{"title":"Author Index for Volume 3","authors":"","doi":"10.1006/mcbr.2000.0246","DOIUrl":"https://doi.org/10.1006/mcbr.2000.0246","url":null,"abstract":"","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 394-395"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0246","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137145591","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}
{"title":"p53 Codon 72 Polymorphism as a Risk Factor in the Development of Breast Cancer","authors":"E.N. Papadakis, D.N. Dokianakis, D.A. Spandidos","doi":"10.1006/mcbr.2000.0241","DOIUrl":"10.1006/mcbr.2000.0241","url":null,"abstract":"<div><p>The p53 gene is polymorphic at amino acid 72 of the protein that it encodes. It has been reported that patients with the arginine form have a higher risk of developing other forms of cancer than those with the proline form. The purpose of this study was to examine whether p53 Arg at the polymorphic position 72 could represent a risk factor for women with breast lesions. The study population included 56 biopsies from patients with breast lesions. Also, 61 normal blood samples were used as controls. There was a difference in the distribution of p53 genotypes between breast cancer lesions and the normal samples. The allele frequency of p53 Arg/Arg was much higher than that of the normal samples (61% versus 20%). Based on the findings of this study, it is suggested that p53 Arg homozygosity could represent a risk factor for the tumorigenesis of the breast.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 389-392"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0241","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862713","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}
{"title":"Normal Breast Epithelial Cells Induce Apoptosis of MCF-7 Breast Cancer Cells through a p53-Mediated Pathway","authors":"Robert-Alain Toillon , Eric Adriaenssens , Danièle Wouters , Severine Lottin , Bénoni Boilly , Hubert Hondermarck , Xuefen Le Bourhis","doi":"10.1006/mcbr.2000.0236","DOIUrl":"10.1006/mcbr.2000.0236","url":null,"abstract":"<div><p>Cancer development depends not only on the nature of the tumor cells themselves but also on the regulatory effects of various normal cells. The present study was performed to better understand the mechanism by which normal breast epithelial cells (NBEC) can control the growth of MCF-7 breast cancer cells. When MCF-7 cells were treated with NBEC conditioned medium, cell growth was inhibited in a concentration-dependent manner. This inhibition was due to an induction of apoptosis without any change in cell cycle progression. The induction of apoptosis was correlated with increased levels of p53, p21<sup>waf1</sup> and decreased levels of bcl-2. Transient transfections of MCF-7 cells with two <em>p53</em> cDNA constructs demonstrated the induction of apoptosis was mediated by endogenous p53. Taken together, our results indicate that NBEC inhibit the growth of MCF-7 breast cancer cells by inducing apoptosis in them via endogenous p53.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 338-344"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0236","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862842","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}
Fabrice Magnino , Marie St-Pierre , Michael Lüthi , Mauricette Hilly , Jean-Pierre Mauger , Jean-François Dufour
{"title":"Expression of Intracellular Calcium Channels and Pumps after Partial Hepatectomy in Rat","authors":"Fabrice Magnino , Marie St-Pierre , Michael Lüthi , Mauricette Hilly , Jean-Pierre Mauger , Jean-François Dufour","doi":"10.1006/mcbr.2000.0242","DOIUrl":"10.1006/mcbr.2000.0242","url":null,"abstract":"<div><p>Ca<sup>2+</sup> signals regulate many cellular functions, including proliferation. They are governed by the inositol 1,4,5-trisphosphate receptor (IP<sub>3</sub>R), the only intracellular hepatic Ca<sup>2+</sup> channel and by the endoplasmic reticulum Ca<sup>2+</sup> pumps, SERCA. To characterise their role in regeneration, expression of their isoforms was studied after 2/3 hepatectomy by real-time quantitative PCR, Western blot and binding studies. We found an early increase in the expression of the IP<sub>3</sub>R isoform 1 which contrasted with the decrease of the expression of the IP<sub>3</sub>R isoforms 2 and 3 and of SERCA3. This results in a transient switch between IP<sub>3</sub>R isoforms 1 and 2, IP<sub>3</sub>R isoform 1 becoming predominant before the first round of mitosis. Binding studies detected a 30% diminution of the IP<sub>3</sub>R population at 24 h. In conclusion, the Ca<sup>2+</sup> signalling machinery is regulated, after hepatectomy, by changes in expression of the IP<sub>3</sub>R and SERCA isoforms to adapt Ca<sup>2+</sup> signals to the regenerative state.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 374-379"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0242","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862847","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}
