作者机构:
[Shi, J.-F.] Institute of Cardiovascular Diseases, University of South China, Hengyang Hunan, 421001, China;[She, M.-H.; Yang, J.] Dept of Biotechnology, Institute of Pharmaceutical and Biological Sciences, University of South China, Hengyang Hunan, 421001, China;[Zhang, X.-H.] Aier Eye Hospital, Hengyang Hunan, 421001, China;First People's Hospital of Changde, Changde Hunan, 415003, China;[Moshe, L.] Neurim Pharmaceuticals Ltd., Israel
通讯机构:
[Zheng, Xing] U;[Zhao, Weili] F;[Zheng, Xing] H;Univ South China, Inst Pharm & Pharmacol, Hengyang 421001, Hunan, Peoples R China.;Fudan Univ, Sch Pharm, Shanghai 201203, Peoples R China.
关键词:
fluorescent probe;palladium;living cell
摘要:
A novel turn-on fluorescent probe for the detection of palladium has been designed. The probe can selectively and sensitively detect palladium in solution, and the limit of detection was calculated to be 11.4 nmol?L~(-1). Furthermore, the probe was successfully used for fluorescence imaging of palladium in living cells.
摘要:
目的预测has-miR-16靶基因并对靶基因的分子功能、生物学过程和信号转导通路富集性分析,全面认识miR-16涉及的生命过程和疾病。方法通过阅读文献结合生物信息学预测的方法得出靶基因集合,用Cytoscape 3.2. 1软件和DAVID(the database for annnotation visualization and integrated discovery)数据库分别对靶基因GO(gene ontology)注释和KEGG(kyoto encyclopedia of genes and genomes)信号转导通路进行富集性分析。结果各物种已知的成熟miR-16序列具有高度保守性。397个靶基因在分子功能上显著富集于蛋白结合、DNA结合、酶类活性、胰岛素样生长因子受体活性等功能,在生物学过程显著富集于发育过程、细胞粘附、神经发生、细胞代谢和细胞周期调控等过程。靶基因显著富集的信号通路有癌症通路、p53信号通路、神经营养因子信号通路等通路。结论从分析结果得出has-miR-16通过调控靶基因参与了人类生命活动和疾病过程的很多方面,尤其在癌症的病理过程是一个值得进一步研究的方向。
作者机构:
[Tian Shuai; Ma Yun] Univ South China, Dept Biochem & Biol, Hengyang 421001, Peoples R China.;[Ma Yun] Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Peoples R China.
通讯机构:
[Ma Yun] U;[Ma Yun] H;Univ South China, Dept Biochem & Biol, Hengyang 421001, Peoples R China.;Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Peoples R China.
关键词:
脆性X综合征;FXR1P学科
摘要:
脆性X综合征(fragile X syndrome,FXS)是最常见的遗传性认知障碍疾病,也是一种与自闭症谱系障碍(autism spectrum disorder,ASD)相关的严重的基因疾病.它主要是由于脆性X智力低下基因1(fragile X mental retardation 1,FMR1)的异常扩增及其上游CpG岛的异常甲基化,导致其编码的脆性X智力低下蛋白(fragile X mental retardation protein,FMRP)表达减少或缺失引起的.FMRP与miRNA(microRNA)均具有翻译抑制活性,而且FMRP在生物化学和遗传学上均与miRNA调控通路有相互作用.此外,越来越多的研究发现miRNA调控通路在FXS的发病和治疗中发挥作用.因此,本文对miRNA的功能及其与脆性X蛋白家族成员间的相互作用进行阐述,为在miRNA水平了解FXS的发病机制奠定基础.
