Molecular cell biology research communications : MCBRC最新文献_第7页

Identification by Array Screening of Altered nm23-M2/PuF mRNA Expression in Mouse Retinal Degeneration 阵列筛选鉴定小鼠视网膜变性中nm23-M2/PuF mRNA表达改变

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0250

Stephen E. Jones, Catherine Jomary, John Grist, Hannah J. Stewart, Michael J. Neal

{"title":"Identification by Array Screening of Altered nm23-M2/PuF mRNA Expression in Mouse Retinal Degeneration","authors":"Stephen E. Jones, Catherine Jomary, John Grist, Hannah J. Stewart, Michael J. Neal","doi":"10.1006/mcbr.2000.0250","DOIUrl":"10.1006/mcbr.2000.0250","url":null,"abstract":"<div><p>In the <em>rd/rd</em> mouse model of inherited retinal degeneration, the majority of photoreceptors die apoptotically between postnatal age (P)10 and 20 days, during which period the inner retina appears morphologically unaffected. To examine mRNA changes associated with the degeneration, we performed differential screening of 588 arrayed murine cDNAs using probes reverse-transcribed from P8 predegenerative and control mouse retinal RNAs. We detected altered expression of the gene encoding nm23-M2, a member of the family of nucleoside diphosphate kinases implicated in diverse processes including metastasis suppression and transcriptional regulation. Retinal nm23 mRNA levels increased during degeneration while control levels decreased over age-matched time-points. <em>In situ</em> hybridization showed the high level of expression at P20 in <em>rd/rd</em> was concentrated in the retinal ganglion cells. Previous studies have indicated upregulation of the stress-response related gene αB-crystallin in the <em>rd/rd</em> inner retina, and increased nm23 levels may be a component of this response to photoreceptor loss and altered retinal architecture.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 1","pages":"Pages 20-25"},"PeriodicalIF":0.0,"publicationDate":"2000-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0250","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83506694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

Loss of Heterozygosity in DNA Mismatch Repair Genes in Human Atherosclerotic Plaques 人类动脉粥样硬化斑块DNA错配修复基因杂合性缺失

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0255

George A. Flouris , Demetrios A. Arvanitis , John T. Parissis , Demetrios L. Arvanitis , Demetrios A. Spandidos

引用次数: 24

Overexpression of Human Amyloid Precursor Protein in Drosophila 人淀粉样前体蛋白在果蝇中的过表达

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0248

Yoshimasa Yagi , Susumu Tomita , Makoto Nakamura , Toshiharu Suzuki

引用次数: 36

Relationship between Cell Cycle Changes and Variations of the Mitochondrial Membrane Potential Induced by Etoposide 依托泊苷诱导细胞周期变化与线粒体膜电位变化的关系

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0251

Michael Facompré, Nicole Wattez, Jérôme Kluza, Amélie Lansiaux, Christian Bailly

{"title":"Relationship between Cell Cycle Changes and Variations of the Mitochondrial Membrane Potential Induced by Etoposide","authors":"Michael Facompré, Nicole Wattez, Jérôme Kluza, Amélie Lansiaux, Christian Bailly","doi":"10.1006/mcbr.2000.0251","DOIUrl":"10.1006/mcbr.2000.0251","url":null,"abstract":"<div><p>Etoposide, a clinically useful anticancer drug, is a potent inhibitor of topoisomerase II. The DNA strand breaks caused by this epipodophyllotoxin lead to apoptotic death of tumor cells. Flow cytometry was used to investigate the relationship between the effects of the drug on the cell cycle of human leukemia HL-60 cells and the variations of the mitochondrial transmembrane potential (ΔΨ<sub>mt</sub>). Three cationic fluorescent probes, DiOC<sub>6</sub>, JC-1, and TMRM, were used to measure drug-induced changes of ΔΨ<sub>mt</sub>. In all three cases, we found that the arrest in the G2/M phase of the cells treated with 0.5 μM etoposide is associated with an increase in the potential of mitochondrial membranes whereas treatment with a tenfold higher drug concentration trigger massive apoptosis and a collapse of ΔΨ<sub>mt</sub>. DNA fragmentation (TUNEL assay) and externalization of phosphatidylserine residues in the outer leaflet of the plasma membrane (annexin V binding) were measured to characterize the apoptotic cell population.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 1","pages":"Pages 37-42"},"PeriodicalIF":0.0,"publicationDate":"2000-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91350631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 44

The Carboxyl-Terminal Fragment of α1-Antitrypsin Is Present in Atherosclerotic Plaques and Regulates Inflammatory Transcription Factors in Primary Human Monocytes α1-抗胰蛋白酶羧基末端片段存在于动脉粥样硬化斑块中并调节原代单核细胞的炎症转录因子

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0256

Wolfgang Dichtl , Fabian Moraga , Mikko P.S Ares , Milita Crisby , Jan Nilsson , Stefan Lindgren , Sabina Janciauskiene

