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Your search keyword '"Zhou, Rong"' showing total 35 results
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12. Clinical, Virological and Immunological Features from Patients Infected with Re-Emergent Avian-Origin Human H7N9 Influenza Disease of Varying Severity in Guangdong Province

Author

Yang, Zi Feng, primary, Mok, Chris Ka Pun, additional, Liu, Xiao Qing, additional, Li, Xiao Bo, additional, He, Jian Feng, additional, Guan, Wen Da, additional, Xu, Yong Hao, additional, Pan, Wei Qi, additional, Chen, Li Yan, additional, Lin, Yong Ping, additional, Wu, Shi Guan, additional, Pan, Si Hua, additional, Huang, Ji Cheng, additional, Ding, Guo Yun, additional, Zheng, Kui, additional, Ke, Chang Wen, additional, Lin, Jin Yan, additional, Zhang, Yong Hui, additional, Lee, Horace Hok Yeung, additional, Liu, Wen Kuan, additional, Yang, Chun Guang, additional, Zhou, Rong, additional, Peiris, Joseph Sriyal Malik, additional, Li, Yi Min, additional, Chen, Rong Chang, additional, Chen, Ling, additional, and Zhong, Nan Shan, additional

Published
2015
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32. A Hepatic Protein, Fetuin-A, Occupies a Protective Role in Lethal Systemic Inflammation

Author

Yan Huang, Zhou Rong-rong, N. Tony Eissa, Kevin J. Tracey, Wei Li, Haichao Wang, Andrew E. Sama, Xing Gong, Ping Wang, Jianhua Li, Xue-Gong Fan, Shu Zhu, Huan Yang, and Willi Jahnen-Dechent

Subjects
Male, Bacterial Diseases, Cytoplasm, Time Factors, alpha-2-HS-Glycoprotein, medicine.medical_treatment, lcsh:Medicine, Pharmacology, Systemic inflammation, Monocytes, Gene Knockout Techniques, Mice, 0302 clinical medicine, HMGB1 Protein, lcsh:Science, 0303 health sciences, Multidisciplinary, biology, Acute-phase protein, Systemic Inflammatory Response Syndrome, Innate Immunity, 3. Good health, Infectious Diseases, Cytokine, Liver, Cytokines, Medicine, Disease Susceptibility, medicine.symptom, Research Article, Immune Cells, Immunology, Inflammation, HMGB1, Immune Suppression, Cell Line, Sepsis, 03 medical and health sciences, In vivo, medicine, Animals, Biology, 030304 developmental biology, Macrophages, lcsh:R, Immunity, Immunoregulation, Immune Defense, medicine.disease, Endotoxemia, Systemic inflammatory response syndrome, Gene Expression Regulation, Immune System, biology.protein, lcsh:Q, Infectious Disease Modeling, 030217 neurology & neurosurgery, Acute-Phase Proteins
Abstract

Background A liver-derived protein, fetuin-A, was first purified from calf fetal serum in 1944, but its potential role in lethal systemic inflammation was previously unknown. This study aims to delineate the molecular mechanisms underlying the regulation of hepatic fetuin-A expression during lethal systemic inflammation (LSI), and investigated whether alterations of fetuin-A levels affect animal survival, and influence systemic accumulation of a late mediator, HMGB1. Methods and Findings LSI was induced by endotoxemia or cecal ligation and puncture (CLP) in fetuin-A knock-out or wild-type mice, and animal survival rates were compared. Murine peritoneal macrophages were challenged with exogenous (endotoxin) or endogenous (IFN-γ) stimuli in the absence or presence of fetuin-A, and HMGB1 expression and release was assessed. Circulating fetuin-A levels were decreased in a time-dependent manner, starting between 26 h, reaching a nadir around 24–48 h, and returning towards base-line approximately 72 h post onset of endotoxemia or sepsis. These dynamic changes were mirrored by an early cytokine IFN-γ-mediated inhibition (up to 50–70%) of hepatic fetuin-A expression. Disruption of fetuin-A expression rendered animals more susceptible to LSI, whereas supplementation of fetuin-A (20–100 mg/kg) dose-dependently increased animal survival rates. The protection was associated with a significant reduction in systemic HMGB1 accumulation in vivo, and parallel inhibition of IFN-γ- or LPS-induced HMGB1 release in vitro. Conclusions These experimental data suggest that fetuin-A is protective against lethal systemic inflammation partly by inhibiting active HMGB1 release.

Published
2011
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33. Identification and Characterization of a Ste20-Like Kinase in Artemia and Its Role in the Developmental Regulation and Resistance to Environmental Stress.

