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3. The emerging roles of UFMylation in the modulation of immune responses.

Author

Liang, Zhengyan, Ning, Rongxuan, Wang, Zhaoxiang, Kong, Xia, Yan, Yubin, Cai, Yafei, He, Zhiwei, Liu, Xin‐guang, Zou, Yongkang, and Zhou, Junzhi

Subjects
BIOLOGICAL systems, RITES & ceremonies, IMMUNOREGULATION, HOMEOSTASIS, IMMUNE response
Abstract

Post‐translational modification is a rite of passage for cellular functional proteins and ultimately regulate almost all aspects of life. Ubiquitin‐fold modifier 1 (UFM1) system represents a newly identified ubiquitin‐like modification system with indispensable biological functions, and the underlying biological mechanisms remain largely undiscovered. The field has recently experienced a rapid growth of research revealing that UFMylation directly or indirectly regulates multiple immune processes. Here, we summarised important advances that how UFMylation system responds to intrinsic and extrinsic stresses under certain physiological or pathological conditions and safeguards immune homeostasis, providing novel perspectives into the regulatory framework and functions of UFMylation system, and its therapeutic applications in human diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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10. A Comprehensive Analysis of Replicative Lifespan in 4,698 Single-Gene Deletion Strains Uncovers Conserved Mechanisms of Aging

Author

McCormick, Mark A, Delaney, Joe R, Tsuchiya, Mitsuhiro, Tsuchiyama, Scott, Shemorry, Anna, Sim, Sylvia, Chou, Annie Chia-Zong, Ahmed, Umema, Carr, Daniel, Murakami, Christopher J, Schleit, Jennifer, Sutphin, George L, Wasko, Brian M, Bennett, Christopher F, Wang, Adrienne M, Olsen, Brady, Beyer, Richard P, Bammler, Theodor K, Prunkard, Donna, Johnson, Simon C, Pennypacker, Juniper K, An, Elroy, Anies, Arieanna, Castanza, Anthony S, Choi, Eunice, Dang, Nick, Enerio, Shiena, Fletcher, Marissa, Fox, Lindsay, Goswami, Sarani, Higgins, Sean A, Holmberg, Molly A, Hu, Di, Hui, Jessica, Jelic, Monika, Jeong, Ki-Soo, Johnston, Elijah, Kerr, Emily O, Kim, Jin, Kim, Diana, Kirkland, Katie, Klum, Shannon, Kotireddy, Soumya, Liao, Eric, Lim, Michael, Lin, Michael S, Lo, Winston C, Lockshon, Dan, Miller, Hillary A, Moller, Richard M, Muller, Brian, Oakes, Jonathan, Pak, Diana N, Peng, Zhao Jun, Pham, Kim M, Pollard, Tom G, Pradeep, Prarthana, Pruett, Dillon, Rai, Dilreet, Robison, Brett, Rodriguez, Ariana A, Ros, Bopharoth, Sage, Michael, Singh, Manpreet K, Smith, Erica D, Snead, Katie, Solanky, Amrita, Spector, Benjamin L, Steffen, Kristan K, Tchao, Bie Nga, Ting, Marc K, Wende, Helen Vander, Wang, Dennis, Welton, K Linnea, Westman, Eric A, Brem, Rachel B, Liu, Xin-guang, Suh, Yousin, Zhou, Zhongjun, Kaeberlein, Matt, and Kennedy, Brian K

Subjects
Genetics, Nutrition, Biotechnology, Aging, Underpinning research, 1.1 Normal biological development and functioning, Generic health relevance, Animals, Basic-Leucine Zipper Transcription Factors, Caenorhabditis elegans, Caloric Restriction, DNA Damage, Gene Deletion, Gene Expression Regulation, Genome, Longevity, Nuclear Pore Complex Proteins, RNA, Transfer, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Biochemistry and Cell Biology, Medical Biochemistry and Metabolomics, Endocrinology & Metabolism
Abstract

Many genes that affect replicative lifespan (RLS) in the budding yeast Saccharomyces cerevisiae also affect aging in other organisms such as C. elegans and M. musculus. We performed a systematic analysis of yeast RLS in a set of 4,698 viable single-gene deletion strains. Multiple functional gene clusters were identified, and full genome-to-genome comparison demonstrated a significant conservation in longevity pathways between yeast and C. elegans. Among the mechanisms of aging identified, deletion of tRNA exporter LOS1 robustly extended lifespan. Dietary restriction (DR) and inhibition of mechanistic Target of Rapamycin (mTOR) exclude Los1 from the nucleus in a Rad53-dependent manner. Moreover, lifespan extension from deletion of LOS1 is nonadditive with DR or mTOR inhibition, and results in Gcn4 transcription factor activation. Thus, the DNA damage response and mTOR converge on Los1-mediated nuclear tRNA export to regulate Gcn4 activity and aging.

