维普中文期刊产品整合服务
13篇 您的检索式:作者名="Michael LD"
    题名 作者 年代 出处 被引量
1Myoblast alignment on 2D wavy patterns: Dependence on feature characteristics and cell - cell interaction 显示文摘Michael SG Casey LD Derin SB 2014Biotechnol Bioeng2014,2,20:1
2Opposite actions of brain --derived neurotrophie factor and neurotrophin--3 on firing features and Ion channel composition of murine spiral gangli- on neurons显示文摘Crista LA Michael AR Robin LD 2002The Journal of Neuroseience2002,22,:1
3Prostaglandin endoperoxide H synthases(cyclooxygenases)-1 and -2显示文摘William L R Michael Garavito David LD 1996J Bio Chem1996,271,33:1
4Bond strength analysis of custom base variables in indirect bonding techniques显示文摘Michael AT James LD Ellen AB 2008Am J Orthod Dentofacial Orthop2008,133,1:1
5Effect of mesenteric ischemia and reperfusion or hemorrhagic shock on intestinal mucosal permeability and ATP content in rats显示文摘SOMKIAT W MICHAEL JM RUSSELL LD 1999Shock1999,12,2:1
6Aspiration and relative risk of medical complications following stroke 显示文摘MARLENE AH KATHLEEN LD MICHAEL JR 1994Arch Neurol1994,51,10:1
7Induction by IL-1 and interferon-γ:tissue distribution, biochemistry, and function of a natural adherence molecule( ICAM- 1 )显示文摘Michael LD Robert R Atul KB 1986J Immunol1986,137,:1
8Autocatalytic oxidation of hemoglobin induced by nitrite: Activation and chemical inhibition 显示文摘Michael PD James GH Russell LD 1985J Free Rad Biol Med1985,1,2:1
9Hypertension, age,and location predict rupture of small intracranial aneu- rysms显示文摘Brian VN Michael LD Thomas Morgan 2005Neurosurgery2005,57,4:1
10Bond strength analysis of custom base variables in indirect bonding techniques显示文摘Michael AT James LD Ellen AB 2008Am J Orthod Dentofacial Orthop2008,133,1:1
11Lymphocyte functionassociated antigen-1 (LFA-1) interaction with intercellular adhesion moleculer-1 (ICAM-1) is one of at least three mechanisms for lymphocyte adhesion to cultured endothelial cell 显示文摘Michael LD Timothy AS Cell bio0,107,:1
12Hypertension, Age, and Location predict rupture of small intracranial aneurysms 显示文摘Bruan VN Michael LD Thomas Morgan et 81 2005Neurosurgery2005,57,4:1
13Inhibition of matrix metalloproteinase-9 secretion by dimethyl sulfoxide and cyclic adenosine monophosphate in human monocytes显示文摘BACKGROUND Matrix metalloproteinases(MMPs),including MMP-9,are an integral part of the immune response and are upregulated in response to a variety of stimuli.New details continue to emerge concerning the mechanistic and regulatory pathways that mediate MMP-9 secretion.There is significant evidence for regulation of inflammation by dimethyl sulfoxide(DMSO)and 3',5'-cyclic adenosine monophosphate(cAMP),thus investigation of how these two molecules may regulate both MMP-9 and tumor necrosis factorα(TNFα)secretion by human monocytes was of high interest.The hypothesis tested in this study was that DMSO and cAMP regulate MMP-9 and TNFαsecretion by distinct mechanisms.AIM To investigate the regulation of lipopolysaccharide(LPS)-stimulated MMP-9 and tumor necrosis factorαsecretion in THP-1 human monocytes by dimethyl sulfoxide and cAMP.METHODS The paper describes a basic research study using THP-1 human monocyte cells.All experiments were conducted at the University of Missouri-St.Louis in the Department of Chemistry and Biochemistry.Human monocyte cells were grown,cultured,and prepared for experiments in the University of Missouri-St.Louis Cell Culture Facility as per accepted guidelines.Cells were treated with LPS for selected exposure times and the conditioned medium was collected for analysis of MMP-9 and TNFαproduction.Inhibitors including DMSO,cAMP regulators,and anti-TNFαantibody were added to the cells prior to LPS treatment.MMP-9 secretion was analyzed by gel electrophoresis/western blot and quantitated by ImageJ software.TNFαsecretion was analyzed by enzyme-linked immuno sorbent assay.All data is presented as the average and standard error for at least 3 trials.Statistical analysis was done using a two-tailed paired Student t-test.P values less than 0.05 were considered significant and designated as such in the Figures.LPS and cAMP regulators were from Sigma-Aldrich,MMP-9 standard and antibody and TNFαantibodies were from R&D Systems,and amyloid-βpeptide was from rPeptide.RESULTS In our investigation of MMP-9 secretion from THP-1 human monocytes,we made the following findings.Inclusion of DMSO in the cell treatment inhibited LPSinduced MMP-9,but not TNFα,secretion.Inclusion of DMSO in the cell treatment at different concentrations inhibited LPS-induced MMP-9 secretion in a dosedependent fashion.A cell-permeable cAMP analog,dibutyryl cAMP,inhibited both LPS-induced MMP-9 and TNFαsecretion.Pretreatment of the cells with the adenylyl cyclase activator forskolin inhibited LPS-induced MMP-9 and TNFαsecretion.Pretreatment of the cells with the general cAMP phosphodiesterase inhibitor IBMX reduced LPS-induced MMP-9 and TNFαin a dose-dependent fashion.Pre-treatment of monocytes with an anti-TNFαantibody blocked LPSinduced MMP-9 and TNFαsecretion.Amyloid-βpeptide induced MMP-9 secretion,which occurred much later than TNFαsecretion.The latter two findings strongly suggested an upstream role for TNFαin mediating LPS-stimulate MMP-9 secretion.CONCLUSION The cumulative data indicated that MMP-9 secretion was a distinct process from TNFαsecretion and occurred downstream.First,DMSO inhibited MMP-9,but not TNFα,suggesting that the MMP-9 secretion process was selectively altered.Second,cAMP inhibited both MMP-9 and TNFαwith a similar potency,but at different monocyte cell exposure time points.The pattern of cAMP inhibition for these two molecules suggested that MMP-9 secretion lies downstream of TNFαand that TNFαmay a key component of the pathway leading to MMP-9 secretion.This temporal relationship fit a model whereby early TNFαsecretion directly led to later MMP-9 secretion.Lastly,antibody-blocking of TNFαdiminished MMP-9 secretion,suggesting a direct link between TNFαsecretion and MMP-9 secretion.Darcy R Denner Maria LD Udan-Johns Michael R Nichols 2021World Journal of Biological Chemistry2021,12,1:0
返回顶部 每页显示:
共1页 首页 上一页 第1页 下一页 末页 /1 跳转

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费