{"title":"The Carboxyl-Terminal Fragment of α1-Antitrypsin Is Present in Atherosclerotic Plaques and Regulates Inflammatory Transcription Factors in Primary Human Monocytes","authors":"Wolfgang Dichtl , Fabian Moraga , Mikko P.S Ares , Milita Crisby , Jan Nilsson , Stefan Lindgren , Sabina Janciauskiene","doi":"10.1006/mcbr.2000.0256","DOIUrl":"10.1006/mcbr.2000.0256","url":null,"abstract":"<div><p>α1-Antitrypsin (AAT) serine proteinase inhibitor is found in most biological fluids, diffuses into most tissues, and is an important factor in controlling tissue damage by proteases in inflammatory diseases such as atherosclerosis. We have previously reported that the C-terminal fragment (C-36) generated during the cleavage of AAT by proteinases forms amyloid fibrils which have biological effects unrelated to precursor functions. Here we show that the C-36 fragment is present in atherosclerotic plaques, particularly within the fibrous cap at the base of the lipid core. We also found that human monocyte stimulation with C-36 fibrils led to a strong activation of both peroxisome proliferator-activated receptors α and γ (PPARα and PPARγ) at 1, 2, and 18 h of cell culture. A parallel increase in the intracellular lipid accumulation was also observed. Furthermore, stimulation of monocytes with C-36 for 18 h led to activator protein-1 (AP-1) and nuclear factor-κB (NF-κB) activation. These data for the first time demonstrate the peptide of AAT as a component of atherosclerotic plaques and as a novel activator of PPARα, PPARγ, NF-κB, and AP-1 in cultured monocytes. Taken together, the effects of the peptide represent a new mechanism of monocyte activation that may be of importance not only in atherogenesis, but also in other inflammatory processes.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 1","pages":"Pages 50-61"},"PeriodicalIF":0.0,"publicationDate":"2000-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0256","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81114974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 42

Suppression of Proliferation of Human Coronary Artery Smooth Muscle Cells by the Nitric Oxide Donor, S-Nitrosoglutathione, Is cGMP-Independent 一氧化氮供体s -亚硝基谷胱甘肽对人冠状动脉平滑肌细胞增殖的抑制是不依赖于cgmp的

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0254

Delano V. Young , Diana Serebryanik, David R. Janero, S.William Tam

{"title":"Suppression of Proliferation of Human Coronary Artery Smooth Muscle Cells by the Nitric Oxide Donor, S-Nitrosoglutathione, Is cGMP-Independent","authors":"Delano V. Young , Diana Serebryanik, David R. Janero, S.William Tam","doi":"10.1006/mcbr.2000.0254","DOIUrl":"10.1006/mcbr.2000.0254","url":null,"abstract":"<div><p>Nitric oxide (NO), delivered by a single addition of <em>S</em>-nitrosoglutathione (GSNO, IC<sub>50</sub> = 60–75 μM), causes the prolonged, multi-day suppression of proliferation of asynchronous, logarithmically growing human (hCASMC, two cell strains), and porcine (porCASMC) coronary artery smooth muscle cells. The inhibition is not cytotoxic, but cytostatic and reversible. Transient exposure (>4–12 h) to GSNO is sufficient to elicit prolonged suppression, but a less than 4 h exposure produces little or no inhibition. Unlike porCASMC and rat and rabbit aortic SMC, hCASMC synthesize little cGMP in response to GSNO stimulation, suggesting loss of NO responsive guanylate cyclase <em>in vitro.</em> The guanylate cyclase inhibitor, ODQ, blocks the slight cGMP synthesis induced by GSNO in hCASMC, but does not prevent GSNO suppression of proliferation. These data support a cGMP independent mechanism for NO induced suppression of hCASMC proliferation which may be significant in the treatment of proliferative coronary artery diseases.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 1","pages":"Pages 32-36"},"PeriodicalIF":0.0,"publicationDate":"2000-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0254","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90012637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 22

MIP-1α Induces Binding of Nuclear Factors to the κB DNA Element in Human B Cells MIP-1α诱导人B细胞核因子与κB DNA元件的结合

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0247

Obe I Omoike , Ryan M Teague , Stephen H Benedict, Marcia A Chan

引用次数: 5

Phosphatidylinositol Transfer Proteins: One Big Happy Family or Strangers with the Same Name? 磷脂酰肌醇转移蛋白:一个快乐的大家庭还是同名的陌生人?

