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Your search keyword '"Zhou, Zhiqiang"' showing total 1,627 results
Start Over Author "Zhou, Zhiqiang" Publication Type Academic Journals
1,627 results on '"Zhou, Zhiqiang"'

10. A transcription factor ZmGLK36 confers broad resistance to maize rough dwarf disease in cereal crops

Author

Xu, Zhennan, Zhou, Zhiqiang, Cheng, Zixiang, Zhou, Yu, Wang, Feifei, Li, Mingshun, Li, Gongjian, Li, Wenxue, Du, Qingguo, Wang, Ke, Lu, Xin, Tai, Yuxin, Chen, Runyi, Hao, Zhuanfang, Han, Jienan, Chen, Yanping, Meng, Qingchang, Kong, Xiaomin, Tie, Shuanggui, Mu, Chunhua, Song, Weibin, Wang, Zhenhua, Yong, Hongjun, Zhang, Degui, Wang, Haiyang, Weng, Jianfeng, and Li, Xinhai

Published
2023
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11. Esketamine Improves Working Memory Impairment in Neuropathic Mice Through Hippocampal BDNF-TrkB Pathway

Author

JIANG Yubin, WANG Xingming, ZHANG Yue, ZHOU Zhiqiang, and YANG Jianjun

Subjects
esketamine, neuropathic pain, working memory, hippocampus, Medicine
Abstract

Objective To explore the effect of esketamine on working memory impairment in neuropathic mice and its underlying mechanism. Methods Fifty clean grade male C57BL/6J mice (2 months) were divided into 5 groups by random number table method: sham+saline (SN group), CCI+saline (CN group), CCI+esketamine(CE group), CCI+ANA-12 (CA group), CCI+ANA-12+esketamine (CAE group), with 10 mice in each group. Chronic constriction injury (CCI) was employed to establish a neuropathic pain model. On the 16th day after modeling, CE group and CAE group were administered ketamine (10 mg/kg), CAE group received ANA-12 (0.5 mg/kg) half an hour before ketamine injection, CA group was only given ANA-12, and SN group and CN group received an equivalent volume of saline. The administration was done through intraperitoneal injection for 5 consecutive days. The open-field test (OFT), paw withdrawal threshold (PWT), paw withdrawal latency (PWL) and Y-maze test were performed from day 21 after surgery. Bromo-2-deoxyUridine (BrdU) was dissolved in saline and intraperitoneally injected into the mice on days 21 to 23 after the surgery. Western blot was performed to determine the expression of Brain-derived neurotrophic factor(BDNF) in hippocampus, the immunofluorescence was performed to determine the number of BrdU and doublecortxin (DCX) positive cells in the dentate gyrus (DG) area of hippocampal. Results Compared with SN group, the other four groups showed significant reductions in both PWT and PWL on day 21 after surgery (all P

Published
2024
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12. Liver-heart cross-talk mediated by coagulation factor XI protects against heart failure

Author

Cao, Yang, Wang, Yuchen, Zhou, Zhenqi, Pan, Calvin, Jiang, Ling, Zhou, Zhiqiang, Meng, Yonghong, Charugundla, Sarada, Li, Tao, Allayee, Hooman, Seldin, Marcus M, and Lusis, Aldons J

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Heart Disease, Cardiovascular, Liver Disease, Digestive Diseases, 1.1 Normal biological development and functioning, Underpinning research, Animals, Bone Morphogenetic Protein 7, Factor XI, Fibrosis, Heart Failure, Humans, Inflammation, Liver, Male, Mice, Mice, Inbred C57BL, Myocardium, Proteolysis, General Science & Technology
Abstract

Tissue-tissue communication by endocrine factors is a vital mechanism for physiologic homeostasis. A systems genetics analysis of transcriptomic and functional data from a cohort of diverse, inbred strains of mice predicted that coagulation factor XI (FXI), a liver-derived protein, protects against diastolic dysfunction, a key trait of heart failure with preserved ejection fraction. This was confirmed using gain- and loss-of-function studies, and FXI was found to activate the bone morphogenetic protein (BMP)-SMAD1/5 pathway in the heart. The proteolytic activity of FXI is required for the cleavage and activation of extracellular matrix-associated BMP7 in the heart, thus inhibiting genes involved in inflammation and fibrosis. Our results reveal a protective role of FXI in heart injury that is distinct from its role in coagulation.

Published
2022

28. Deletion of ABCB10 in beta-cells protects from high-fat diet induced insulin resistance

Author

Shum, Michael, Segawa, Mayuko, Gharakhanian, Raffi, Viñuela, Ana, Wortham, Matthew, Baghdasarian, Siyouneh, Wolf, Dane M, Sereda, Samuel B, Nocito, Laura, Stiles, Linsey, Zhou, Zhiqiang, Gutierrez, Vincent, Sander, Maike, Shirihai, Orian S, and Liesa, Marc

Subjects
Biochemistry and Cell Biology, Biological Sciences, Obesity, Diabetes, Nutrition, Genetics, 2.1 Biological and endogenous factors, Metabolic and endocrine, ATP-Binding Cassette Transporters, Animals, Blood Glucose, Diabetes Mellitus, Type 2, Diet, High-Fat, Female, Glucose, Glucose Tolerance Test, Insulin, Insulin Resistance, Insulin Secretion, Insulin-Secreting Cells, Islets of Langerhans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mitochondria, Insulin resistance, Beta-cell, ABCB10, Physiology, Biochemistry and cell biology
Abstract