Published
2015

12. Clonal hematopoiesis in unexplained cytopenias

Author

Wu, Han‐yang, primary, Gu, Chao‐yang, additional, Liu, Shuang, additional, Dong, Qiao‐feng, additional, Dong, Lin, additional, Wang, Liang, additional, Wang, Xin‐ru, additional, Cui, Si‐yuan, additional, Li, Zhao, additional, Liu, Xin‐guang, additional, Ma, Dao‐xin, additional, and Ji, Chun‐yan, additional

Published
2023
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17. The Distribution, Drug Susceptibility, and Dynamic Trends of Pseudomonas aeruginosa Infection in a Tertiary Hospital in China During 2016‒2022

Author

Li,Xiao-Yan, Liu,Xin-Guang, Dong,Zhi-Ling, Chai,Liang-Ting, Liu,Yan-Jun, Qi,Jie, and Zhao,Jie

Subjects
Infection and Drug Resistance
Abstract

Xiao-Yan Li,1 Xin-Guang Liu,2 Zhi-Ling Dong,1 Liang-Ting Chai,3 Yan-Jun Liu,4 Jie Qi,3 Jie Zhao1 1Department of Clinical Laboratory, Handan Central Hospital, Handan, Hebei, People’s Republic of China; 2Department of Clinical Laboratory, Children’s Hospital of Hebei, Shijiazhuang, Hebei, People’s Republic of China; 3Department of Clinical Laboratory, Handan First Hospital, Handan, Hebei, People’s Republic of China; 4Department of General Surgery, Handan Central Hospital, Handan, Hebei, People’s Republic of ChinaCorrespondence: Jie Zhao, No. 59 Congtai North Road, Congtai District, Handan City, Hebei Province, 057150, People’s Republic of China, Tel +86-18003205055, Email zjlxy8160@163.comBackground: Drug-resistant Pseudomonas aeruginosa infections rapidly increased and contributed to life-threatening nosocomial infections; however, the distribution, species, drug susceptibility and dynamic trends of P. aeruginosa infection in China remained unclear. This study was conducted to better understand the epidemiological data of increased P. aeruginosa infections from 2016 to 2022 in a hospital in China.Methods: This study involved 3301 patients infected with P. aeruginosa, diagnosed using a nosocomial infection surveillance system in a tertiary hospital between 2016 and 2022. The P. aeruginosa infections from 2016 to 2022 were assessed according to the hospital department and species, and the drug susceptibility was evaluated using 16 antimicrobial agents.Results: The P. aeruginosa infection prevalence in the hospital department was: Neurosurgery (14.30%), Emergency (13.30%), and Critical Care Medicine (11.69%). Samples for P. aeruginosa infection identification were from sputum (72.52%) and other secreta (9.91%). The P. aeruginosa infections demonstrated a greater sensitivity to amikacin (AMK, 91.82%), tobramycin (TOB, 82.79%), and gentamycin (GEN, 82.01%); however, P. aeruginosa infection demonstrated greater resistance to ticarcillin (22.57%), levofloxacin (21.63%), and ciprofloxacin (18.00%).Conclusion: The P. aeruginosa infections were commonly observed in the Neurosurgery, Emergency, and Critical Care Medicine departments and demonstrated greater sensitivity to AMK, TOB, and GEN than the other drugs.Keywords: Pseudomonas aeruginosa, distribution, drug susceptibility, dynamic trend

Published
2023

18. Chinese guidelines for treatment of adult primary immune thrombocytopenia

Author

Liu, Xin-guang, Bai, Xiao-chuan, Chen, Fang-ping, Cheng, Yun-feng, Dai, Ke-sheng, Fang, Mei-yun, Feng, Jian-Ming, Gong, Yu-ping, Guo, Tao, Guo, Xin-hong, Han, Yue, Hong, Luo-jia, Hu, Yu, Hua, Bao-lai, Huang, Rui-bing, Li, Yan, Peng, Jun, Shu, Mi-mi, Sun, Jing, Sun, Pei-yan, Sun, Yu-qian, Wang, Chun-sen, Wang, Shu-jie, Wang, Xiao-min, Wu, Cong-ming, Wu, Wen-man, Yan, Zhen-yu, Yang, Feng-e, Yang, Lin-hua, Yang, Ren-Chi, Yang, Tong-hua, Ye, Xu, Zhang, Guang-sen, Zhang, Lei, Zheng, Chang-cheng, Zhou, Hu, Zhou, Min, Zhou, Rong-fu, Zhou, Ze-ping, Zhu, Hong-li, Zhu, Tie-nan, and Hou, Ming

Published
2018
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30. Pathogenesis-oriented approaches for the management of corticosteroid-resistant or relapsedprimary immune thrombocytopenia