作者机构:
[Hong Zhao] Institute of Pharmacy and Pharmacology, Hunan Province Cooperative innovation Center for Molecular Target New Drugs Study, University of South China, Hengyang 421001, China;[Pingbo Yao] Intensive Care Units of the Affiliated Nanhua Hospital, University of South China, Hengyang 421002, China;[Lanfang Li; Linxi Chen] Institute of Pharmacy and Pharmacology, Hunan Province Cooperative innovation Center for Molecular Target New Drugs Study, University of South China, Hengyang 421001, China llfwjl@126.com lxchen6@126.com
通讯机构:
[Li, L.] I;Institute of Pharmacy and Pharmacology, Hunan Province Cooperative Innovation Center for Molecular Target New Drugs Study, University of South China, Hengyang, China
关键词:
Apelin;mechanism;polarization
摘要:
Cellular polarization is common to many types of cells, such as vascular endothelial cells (ECs), macrophages, and epithelial cells [1]. An individual cell has opposite sides and the directions of imaginary axes connecting opposite sides are highly coordinated. This coordination of the polarization axes is essential for the function of organs, named planar cell polarity (PCP) [2]. It occurs when cell organelles, cytoskeleton, and/or adhesion complexes display unidirectional organization along an axis. The ECs are continuously exposed to shear stress, and they directly exhibit profound morphological adaptations, such as planar cell polarization, elongation, and alignment of microtubules. In addition, the state of cell junctions and dynamic rearrangements of cytoskeleton are important for the establishment of flow-induced EC polarization, which is a significant determinant of maintaining vascular homeostasis.
摘要:
Autophagy is conserved in nature from lower eukaryotes to mammals and is an important self-cannibalizing, degradative process that contributes to the elimination of superfluous materials. Cardiac hypertrophy is primarily characterized by excess protein synthesis, increased cardiomyocyte size, and thickened ventricular walls and is a major risk factor that promotes arrhythmia and heart failure. In recent years, cardiomyocyte autophagy has been considered to play a role in controlling the hypertrophic response. However, the beneficial or aggravating role of cardiomyocyte autophagy in cardiac hypertrophy remains controversial. The exact mechanism of cardiomyocyte autophagy in cardiac hypertrophy requires further study. In this review, we summarize the controversies associated with autophagy in cardiac hypertrophy and provide insights into the role of autophagy in the development of cardiac hypertrophy. We conclude that future studies should emphasize the relationship between autophagy and the different stages of cardiac hypertrophy, as well as the autophagic flux and selective autophagy. Autophagy will be a potential therapeutic target for cardiac hypertrophy.
作者机构:
[Lanfang Li; Di Wu] Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China;[Linxi Chen] Institute of Pharmacy and Pharmacology, University of South China, Hengyang 421001, China lxchen6@126.com
通讯机构:
[Chen, L.] I;Institute of Pharmacy and Pharmacology, University of South China, Hengyang, China
关键词:
应激性疾病;肿瘤转移;治疗;通道;敏感;癌症患者;转移过程;肿瘤细胞
摘要:
Cancer metastasis is a process that cancer cells deviate from the primary site and spread to the other areas to form new colonies, which is the leading cause of death in cancer patients. During metastatic progression, circulating cancer cells lodge within the microvasculature of end organs, where most of them die from mechanical deformation. However, cancer cells can survive from mechanical deformation by unknown mechanisms. Recently, Furlow et al. identified a mutation truncated form of pannexin-1 (Panx-1), PANX1~(1–89), which was significantly enriched in highly metastatic cancer cells. PANX1~(1–89) augmented Panx-1 channel-mediated adenosine triphosphate (ATP) release and enhanced the efficiency of metastasis by promoting metastatic breast cancer cells survival during physical deformation. Additionally, carbenoxolone (CBX), a Panx-1 inhibitor, was proved to reduce the efficiency of breast cancer metastasis. These results suggested that Panx-1 is one of the molecular bases for metastatic cell survival in microvasculature-induced biomechanical trauma.
作者机构:
[Xu Jin; Lu Liqun; Li Lanfang] Institute of Pharmacy and Pharmacology, University of South China, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study;[Xu Jin; Lu Liqun; Li Lanfang] Learning Key Laboratory for Pharmacoproteomics, Hengyang, 421001
通讯机构:
[Li, L.] H
关键词:
promising;therapy target;inflammatory
摘要:
NLRP3 inflammasome is a multi-protein complex that is critical for the activation of caspases-1, maturation, and secretion of proinflammatory cytokines such as interleukin (IL)-1β and IL-18. NLRP3 has three parts: an amino-terminal pyrin domain (PYD), a central nucleotide-binding domain (NBD), and a C-terminal leucinerich repeat (LRR). The interactions among NLRP3, the adapter apoptosis-associated speck-like protein (ASC), and pro-caspase-1 are closely associated with the formation of NLRP3 inflammasome. Under the pathological conditions, the NLRP3-activating stimuli contribute to the inflammasome assembly and activation of the NLRP3 inflammasome, which consists of NLRP3 oligomerization of ASC and activation of caspase-1. This process leads to the secretion and maturation of IL-1β and IL-18, which eventually triggers cell damage and death. NLRP3 inflammasome is involved in the initiation and development of several pathophysiological events, such as gout, atherosclerosis, Type 2 diabetes, metabolic syndrome, agerelated macular degeneration, Alzheimer's disease, multiple sclerosis, and inflammatory bowel disease.
