pan, Zhang, Xiaomeng, Zhang, Mingyang, Li, Guohua, Hu, Lang, Zhao, Huishou, Zhu, Xiaoxing, Wu, Juan, Wang, Xihui, Wang, Kaiyan, Zhang, Jing, Ren, Minggang, Chen, Baoying, Zhu, Xiaoling, Zhu, Miaozhang, and Yu, Jun

Subjects
GLUCOSE-regulated proteins, MICE, EXERCISE, SUPEROXIDE dismutase, ENDOPLASMIC reticulum, OXIDATIVE stress
Abstract

The purpose of the present study was to explore aging-associated cardiac dysfunction and the possible mechanism by which swimming exercise modulates cardiac dysfunction in aged mice. Aged mice were divided into two groups: i) Aged mice; and ii) aged mice subjected to swimming exercises. Another cohort of 4-month-old male mice served as the control group. Cardiac structure and function in mice were analyzed using hematoxylin and eosin staining, and echocardiography. The levels of oxidative stress were determined by measuring the levels of superoxide dismutase, malondialdehyde and reactive oxygen species (ROS). Levels of the endoplasmic reticulum (ER) stress-related protein PKR-like ER kinase, glucose-regulated protein 78 and C/EBP homologous protein were determined to evaluate the level of ER stress. The aged group exhibited an abnormal cardiac structure and decreased cardiac function, both of which were ameliorated by swimming exercise. The hearts of the aged mice exhibited pronounced oxidative and ER stress, which were ameliorated by exercise, and was accompanied by the reactivation of myocardial cGMP and suppression of cGMP-specific phosphodiesterase type 5 (PDE5). The inhibition of PDE5 attenuated age-induced cardiac dysfunction, blocked ROS production and suppressed ER stress. An ER stress inducer abolished the beneficial effects of the swimming exercise on cardiac function and increased ROS production. The present study suggested that exercise restored cardiac function in mice with age-induced cardiac dysfunction by inhibiting oxidative stress and ER stress, and increasing cGMP-protein kinase G signaling. [ABSTRACT FROM AUTHOR]

Published
2020
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15. Glycoprotein M6B Interacts with TβRI to Activate TGF-β-Smad2/3 Signaling and Promote Smooth Muscle Cell Differentiation

Author

Zhang, Xiaomeng, primary, Xie, Huaning, additional, Chang, Pan, additional, Zhao, Huishou, additional, Xia, Yunlong, additional, Zhang, Ling, additional, Guo, Xiong, additional, Huang, Chong, additional, Yan, Feng, additional, Hu, Lang, additional, Lin, Chen, additional, Li, Yueyang, additional, Xiong, Zhenyu, additional, Wang, Xiong, additional, Li, Guohua, additional, Deng, Longxiang, additional, Wang, Shan, additional, and Tao, Ling, additional

Published
2018
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19. Adiponectin determines farnesoid X receptor agonism-mediated cardioprotection against post-infarction remodelling and dysfunction

Author

Xia, Yunlong, primary, Zhang, Fuyang, additional, Zhao, Shihao, additional, Li, Yueyang, additional, Chen, Xiyao, additional, Gao, Erhe, additional, Xu, Xinyue, additional, Xiong, Zhenyu, additional, Zhang, Xiaomeng, additional, Zhang, Jinglong, additional, Zhao, Huishou, additional, Wang, Wei, additional, Wang, Helin, additional, Guo, Yanjie, additional, Liu, Yi, additional, Li, Congye, additional, Wang, Shan, additional, Zhang, Ling, additional, Yan, Wenjun, additional, and Tao, Ling, additional

Published
2018
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21. GW27-e1159 Branched chain amino acids induced downregulation of AKT2 protein in hepatocytes, promoted high fat diet induced mice liver insulin resistance

Author

Tao Ling and Zhao Huishou

Subjects
chemistry.chemical_classification, Gene isoform, medicine.medical_specialty, business.industry, Insulin sensitivity, High fat diet, AKT2, medicine.disease, Amino acid, Endocrinology, Insulin resistance, chemistry, Downregulation and upregulation, Internal medicine, medicine, Cardiology and Cardiovascular Medicine, business, Protein kinase B
Abstract

To investigate the effect of BCAA on liver insulin sensitivity, and to investigate whether BCAA contributes to the development of liver insulin resistance through changing the protein level of AKT and the isoforms. 1.Cell experiments HepG2 cells were divided into control group, palmitate treatment

Published
2016

22. Branched Chain Amino Acids Cause Liver Injury in Obese/Diabetic Mice by Promoting Adipocyte Lipolysis and Inhibiting Hepatic Autophagy

Author

Zhang, Fuyang, primary, Zhao, Shihao, additional, Yan, Wenjun, additional, Xia, Yunlong, additional, Chen, Xiyao, additional, Wang, Wei, additional, Zhang, Jinglong, additional, Gao, Chao, additional, Peng, Cheng, additional, Yan, Feng, additional, Zhao, Huishou, additional, Lian, Kun, additional, Lee, Yan, additional, Zhang, Ling, additional, Lau, Wayne Bond, additional, Ma, Xinliang, additional, and Tao, Ling, additional