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0253

Geraint M.H. Thomas, Jef A. Pinxteren

引用次数: 3

Cross-Regulation of Intracellular cGMP and cAMP in Cultured Human Corpus Cavernosum Smooth Muscle Cells 体外培养人海绵体平滑肌细胞内cGMP与cAMP的交叉调控

Molecular cell biology research communications : MCBRC Pub Date : 2000-07-01 DOI: 10.1006/mcbr.2000.0249

Noel N. Kim , Yue-hua Huang , Robert B. Moreland , Sandra S. Kwak , Irwin Goldstein , Abdulmaged Traish

{"title":"Cross-Regulation of Intracellular cGMP and cAMP in Cultured Human Corpus Cavernosum Smooth Muscle Cells","authors":"Noel N. Kim , Yue-hua Huang , Robert B. Moreland , Sandra S. Kwak , Irwin Goldstein , Abdulmaged Traish","doi":"10.1006/mcbr.2000.0249","DOIUrl":"10.1006/mcbr.2000.0249","url":null,"abstract":"<div><p>The goal of this study was to assess the potential cross-regulation of cyclic nucleotides in human corpus cavernosum (HCC). Incubation of primary cultures of HCC smooth muscle cells with either the NO donor sodium nitroprusside (SNP, 10 μM) or the phosphodiesterase type 5 (PDE 5) inhibitor sildenafil (50 nM) produced little or no changes in the intracellular cGMP levels. Incubation with both SNP and sildenafil produced marked increases in cGMP. Interestingly, incubation of cells with 10 μM of forskolin or PGE<sub>1</sub> produced significant enhancement of cGMP accumulation. These increases were not further enhanced by the addition of SNP and sildenafil. Kinetic analyses of cGMP hydrolysis by PDE 5 showed that high concentrations of cAMP reversibly inhibited the enzyme with a <em>K</em><sub>i</sub> of 258 ± 54 μM. The increase in cGMP levels in response to cAMP generating agents is not due to assay artifact since cAMP did not cross-react with cGMP antibody. Our data suggest that cAMP up-regulates intracellular levels of cGMP, in part, by inhibition of PDE 5. We also noted that cGMP down-regulates cAMP synthesis via a mechanism requiring G-protein coupling of adenylyl cyclase. These observations may have important implications in the utility of pharmacotherapeutic agents targeting cyclic nucleotide metabolism for the treatment of erectile dysfunction.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"4 1","pages":"Pages 10-14"},"PeriodicalIF":0.0,"publicationDate":"2000-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0249","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81540184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 55

Downregulation of Cyclin D1 Alters cdk 4- and cdk 2-Specific Phosphorylation of Retinoblastoma Protein 细胞周期蛋白D1的下调改变视网膜母细胞瘤蛋白cdk4 -和cdk2特异性磷酸化

Molecular cell biology research communications : MCBRC Pub Date : 2000-06-01 DOI: 10.1006/mcbr.2000.0238

Bo Yu , Maureen E. Lane , Richard G. Pestell , Chris Albanese , Scott Wadler

{"title":"Downregulation of Cyclin D1 Alters cdk 4- and cdk 2-Specific Phosphorylation of Retinoblastoma Protein","authors":"Bo Yu , Maureen E. Lane , Richard G. Pestell , Chris Albanese , Scott Wadler","doi":"10.1006/mcbr.2000.0238","DOIUrl":"10.1006/mcbr.2000.0238","url":null,"abstract":"<div><p>Progression of cells through the G1 phase of the cell cycle requires the assembly and activation of specific cyclin:cyclin-dependent kinase (cdk) complexes in a tightly regulated, sequential fashion. To more clearly define the temporal events leading to the G1/S transition, sequential changes in the expression of cyclin E and cdks 2, 4, and 6, as well as the phosphorylation of the retinoblastoma protein (pRb), were assayed in RA28 cells, a variant of human colon cancer RKO cells which were modified by transfection of an ecdysone-inducible antisense (AS) CD1 expression system. Induction of cyclin D1 antisense mRNA by the ecdysteroid, ponasterone A, resulted in a 55% decrease in cyclin D1 mRNA and a 58% decrease in CD1 protein levels. There was a 2.4-fold decrease in the ratio of hyperphosphorylated pRb (ppRb) to hypophosphorylated pRb, as well as a 60–75% decrease in cdk 2- and cdk 4-specific phosphorylated pRb proteins. Of interest, cyclin E-dependent phosphorylation (cdk2) decreased 2.5-fold at 3 h despite only a 30% decrease in cyclin E protein level. Levels of cdk 2, cdk 4, and cdk 6 decreased 40–70%, while levels of cyclin A and B were unaffected by induction of CD1 antisense. Induction of a CD1 antisense gene in a human colon cancer cell line resulted in rapid, concomitant changes in CD1 mRNA and protein, cyclin E, cdk2, cdk4, and cdk6, as well as the ratio of ppRb to pRb. In this system, growth regulatory events are tightly regulated and the perturbed expression of a single protein, CD1, rapidly alters expression of multiple regulatory proteins involved in the G1/S transition phase of cell cycle progression.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 352-359"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0238","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 43