作者：
Wang Wen-jing;Wang Yi-fu;Jin Ya-jie;Song Wu-qiang;Lin Jia-meng;...
期刊：
农业科学学报(英文),2023年22(1):320-324 ISSN：2095-3119
作者机构：
[Wang Wen-jing; Tu Jian; Wang Yi-fu] Univ South China, Inst Pharm & Pharmacol, Hunan Prov Key Lab Tumor Microenvironm Respons Dr, Hengyang 421001, Peoples R China.;[Wang Wen-jing; Tong Xin-ru; Jin Ya-jie; Lin Jia-meng; Zhang Yan; Wang Yi-fu; Li Tao; Song Wu-qiang] Chinese Acad Agr Sci, Shanghai Vet Res Inst, Shanghai 200241, Peoples R China.;[Tu Jian] Guilin Med Univ, Guilin 541199, Peoples R China.;[Li Rui-chao] Yangzhou Univ, Coll Vet Med, Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Jiangsu, Peoples R China.
摘要：
An extensively drug-resistant (XDR) Escherichia coli strain 258E was isolated from an anal swab sample of a chicken farm of Anhui Province in China. Genomic analyses indicated that the strain 258E harbors an incompatibility group N (IncN) plasmid pEC258-3, which co-produces bla_(CTX-M-3), bla_(KPC-2), bla_(TEM-1B), qnrS1, aac(6')-Ib-cr, dfrA14, arr-3, and aac(6')-Ib3. Multiple genome arrangement analyses indicated that pEC258-3 is highly homologous with pCRKP-1-KPC discovered in Klebsiella pneumoniae from a patient. Furthermore, conjugation experiments proved that plasmid pEC258-3 can be transferred horizontally and may pose a significant potential threat in animals, community and hospital settings.
作者：
Yang Zhisheng;Chen Zhe;Chen Linxi;Xiong Guozuo
期刊：
生物化学与生物物理学报,2023年55(1):169-171 ISSN：1672-9145
通讯作者：
Chen, L.;Xiong, G.
作者机构：
[Xiong Guozuo; Yang Zhisheng] Department of Vascular Surgery, The Second Affiliated Hospital of University of South China, Hengyang, 421001, China;[Chen Zhe; Chen Linxi] Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, College of Basic Medical Science, Hengyang Medical School, University of South China, Hengyang, 421001, China
通讯机构：
[Chen, L.] I;[Xiong, G.] D;Institute of Pharmacy and Pharmacology, China;Department of Vascular Surgery, China
摘要：
G protein-coupled receptor 35 (GPR35), originally an orphan receptor, was discovered in 1998. At that time, the lack of pharmacological tools and convincingly defined endogenous ligands of GPR35 hindered the understanding of its functions and therapy. De Giovanni et al. recently discovered that 5- hydroxyindoleacetic acid (5-HIAA) is a new ligand of GPR35. Notably, 5-HIAA can promote neutrophil recruitment to inflammatory sites to clear pathogenic bacteria by activating GPR35. Interestingly, this new ligand is derived from platelets and mast cells. Based on this, we briefly commented that platelet and mast cell-derived 5-HIAA activates GPR35 on neutrophils to promote the inflammatory process.