作者机构:
College of Laboratory Medicine, Hunan University of Medicine, Huaihua, Hunan 418000, China;Division of Basic Medical Sciences, Hunan University of Medicine, Huaihua, Hunan 418000, China;Institute of Cardiovascular Disease, University of South China Medical College, Hengyang, Hunan 412000, China;Department of Experimental Animal, University of South China, Hengyang, Hunan 412000, China;[Moshe, L.] Neurim Pharmaceuticals Ltd, Tel-Aviv, 69710, Israel
通讯机构:
[Cai, S.-C.] D;Division of Basic Medical Sciences, Hunan University of Medicine, Huaihua, Hunan, China
作者机构:
[孙四玉; 邱飞; 杨冬梅] School of Pharmacy, Hunan University of Chinese Medicine, Changsha, 410208, China;[阳巍; 张彩平; 熊国祚] Institute of Pharmacy and Pharmacology, University of South China, Hengyang Hunan, 421001, China;[陈剑雄] Integrative Heart and Brain Disease Prevention and Control Laboratory, Hunan University of Chinese Medicine, Changsha, 410208, China;School of Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China;[庹勤慧] Institute of Pharmacy and Pharmacology, University of South China, Hengyang Hunan, 421001, China, School of Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China
摘要:
Macrophage-activating lipopeptide-2 (MALP-2) has been shown to promote the development of atherosclerosis. ATP-binding cassette transporter A1 (ABCA1), a transmembrane protein, plays a critical role in mediating cholesterol export from macrophages to apolipoprotein A-I (apoA-I). However, whether MALP-2 can regulate the expression of ABCA1 is still largely unknown. The aim of this study was to explore the effects of MALP-2 on ABCA1 expression in THP-1 macrophages and the underlying mechanisms. Our results showed that the treatment of cells with MALP-2 decreased ABCA1 level and suppressed cholesterol efflux in both concentration- and time-dependent manners. The contents of intracellular cholesterol were significantly increased in the presence of MALP-2. Moreover, MALP-2-mediated inhibition of ABCA1 expression was abolished by siRNA of either Toll-like receptor 2 (TLR2) or nuclear factor κB (NF-κB). A similar effect was produced by treatment with the NF-κB inhibitor pyrrolidine dithiocarbamate. In addition, MALP-2-induced activation of NF-κB markedly increased zinc finger protein 202 (ZNF202) level, and ZNF202 siRNA impaired the effects of MALP-2 on ABCA1 expression. Taken together, these results suggest that MALP-2 can decrease ABCA1 expression and subsequent cholesterol efflux through activation of the TLR2/NF-κB/ZNF202 signaling pathway in THP-1 macrophages.
作者机构:
Institute of Cardiovascular Disease,University of South China, Key Laboratory for Arteriosclerology of Hunan Province;[Li Lanfang] Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang, 421001;Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang, 421001;Institute of Cardiovascular Disease, University of South China, Key Laboratory for Arteriosclerology of Hunan Province, Hengyang, 421001;[Li Lanfang] Institute of Cardiovascular Disease,University of South China, Key Laboratory for Arteriosclerology of Hunan Province
通讯机构:
[Chen, L.] H;Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hengyang, China
关键词:
initially;identified;closest
摘要:
APJ, which was initially identified as a gene with closest homology to the angiotensin II type 1 receptor, is a seven transmembrane G protein-coupled receptor. Apelin is an endogenous ligand of the APJ originally isolated from bovine stomach extracts. There are several isoforms of apelin. Apelin preproproteins contain 77 amino-acid residues, which can be cleaved to form shorter bioactive isoforms, including apelin-36, apelin-17, apelin-13, apelin-12, and so on. Apelin/APJ receptor is extensively distributed in the central nervous system and peripheral tissues. Apelin/APJ system involves in a wide range of physiological and pathological functions. For example, apelin lowers blood pressure via a NO/cGMP-dependent mechanism. Apelin-13 maintains the Ca~(2+) transient against ischemia/reperfusion in cardiomyocytes. Furthermore, apelin-13 promotes cell proliferation and angiogenesis via PI3K/AKT activation.