ObjectiveThe contribution of beta-cell dysfunction to type 2 diabetes (T2D) is not restricted to insulinopenia in the late stages of the disease. Elevated fasting insulinemia in normoglycemic humans is a major factor predicting the onset of insulin resistance and T2D, demonstrating an early alteration of beta-cell function in T2D. Moreover, an early and chronic increase in fasting insulinemia contributes to insulin resistance in high-fat diet (HFD)-fed mice. However, whether there are genetic factors that promote beta-cell-initiated insulin resistance remains undefined. Human variants of the mitochondrial transporter ABCB10, which regulates redox by increasing bilirubin synthesis, have been associated with an elevated risk of T2D. The effects of T2D ABCB10 variants on ABCB10 expression and the actions of ABCB10 in beta-cells are unknown.MethodsThe expression of beta-cell ABCB10 was analyzed in published transcriptome datasets from human beta-cells carrying the T2D-risk ABCB10 variant. Insulin sensitivity, beta-cell proliferation, and secretory function were measured in beta-cell-specific ABCB10 KO mice (Ins1Cre-Abcb10flox/flox). The short-term role of beta-cell ABCB10 activity on glucose-stimulated insulin secretion (GSIS) was determined in isolated islets.ResultsCarrying the T2Drisk allele G of ABCB10 rs348330 variant was associated with increased ABCB10 expression in human beta-cells. Constitutive deletion of Abcb10 in beta-cells protected mice from hyperinsulinemia and insulin resistance by limiting HFD-induced beta-cell expansion. An early limitation in GSIS and H2O2-mediated signaling caused by elevated ABCB10 activity can initiate an over-compensatory expansion of beta-cell mass in response to HFD. Accordingly, increasing ABCB10 expression was sufficient to limit GSIS capacity. In health, ABCB10 protein was decreased during islet maturation, with maturation restricting beta-cell proliferation and elevating GSIS. Finally, ex-vivo and short-term deletion of ABCB10 in islets isolated from HFD-fed mice increased H2O2 and GSIS, which was reversed by bilirubin treatments.ConclusionsBeta-cell ABCB10 is required for HFD to induce insulin resistance in mice by amplifying beta-cell mass expansion to maladaptive levels that cause fasting hyperinsulinemia.

Published
2022

29. Sex differences in heart mitochondria regulate diastolic dysfunction

Author

Cao, Yang, Vergnes, Laurent, Wang, Yu-Chen, Pan, Calvin, Chella Krishnan, Karthickeyan, Moore, Timothy M, Rosa-Garrido, Manuel, Kimball, Todd H, Zhou, Zhiqiang, Charugundla, Sarada, Rau, Christoph D, Seldin, Marcus M, Wang, Jessica, Wang, Yibin, Vondriska, Thomas M, Reue, Karen, and Lusis, Aldons J

Subjects
Biological Sciences, Genetics, Cardiovascular, Heart Disease, Underpinning research, 2.1 Biological and endogenous factors, Aetiology, 1.1 Normal biological development and functioning, Animals, Coenzyme A Ligases, Diastole, Female, Heart Failure, Humans, Male, Mice, Mitochondria, Heart, Sex Characteristics, Stroke Volume
Abstract

Heart failure with preserved ejection fraction (HFpEF) exhibits a sex bias, being more common in women than men, and we hypothesize that mitochondrial sex differences might underlie this bias. As part of genetic studies of heart failure in mice, we observe that heart mitochondrial DNA levels and function tend to be reduced in females as compared to males. We also observe that expression of genes encoding mitochondrial proteins are higher in males than females in human cohorts. We test our hypothesis in a panel of genetically diverse inbred strains of mice, termed the Hybrid Mouse Diversity Panel (HMDP). Indeed, we find that mitochondrial gene expression is highly correlated with diastolic function, a key trait in HFpEF. Consistent with this, studies of a "two-hit" mouse model of HFpEF confirm that mitochondrial function differs between sexes and is strongly associated with a number of HFpEF traits. By integrating data from human heart failure and the mouse HMDP cohort, we identify the mitochondrial gene Acsl6 as a genetic determinant of diastolic function. We validate its role in HFpEF using adenoviral over-expression in the heart. We conclude that sex differences in mitochondrial function underlie, in part, the sex bias in diastolic function.

Published
2022

46. Genomic prediction of yield performance among single-cross maize hybrids using a partial diallel cross design

Author

Luo, Ping, Wang, Houwen, Ni, Zhiyong, Yang, Ruisi, Wang, Fei, Yong, Hongjun, Zhang, Lin, Zhou, Zhiqiang, Song, Wei, Li, Mingshun, Yang, Jie, Weng, Jianfeng, Meng, Zhaodong, Zhang, Degui, Han, Jienan, Chen, Yong, Zhang, Runze, Wang, Liwei, Zhao, Meng, Gao, Wenwei, Chen, Xiaoyu, Li, Wenjie, Hao, Zhuanfang, Fu, Junjie, Zhang, Xuecai, and Li, Xinhai

Published
2023
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