作者机构：
[Yuxin Liu; Xiaoyan Ni; Huini Liu] School of Nursing, University of South China, Hengyang, Hunan, China;[Rong Wang] Department of Internal Medicine-Oncology, The First Affiliated Hospital, University of South China, Hengyang, Hunan, China;Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan, China;[Zifen Guo] School of Nursing, University of South China, Hengyang, Hunan, China<&wdkj&>Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan, China
通讯机构：
[Zifen Guo] S;School of Nursing, University of South China, Hengyang, Hunan, China<&wdkj&>Institute of Pharmacy and Pharmacology, University of South China, Hengyang, Hunan, China
作者机构：
[Ouyang Xueqian; Chen Linxi; Chen Wei; Li Lanfang] Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, China
通讯机构：
[Chen, L.; Li, L.] I;Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China
摘要：
Endoplasmic reticulum(ER)is the largest organelle in eukaryotic cells, which can participate in the maintenance of calcium(Ca~(2+))homeostasis, protein synthesis and organelle communication[1]. Endoplasmic reticulum autophagy(ER-phagy)is a cellular quality control pathway mediated by autophagy receptors. ER-phagy involves the engulfing of excess or misfolded proteins and superfluous ER membrane to form autophagosomes which are degraded by lysosome[1]. ER-phagy occurs under normal conditions and is enhanced during starvation. At present, the receptors of ER-phagy in mammalian cells include family sequence similarity 134[1], membrane B(FAM134B), SEC62, reticulin 3(RTN3), cell cycle progression 1(CCPG1), atlastin GTPase 3(ATL3), testis expressed gene 264(TEX264), tripartite motif containing 13(TRIM13, also known as RFP2), and coiled-coil domain protein 1(CALCOCO1)[2]. FAM134B is recognized as the most characteristic receptor for ER-phagy in mammalian cells[1]. FAM134B consists of a reticulonhomology domain(RHD), a C-terminal cytoplasmic domain and an N-terminal cytoplasmic domain[1]. The RHD region of FAM134B senses and induces ER membrane curvature for ER-phagy. The LC3-interacting region(LIR), located in the C-terminal cytoplasmic domain of FAM134B, is responsible for recruiting and binding the autophagy modifiers LC3 and GABARAP, which involves the engulfing of degradable cargo to phagophore membranes for ER-phagy[1,3]. FAM134B plays a critical role in ER function and quality control through mediating ER-phagy. Inhibition of FAM134B expression leads to ER expansion. Contrarily, up-regulation of FAM134B level results in ER fragmentation[1].
作者机构：
Changde Research Centre for Artificial Intelligence and Biomedicine, College of Life and Environmental Sciences, Hunan University of Arts and Science,,Institute of Pharmacy and Pharmacology, College of Basic Medical Science, Hengyang Medical School, Unive;Institute of Pharmacy and Pharmacology, College of Basic Medical Science, Hengyang Medical School, University of South China;Department of Pharmacology, Yongzhou Vocational Technical College;Institute of Pharmacy and Pharmacology, College of Basic Medical Science, Hengyang Medical School, University of South China,,The First Affiliated Hospital, Department of Pharmacy, Hengyang Medical School, University of South China;[Chen Linxi; Chen Zhe] Institute of Pharmacy and Pharmacology, College of Basic Medical Science, Hengyang Medical School, University of South China, Hengyang, 421200, China
通讯机构：
[Fu, C.; Chen, L.] I;Institute of Pharmacy and Pharmacology, China
摘要：
The phospholipid molecules forming the phospholipid bilayer membrane have difficulties to complete spontaneous trans-bilayer shuttling due to the physicochemical properties and biological functions of the membrane bilayer. However, this transbilayer phospholipid transport is essential in biology. Phospholipid synthesis is concentrated on the membrane of the endoplasmic reticulum (ER) of cells, which occurs only in the monolipid layer on the cytoplasmic side. Therefore, the formation of a complete bilayer membrane requires the phospholipids to be flipped to the other side. Transmembrane translocation of lipids controls transbilayer lipid asymmetry in membranes. ATP-independent scramblases and energy-driven flippases are key factors in maintaining asymmetric phospholipid distribution by promoting transbilayer movement of specific lipids across the cytoplasmic leaflet. ER scramblases promote rapid turnover of lipids and allow them to equilibrate between two membrane leaflets in an ATP-independent manner. Intriguingly, ER transmembrane protein 41B (TMEM41B) was recently identified as a lipid scramblase which mediates transbilayer phospholipid movement and plays a prominent role in maintaining lipoprotein biogenesis and lipid metabolism. The ER is considered to initiate protein and lipid synthesis/transport in eukaryotic cells. Many neutral lipids, including phospholipids and cholesterol utilized for lipoprotein assembly, are synthesized in the ER lumen lipoproteins, indicating that there are tissue-specific phospholipid biosynthetic pathways that vigorously produce phospholipids on the rough ER membrane of liver or intestinal cells. One recent study revealed that the transmembrane cargo receptor SURF4 selectively transports hepatic lipid-carrying lipoproteins from the ER to the Golgi through coat protein complex II (COPII)-coated transport vesicles. Synergistic pairing between SURF4 and the molecular switch SAR1B operates a sensitive transport program for hepatic lipoprotein secretion and maintains circulating lipid homeostasis (Figure 1). Furthermore, TMEM41B is detected in a hepatic protein complex of SURF4 and lipoproteins, which is present in the SURF4-mediated ER transport of lipid cargos and implicated in lipid equilibration between the membrane leaflets.