Author

Zhou, Rong, Sun, Yu-Xia, Yang, Wei-Jun, and Yang, Fan

Subjects
*PROTEIN kinases, *ARTEMIA, *DEVELOPMENTAL biology, *ENVIRONMENTAL engineering, *CRUSTACEA, *ULTRAVIOLET radiation
Abstract

Background: To adapt to extreme environments, the crustacean Artemia has evolved two alternative reproductive pathways. During ovoviviparous (direct) development, nauplius larvae are produced. In contrast, Artemia females release encysted diapause embryos (cysts) via the oviparous pathway. To date, the cellular mechanisms that regulate stress resistance of Artemia remain largely unknown. Ste20-like kinase (SLK) participates in multiple biological processes, including stress responses, apoptosis, and cell cycle progression. Principal Finding: We isolated and characterized a member of the SLK superfamily termed ArSLK from Artemia parthenogenetica. The ArSLK gene is transcribed throughout both ovoviviparous and oviparous development; however, the protein is located mainly in the nuclei of stress-resistant diapause cysts, unlike the nauplii and nauplius-destined embryos where it is cytoplasmic. Interestingly, exposure of nauplii to heat shock, acidic pH, and UV irradiation induced the translocation of ArSLK from cytoplasm to nucleus. This translocation was reversed following stress removal. Moreover, under physiologically-stressful conditions, the nauplius larvae produced by adults after gene knockdown of endogenous ArSLK by RNAi, lost the ability of free-swimming much earlier than those of control larvae from females injected with GFP dsRNA. Conclusions/Significance: Taken together, this study demonstrated that trafficking of ArSLK between the cytoplasm and the nucleus participates in regulating the stress resistance of Artemia. Our findings may provide significant insight into the functions of members of the SLK superfamily. [ABSTRACT FROM AUTHOR]

Published
2014
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34. Effects of DNMT1 and HDAC Inhibitors on Gene-Specific Methylation Reprogramming during Porcine Somatic Cell Nuclear Transfer

Author

Xu, Weihua, Li, Zicong, Yu, Bo, He, Xiaoyan, Shi, Junsong, Zhou, Rong, Liu, Dewu, and Wu, Zhenfang

Subjects
HISTONE deacetylase inhibitors, SOMATIC cells, TRANSPLANTATION of cell nuclei, GENOMIC imprinting, LABORATORY swine, DNA methylation, MOLECULAR genetics
Abstract

Somatic cell nuclear transfer (SCNT) in mammalian cloning currently remains inefficient. Incomplete or erroneous epigenetic reprogramming of specialized donor somatic nuclear and resulting aberrant gene expression during development of cloned embryos is commonly believed as the main reason that causes the low efficiency of SCNT. Use of small molecular reprogramming modifiers to assist the somatic nucleus to mimic naturally occurring DNA methylation and chromatin remodeling in nucleus of fertilization-derived zygotes, has been widely attempted to improve cloning efficiency. However, impacts of these small modifiers on gene-specific methylation dynamics and their potential effects on methylation of imprinted gene have rarely been traced. Here, we attempted two relatively novel DNMT1 inhibitor (DNMTi) and histone deacetylase inhibitor (HDACi), scriptaid and RG108, and demonstrated their effects on dynamics of gene-specific DNA methylation and transcription of porcine SCNT embryos. We found that scriptaid and RG108 had synergetic effects on rescuing the disrupted methylation imprint of H19 during SCNT at least partially by repression over-expressed MBD3 in eight-cell cloned embryos. Furthermore, we firstly identified a differential methylation regions (DMRs) at 5′ flanking regions of XIST gene and found that scriptaid alone and its combination with RG108 modify the dynamics of both transcription and DNA methylation levels in cloned embryos, by different manners. Additionally, we found that scriptaid alone and its combination with RG108 can significantly promote the transcription of NANOG in cloned embryos and enhance their pre-implantation developmental capacity. Our results would contribute to uncovering the epigenetic reprogramming mechanisms underlying the effects of assisted small molecules on improvement of mammalian cloning efficiency. [ABSTRACT FROM AUTHOR]

Published
2013
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35. Acetylation of Chromatin-Associated Histone H3 Lysine 56 Inhibits the Development of Encysted Artemia Embryos.

Author

Zhou, Rong, Yang, Fan, Chen, Dian-Fu, Sun, Yu-Xia, Yang, Jin-Shu, and Yang, Wei-Jun

Subjects
*ACETYLATION, *CHROMATIN, *HISTONES, *LYSINE, *ARTEMIA, *EMBRYOS, *DEACETYLATION, *ENZYME inhibitors
Abstract

Background: As a response to harsh environments, the crustacean artemia produces diapause gastrula embryos (cysts), in which cell division and embryonic development are totally arrested. This dormant state can last for very long periods but be terminated by specific environmental stimuli. Thus, artemia is an ideal model organism in which to study cell cycle arrest and embryonic development. Principal Finding: Our study focuses on the roles of H3K56ac in the arrest of cell cycle and development during artemia diapause formation and termination. We found that the level of H3K56ac on chromatin increased during diapause formation, and decreased upon diapause termination, remaining basal level throughout subsequent embryonic development. In both HeLa cells and artemia, blocking the deacetylation with nicotinamide, a histone deacetylase inhibitor, increased the level of H3K56ac on chromatin and induced an artificial cell cycle arrest. Furthermore, we found that this arrest of the cell cycle and development was induced by H3K56ac and dephosphorylation of the checkpoint protein, retinoblastoma protein. Conclusions/Significance: These results have revealed the dynamic change in H3K56ac on chromatin during artemia diapause formation and termination. Thus, our findings provide insight into the regulation of cell division during arrest of artemia embryonic development and provide further insight into the functions of H3K56ac. [ABSTRACT FROM AUTHOR]

Published
2013
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