Author

Liu Xin-guang and Hou Ming

Subjects
itp, pathogenesis, management, Medicine
Abstract

Primary immune thrombocytopenia (ITP) is a complex autoimmune disorder in which the patient’s immune system reacts with platelet autoantigens resulting in immune-mediated platelet destruction and/or suppression of platelet production. Corticosteroids can induce sustained remission rates in 50% to 75% of patients with active ITP. For these patients who are unresponsive to glucocorticoids, or relapsed after an initial response, multiple second-line treatment modalities can be chosen. However, how to make an optimal therapeutic strategy for a specific patient still remains a major challenge. As the pathogenetic heterogeneity of the ITP is increasingly identified, pathogenesis-oriented approach might offer an opportunity to improve the outcome of corticosteroid-resistant or relapsed ITP.

Published
2016
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37. Overexpression of Progerin Results in Impaired Proliferation and Invasion of Non-Small Cell Lung Cancer Cells

Author

Hu, Xiao-Ting, Song, Hao-Chang, Yu, Hui, Wu, Zu-Chun, Liu, Xin-Guang, and Chen, Wei-Chun

Subjects
integumentary system, A549 lung cancer cells, progerin, DNA damage, cell cycle, respiratory system, invasion, OncoTargets and Therapy, respiratory tract diseases, Original Research
Abstract

Xiao-Ting Hu, Hao-Chang Song, Hui Yu, Zu-Chun Wu, Xin-Guang Liu, Wei-Chun Chen Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Institute of Aging Research, Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Dongguan, Guangdong, People’s Republic of ChinaCorrespondence: Wei-Chun Chen; Xin-Guang LiuGuangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Institute of Aging Research, Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Dongguan, Guangdong, People’s Republic of ChinaTel +86759 22896026Email chenwchun@126.com; xgliu64@126.comPurpose: The accumulation of progerin (PG) in patients is responsible for the pathogenesis of Hutchinson-Gilford Progeria Syndrome (HGPS) because it triggers accelerated aging of cells. However, there are few studies on the effects of progerin on tumor cells. Lung cancer is one of the most common malignant cancers with high global morbidity and mortality rates; non-small cell lung cancer accounts for the majority of cases. The purpose of this study was to determine the effects of progerin on A549 cell proliferation, cell cycle, invasion, migration, sensitivity to DNA damaging agents, senescence and apoptosis with a goal of exploring new ideas for lung cancer treatment.Methods: A549 cells overexpressing progerin (A549-PG) and a corresponding blank control (A549-GFP) were constructed by lentiviral infection. A nuclear staining assay was utilized to detect abnormal nuclear morphology. The proliferation, cell cycle, colony formation, invasion and migration abilities of A549-PG were compared with those of A549-GFP via EdU assays, flow cytometry, colony formation experiments, and Matrigel invasion and migration assays, respectively. SA‐β‐gal staining was used to measure senescence in cells.Results: The expression of progerin was significantly higher in A549-PG than A549-GFP. About 20% of A549-PG possessed abnormal nuclei. Overexpression of progerin in A549 cells inhibited cell proliferation, migration and invasion, and associated proteins (CDK4, pRB, ANLN, MMP7 and MMP9) were downregulated. DNA damage repair was also impaired. Progerin did not cause cells to senesce, and there was no difference in apoptosis.Conclusion: A549-PG generated some cellular changes, including the nuclear skeleton, the cell cycle, DNA damage repair, and migration and invasion abilities. Our data indicate that progerin could cause an imbalance in the steady state in A549 cells and increase their sensitivity to chemotherapeutic drugs.Keywords: A549 lung cancer cells, progerin, cell cycle, invasion, DNA damage

Published
2020

38. Effect of the 5-HT4 receptor and serotonin transporter on visceral hypersensitivity in rats

Author

Chi Yan, Liu Xin-Guang, Wang Hua-Hong, Li Jun-Xia, and Li Yi-Xuan

Subjects
5-Hydroxytryptamine receptor, Serotonin, Serotonin transport protein, Visceral hypersensitivity, SERT expression, Medicine (General), R5-920, Biology (General), QH301-705.5
Abstract