作者机构：
[Hong L.; Fangqun L.] Department of Pharmacy, Changsha Central Hospital Affiliated to University of South China, Changsha, 410004, China;[Chaohui Z.] Department of Pharmacy, Changsha Sanyi Rehabilitation Hospital, Changsha, 410004, China;[Hengbei Z.] Office of Drug Use and Adverse Reaction Supervision, Changsha Administration for Market Regulation, Changsha, 410013, China
通讯机构：
[Hong, L.] D;Department of Pharmacy, Changsha Central Hospital Affiliated to University of South China, Changsha, China
作者机构：
[苏琦; 曹振华; 李志敏; 刘芳] Cancer Research Institute, Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan Provincial University Hengyang, Hunan, 421001, China;Clinical Anatomy and Reproductive Medicine Application Institute, Hunan, Hengyang, 421001, China;Institute of Pharmacy and Pharmacology, Hengyang Medical School, University of South China, Hunan, Hengyang, 421001, China;[苏波] Cancer Research Institute, Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan Provincial University Hengyang, Hunan, 421001, China, Institute of Pharmacy and Pharmacology, Hengyang Medical School, University of South China, Hunan, Hengyang, 421001, China;[何慧] Cancer Research Institute, Key Laboratory of Cancer Cellular and Molecular Pathology of Hunan Provincial University Hengyang, Hunan, 421001, China, Clinical Anatomy and Reproductive Medicine Application Institute, Hunan, Hengyang, 421001, China
作者机构：
[Chen L.; Li L.; Fan S.; Chen W.] Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, 421001, China
通讯机构：
[Chen, L.; Li, L.] I;Institute of Pharmacy and Pharmacology, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, China
关键词：
DRUGS;ORGANS;TREATMENT
摘要：
Fibrosis, the self-repair process of the body after tissue damage, is a common pathological feature of many chronic inflammatory diseases. It occurs in a variety of organs, leading to structural destruction and hypofunction, and even organ failure. Fibrosis in organ tissues is characterized by chronic inflammation, excessive accumulation of extracellular matrix (ECM) components, and the decrease of parenchymal cells. Fibrosis is caused by persistent infections, toxins, autoimmune diseases, radiation, and mechanical injury. To date, there are various therapeutic strategies for organ fibrosis, such as changing lifestyle, using antiviral drugs, anti-in-flammatory treatment, using interferon, and organ transplantation. Currently, there are only two FDA-approved drugs for the treatment of idiopathic pulmonary fibrosis (IPF), i.e., pirfenidone and nintedanib. Nevertheless, the mechanisms of action of these drugs are not fully understood, the cost is high, and there is no way to prevent or reverse the disease process. Consequently, it is extremely important for us to better understand the pathogenesis of fibrosis, strengthen the screening and evaluation of new drugs, and improve the existing drugs. And it can also help us to treat and prevent fibrosis in the future.
作者：
Yang Wu-Zhou;Li Heng;Yu Xiao-Hua;Zhang Jie;Huang Xin-Yun;...
期刊：
生物化学与生物物理进展,2022年49(2):401-412 ISSN：1000-3282
通讯作者：
Cao Qi;Tang, CK
作者机构：
[Li Heng; Cao Qi; Yang Wu-Zhou; Zhao Zhen-Wang; Zhang Jie; Tang Chao-Ke; Huang Xin-Yun] Univ South China, Key Lab Arteriosclerol Hunan Prov, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Affiliated Hosp 2,Inst Cardiovasc Dis, Hengyang 421001, Peoples R China.;[Yu Xiao-Hua] Hainan Med Univ, Inst Clin Med, Affiliated Hosp 2, Haikou 460106, Peoples R China.