Published
2016
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24. Glycoprotein M6B Interacts with TβRI to Activate TGF‐β‐Smad2/3 Signaling and Promote Smooth Muscle Cell Differentiation

Author

Zhang, Xiaomeng, Xie, Huaning, Chang, Pan, Zhao, Huishou, Xia, Yunlong, Zhang, Ling, Guo, Xiong, Huang, Chong, Yan, Feng, Hu, Lang, Lin, Chen, Li, Yueyang, Xiong, Zhenyu, Wang, Xiong, Li, Guohua, Deng, Longxiang, Wang, Shan, and Tao, Ling

Abstract

Smooth muscle cells (SMCs), which form the walls of blood vessels, play an important role in vascular development and the pathogenic process of vascular remodeling. However, the molecular mechanisms governing SMC differentiation remain poorly understood. Glycoprotein M6B (GPM6B) is a four‐transmembrane protein that belongs to the proteolipid protein family and is widely expressed in neurons, oligodendrocytes, and astrocytes. Previous studies have revealed that GPM6B plays a role in neuronal differentiation, myelination, and osteoblast differentiation. In the present study, we found that the GPM6B gene and protein expression levels were significantly upregulated during transforming growth factor‐β1 (TGF‐β1)‐induced SMC differentiation. The knockdown of GPM6B resulted in the downregulation of SMC‐specific marker expression and repressed the activation of Smad2/3 signaling. Moreover, GPM6B regulates SMC Differentiation by Controlling TGF‐β‐Smad2/3 Signaling. Furthermore, we demonstrated that similar to p‐Smad2/3, GPM6B was profoundly expressed and coexpressed with SMC differentiation markers in embryonic SMCs. Moreover, GPM6B can regulate the tightness between TβRI, TβRII, or Smad2/3 by directly binding to TβRI to activate Smad2/3 signaling during SMC differentiation, and activation of TGF‐β‐Smad2/3 signaling also facilitate the expression of GPM6B. Taken together, these findings demonstrate that GPM6B plays a crucial role in SMC differentiation and regulates SMC differentiation through the activation of TGF‐β‐Smad2/3 signaling via direct interactions with TβRI. This finding indicates that GPM6B is a potential target for deriving SMCs from stem cells in cardiovascular regenerative medicine. Stem Cells2018StemCells2019;37:190–201 In summary, the present study revealed that GPM6B play a crucial role in SMC differentiation. GPM6B promotes SMC differentiation through the activation of TGF‐β‐Smad2/3 signaling via regulating the tightness between TβRI and TβRII or Smad2/3 by directly binding to TβRI to activate Smad2/3 signaling, and activation of TGF‐β‐Smad2/3 signaling also facilitate the expression of GPM6B.

Published
2019
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25. Decreased Mrpl42 expression exacerbates myocardial ischemia and reperfusion injury by inhibiting mitochondrial translation.

Author

Zhang X, Chang X, Deng J, Li C, Li Y, Zheng Y, Yang R, Xu X, Yan W, Zhang F, Xia Y, Zhao H, Xing P, Guo G, Ding F, Tao L, and Wang S

Abstract

Mammalian mitochondrial DNA (mtDNA) encodes a total of 13 proteins, all of which are subunits of enzyme complexes of the oxidative phosphorylation. The mtDNA-encoded protein synthesis depends on the mitochondrial ribosomal proteins (MRPs), which assemble to form a specialized form of ribosome. Some mtDNA-encoded proteins have been reported to be reduced after myocardial ischemic injury. However, the molecular mechanisms responsible for this decrease and whether this decrease is involved in myocardial ischemia/reperfusion (I/R) injury remains unknown. Here, we found that the mtDNA-encoded protein levels were significantly decreased after I/R injury, while the mRNA levels of these genes were either increased or had no significant change. Subsequently, by querying and analyzing public database resources, we found that the expression of many mitochondrial translation-related proteins tended to decrease after myocardial infarction injury, and the reduction in the expression of these proteins was most obvious for Mrpl42. Furthermore, we found that cardiac Mrpl42 knockdown aggravated I/R-induced cardiac contractile dysfunction and cardiomyocyte death, while restoring Mrpl42 expression in the heart reduced I/R injury. Mrpl42 knockdown impaired the translation of mtDNA-encoded genes, ultimately led to aberrations in mitochondrial morphology and respiratory function. In addition, we found that the decrease in the expression of Mrpl42 after I/R injury was caused by the downregulation of Nrf2, which directly regulates Mrpl42 transcription. Our study revealed that ischemic downregulation of Mrpl42 expression and subsequent inhibition of mitochondrial translation contribute to cardiac I/R injury. Targeting Mrpl42 may be a novel therapeutic intervention for cardiac I/R injury and myocardial infarction., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Published
2024
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