Visceral hypersensitivity plays an important role in motor and sensory abnormalities associated with irritable bowel syndrome, but the underlying mechanisms are not fully understood. The present study was designed to evaluate the expression of the 5-HT4 receptor and the serotonin transporter (SERT) as well as their roles in chronic visceral hypersensitivity using a rat model. Neonatal male Sprague-Dawley rats received intracolonic injections of 0.5% acetic acid (0.3-0.5 mL at different times) between postnatal days 8 and 21 to establish an animal model of visceral hypersensitivity. On day 43, the threshold intensity for a visually identifiable contraction of the abdominal wall and body arching were recorded during rectal distention. Histological evaluation and the myeloperoxidase activity assay were performed to determine the severity of inflammation. The 5-HT4 receptor and SERT expression of the ascending colon were monitored using immunohistochemistry and Western blot analyses; the plasma 5-HT levels were measured using an ELISA method. As expected, transient colonic irritation at the neonatal stage led to visceral hypersensitivity, but no mucosal inflammation was later detected during adulthood. Using this model, we found reduced SERT expression (0.298 ± 0.038 vs 0.634 ± 0.200, P < 0.05) and increased 5-HT4 receptor expression (0.308 ± 0.017 vs 0.298 ± 0.021, P < 0.05). Treatment with fluoxetine (10 mg·kg-1·day-1, days 36-42), tegaserod (1 mg·kg-1·day-1, day 43), or the combination of both, reduced visceral hypersensitivity and plasma 5-HT levels. Fluoxetine treatment increased 5-HT4 receptor expression (0.322 ± 0.020 vs 0.308 ± 0.017, P < 0.01) but not SERT expression (0.219 ± 0.039 vs 0.298 ± 0.038, P = 0.654). These results indicate that both the 5-HT4 receptor and SERT play a role in the pathogenesis of visceral hypersensitivity, and its mechanism may be involved in the local 5-HT level.

Published
2012

39. Research letters

Author

Chhina, Amitoj Singh, Shenoi, Arvind, Nagendra, Namrata, Rao, Nilesh, Raja, Malathi, Fan, Qiu-Xia, Wang, Chun-Mei, Chen, Shu-Xia, Liu, Xin-Guang, and Han, Bo

Published
2016
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45. Two new sesquiterpenes from the rhizomes of Atractylodes macrocephala and their biological activities

Author

Zhao, Yi-Nan, Gao, Gai, Ma, Jin-Lian, Xu, Rui-Zhu, Guo, Tao, Wu, Li-Min, Liu, Xin-Guang, Xie, Zhi-Shen, Xu, Jiang-Yan, Zhang, Zhen-Qiang, and Wang, Pan

Abstract

Two new sesquiterpenes, named selina-4(14),7,11-trien-9-ol (1) and selina-4(14),11-dien-7-ol (2), along with two known compounds were isolated from rhizomes of Atractylodes macrocephala Koidz. All structures were assigned on the basis of detailed spectroscopic analyses. The absolute configuration of 1 was established by TDDFT-ECD calculations. Compound 1 was found to moderately inhibit LSD1 activity with IC50 value of 34.0 μM. Compounds 1 and 4 exhibited a regulate effect on Keap1-Nrf2-ARE pathway.

Published
2021
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49. Overexpression of Progerin Results in Impaired Proliferation and Invasion of Non-Small Cell Lung Cancer Cells

Author

Hu,Xiao-Ting, Song,Hao-Chang, Yu,Hui, Wu,Zu-Chun, Liu,Xin-Guang, Chen,Wei-Chun, Hu,Xiao-Ting, Song,Hao-Chang, Yu,Hui, Wu,Zu-Chun, Liu,Xin-Guang, and Chen,Wei-Chun

Abstract

Xiao-Ting Hu, Hao-Chang Song, Hui Yu, Zu-Chun Wu, Xin-Guang Liu, Wei-Chun Chen Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Institute of Aging Research, Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Dongguan, Guangdong, People’s Republic of ChinaCorrespondence: Wei-Chun Chen; Xin-Guang LiuGuangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Institute of Aging Research, Institute of Biochemistry & Molecular Biology, Guangdong Medical University, Dongguan, Guangdong, People’s Republic of ChinaTel +86759 22896026Email chenwchun@126.com; xgliu64@126.comPurpose: The accumulation of progerin (PG) in patients is responsible for the pathogenesis of Hutchinson-Gilford Progeria Syndrome (HGPS) because it triggers accelerated aging of cells. However, there are few studies on the effects of progerin on tumor cells. Lung cancer is one of the most common malignant cancers with high global morbidity and mortality rates; non-small cell lung cancer accounts for the majority of cases. The purpose of this study was to determine the effects of progerin on A549 cell proliferation, cell cycle, invasion, migration, sensitivity to DNA damaging agents, senescence and apoptosis with a goal of exploring new ideas for lung cancer treatment.Methods: A549 cells overexpressing progerin (A549-PG) and a corresponding blank control (A549-GFP) were constructed by lentiviral infection. A nuclear staining assay was utilized to detect abnormal nuclear morphology. The proliferation, cell cycle, colony formation, invasion and migration abilities of A549-PG were compared with those of A549-GFP via EdU assays, flow cytometry, colony formation experiments, and Matrigel invasion and migration assays, respectively. SA‐β‐gal staining was used to measure senescence in cells.Results: The expression of progerin was significantly higher in A549-PG than A549-GFP. About 20% of A549-PG possessed ab

Published
2020

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