通讯机构：
[Cao, Q; Tang, CK ] U;Univ South China, Key Lab Arteriosclerol Hunan Prov, Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Affiliated Hosp 2,Inst Cardiovasc Dis, Hengyang 421001, Peoples R China.
关键词：
miR-216b;ABCG1
摘要：
Objective To investigated the function and the target gene of miR-216b in osteoclast differentiation and explored its effect on osteoclast cholesterol efflux.Methods The cell model of RAW264.7 osteoclast precursor cell differentiation induced by RANKL stimulation was established.Tartrate-resistant acid phosphatase(TRAP)staining assay was conducted to evaluate osteoclasts differentiation.MiR-216b target gene,ABCG1 3' untranslated region(3'UTR)sequence and free energy were predicted and analyzed by bioinformatics analyses and dual-luciferase reporter assays.MiR-216b mimic or inhibitor transfection was performed to verify the role of miR-216b in osteoclast differentiation.Liquid scintillation counting was used to measure [3H]-labeled cholesterol efflux from RAW264.7 macrophage-derived osteoclasts.The lipid accumulation in RAW264.7 macrophages was detected by high performance liquid chromatography(HPLC).Real-time quantitative PCR(RT-qPCR)and Western blot assays were used to assess the transcriptional and post-transcriptional levels of ABCG1 in osteoclasts.Results Our results showed that the number of osteoclasts,the average diameter of osteoclasts and the fusion index were significantly increased when cells were transfected with miR-216b mimic,as revealed by tartrate-resistant acid phosphatase-positive staining and microscopy assay.MiR-216b inhibitor showed the complete opposite outcome which brought additional evidence to our findings.Bioinformatics analysis and dualluciferase reporter assays showed that miR-216b targets the 3'UTR of ABCG1.Moreover,miR-216b suppressed both the mRNA and protein levels of ABCG1 in osteoclasts.Besides,we found that silencing of ABCG1 by ABCG1 siRNA increased the number of osteoclasts,the average diameter of osteoclasts and the fusion index.MiR-216b reduced cholesterol efflux from osteoclasts by inhibiting ABCG1 expression.Conclusion Collectively,these findings suggest that miR-216b downregulates ABCG1 expression and inhibits osteoclast cholesterol efflux,which disturbs cholesterol homeostasis and promotes osteoclastogenesis.
作者：
Hu Xiao-Bo;Duan Ting-Ting;Liu Jun;Zhu Gao-Lu;Cao Zhao-Hui;...
期刊：
中华医学杂志(英文版),2021年134(1):41-43 ISSN：0366-6999
作者机构：
[Duan Ting-Ting; Zhu Gao-Lu] The Key Laboratory of Ecological Environment and Critical Human Diseases Prevention, Education Department of Hunan Province, Department of Biochemistry, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China;The Key Laboratory of Typical Environmental Pollution and Health Hazards, Hunan Province, University of South China, Hengyang, Hunan 421001, China;[Feng Shao-Long] The Institute of Preventive Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi 541004, China.;[Hu Xiao-Bo; Liu Jun; Cao Zhao-Hui] The Key Laboratory of Ecological Environment and Critical Human Diseases Prevention, Education Department of Hunan Province, Department of Biochemistry, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China<&wdkj&>The Key Laboratory of Typical Environmental Pollution and Health Hazards, Hunan Province, University of South China, Hengyang, Hunan 421001, China
摘要：
Type 1 diabetes (T1D) is an organ-specific autoimmune disease with loss of pancreatic β-cells, characterized by reduced insulin levels and increased blood glucose. The incidence of T1D is increasing by approximately 2% to 5% worldwide every year and becoming a global health problem. Vitamin D (VD) deficiency was reported to be a risk factor in the development of T1D. Recent studies showed that supplementation of VD alleviated disease symptoms in T1D patients. However, a few randomized controled trials (RCTs) demonstrated the clinical effect of VD treatment with inconsistent findings. This article aimed to evaluate the effect of VD supplementation in T1D, which is helpful to develop an adjuvant therapy for T1D.
摘要：
Endoplasmic reticulum (ER) stress plays a critical role in pancreatic beta cell destruction which leads to the pathogenesis of type 1 diabetes mellitus (T1DM). Vitamin D (VD) has been reported to reduce the risk of T1DM; however, it remains unknown whether VD affects ER stress in pancreatic beta cells. In this study, we investigated the role of the active form of VD, 1,25-dihydroxyvitamin D3 [1,25-(OH)(2)D-3], in ER stress-induced beta cell apoptosis and explored its potential mechanism in mouse insulinoma cell line mouse insulinoma 6 (MIN6). The results of cell counting kit-8 (CCK8) and flow cytometric analyses showed that 1,25-(OH)(2)D-3 caused a significant increase in the viability of MIN6 cells injured by H2O2. The protein kinase like ER kinase (PERK) signal pathway, one of the most conserved branches of ER stress, was found to be involved in this process. H2O2 activated the phosphorylation of PERK, upregulated the activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP) expression, and subsequently initiated cell apoptosis, which were significantly reversed by 1,25-(OH)(2)D-3 pretreatment. In addition, GSK2606414, a specific inhibitor of PERK, suppressed PERK phosphorylation and reduced the expressions of ATF4 and CHOP, leading to a significant decrease in beta cell apoptosis induced by H2O2. Taken together, the present findings firstly demonstrated that 1,25-(OH)(2)D-3 could prevent MIN6 cells against ER stress-associated apoptosis by inhibiting the PERK-ATF4-CHOP pathway. Therefore, our results suggested that 1,25-(OH)(2)D-3 might serve as a potential therapeutic target for preventing pancreatic beta cell destruction in T1DM.
作者机构：
[Zhaohui Cao; Wenjie Wei; Zhijie He; Yuqing Xiong; Tingting Duan; Xiaobo Hu] Department of Biochemistry,Hengyang Medical School,University of South China,Hengyang 421001,China
关键词：
STASIS;DISEASES;STRESS
摘要：
Cell–cell communication plays a critical role in cell proliferation, differentiation, morphogenesis, functiogenesis, and tissue homoeostasis in multicellular organisms, while abnormal communication among cells may disrupt biological processes [1]. Intercellular communication is largely mediated by gap junctions (GJs), consisting of arrays of intercellular channels that enable cells to communicate by allowing ions and small molecules to directly transfer between neighboring cells [2]. Three families of integral membrane proteins forming GJ have been identified as innexins, connexins, and pannexins [2]. In vertebrates, six connexins (Cxs) oligomerized to connexons function as hemichannels and assemble into GJs, providing a channel for direct exchange of small signaling molecules between adjacent cells [2]. Cx43, a 43-kDa protein, as the most widely expressed Cx, plays essential roles in regulating many physiological and pathological processes in various tissues [3–7]. Recently, accumulating studies implicated that increased intercellular GJ activity and Cx43 expression play a critical role in the pathogenesis of atherosclerosis [3], chronic kidney disease [4], rheumatoid arthritis [5], osteoarthritis [6], and neurodegenerative diseases [7], which are associated with chronic inflammation and cellular stress. These findings suggested that increased intercellular communication might be a common feature of conditions characterized by various cellular stresses.
作者机构：
[简雪婷; 冯晓祎; 熊菀伶; 谢灵兮; 谭俊艳; 王萍; 刘阳] Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hunan Provincial Key Laboratory of Tumor Microenvironment Responsive Drug Research, College of Pharmacy, University of South China, Hengyang;421001, China;[简雪婷; 冯晓祎; 熊菀伶; 谢灵兮; 谭俊艳; 王萍; 刘阳] 421001, China
通讯机构：
[Liu, Y.] H;Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, China