{"title":"Author Index for Volume 3, Number 6","authors":"","doi":"10.1006/mcbr.2000.0245","DOIUrl":"https://doi.org/10.1006/mcbr.2000.0245","url":null,"abstract":"","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Page iv"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0245","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137288548","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}
Amy D. Bradshaw , James A. Bassuk , A. Francki , E.Helene Sage
{"title":"Expression and Purification of Recombinant Human SPARC Produced by Baculovirus","authors":"Amy D. Bradshaw , James A. Bassuk , A. Francki , E.Helene Sage","doi":"10.1006/mcbr.2000.0237","DOIUrl":"10.1006/mcbr.2000.0237","url":null,"abstract":"<div><p>SPARC (secreted protein acidic and rich in cysteine/osteonectin/BM-40), a matrix-associated protein, disrupts cell adhesion and inhibits the proliferation of many cultured cells. We report the expression of recombinant human protein (rhSPARC) in a baculovirus expression system. This procedure routinely yields ∼1 mg of purified protein per 500 ml of culture supernate. rhSPARC produced by insect cells migrates at the appropriate molecular weight under reducing and nonreducing conditions. The rhSPARC purified from insect cell media appeared structurally similar to SPARC purified from mammalian tissue culture by the criterion of circular dichroism. In addition, a series of anti-SPARC and anti-SPARC peptide antibodies recognized insect cell rhSPARC. We also show that rhSPARC produced in this system is glycosylated and is biologically active, as assessed by inhibition of endothelial cell proliferation and induction of collagen I mRNA in mesangial cells. Significant amounts of rhSPARC can now be generated in the absence of contaminating mammalian proteins for structure/function assays of SPARC activities.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 345-351"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0237","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862843","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}
Alan W. Stitt , Tisha Bhaduri, C.B.Tara McMullen, Thomas A. Gardiner, Desmond B. Archer
{"title":"Advanced Glycation End Products Induce Blood–Retinal Barrier Dysfunction in Normoglycemic Rats","authors":"Alan W. Stitt , Tisha Bhaduri, C.B.Tara McMullen, Thomas A. Gardiner, Desmond B. Archer","doi":"10.1006/mcbr.2000.0243","DOIUrl":"10.1006/mcbr.2000.0243","url":null,"abstract":"<div><p>Advanced glycation end products (AGEs) have been implicated in the progressive vascular dysfunction which occurs during diabetic retinopathy. In the current study we have examined the role of these adducts in blood–retinal barrier (BRB) breakdown and investigated expression of the vasopermeabilizing agent vascular endothelial growth factor (VEGF) in the retina. When normoglycemic rats were injected with AGE-modified albumin daily for up to 10 days there was widespread leakage of FITC-dextran and serum albumin from the retinal vasculature when compared to control animals treated with nonmodified albumin. Ultrastructural examination of the vasculature revealed areas of attenuation of the retinal vascular endothelium and increased vesicular organelles only in the AGE-exposed rats. Quantitative RT-PCR and <em>in situ</em> hybridization demonstrated a significant increase in retinal VEGF mRNA expression (<em>P</em> < 0.05). These results suggest that AGEs can initiate BRB dysfunction in nondiabetic rats and a concomitant increase in retinal VEGF expression. These findings may have implications for the role of AGEs in the pathogenesis of diabetic retinopathy.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 380-388"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0243","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862848","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}
Anne Dubouix, Isabelle Gennero, Michèle Niéto, Nicole Ser, Hélène Hannaire-Broutin, Jean Pierre Tauber, Jacques Pourrat, Josette Fauvel, Philippe Barthe, Hugues Chap, Jean Pierre Salles
{"title":"Polymorphism of the 5' Untranslated Region of NHE1 Gene Associated with Type-I Diabetes","authors":"Anne Dubouix, Isabelle Gennero, Michèle Niéto, Nicole Ser, Hélène Hannaire-Broutin, Jean Pierre Tauber, Jacques Pourrat, Josette Fauvel, Philippe Barthe, Hugues Chap, Jean Pierre Salles","doi":"10.1006/mcbr.2000.0244","DOIUrl":"https://doi.org/10.1006/mcbr.2000.0244","url":null,"abstract":"","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Page 393"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0244","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137288549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cellular Responses to Sodium Butyrate Exhibit the Dominance of One Parental Phenotype in Somatic Cell Hybrids","authors":"G.Stanley Cox","doi":"10.1006/mcbr.2000.0235","DOIUrl":"10.1006/mcbr.2000.0235","url":null,"abstract":"<div><p>The glycoprotein hormone α-subunit (GPHα) gene is inducible by sodium butyrate (NaBtr) in nontrophoblastic tumor cell lines such as HeLa (cervical carcinoma) but not in trophoblastic tumor cell lines such as JEG-3 (choriocarcinoma). The studies summarized in this report examined the ability of NaBtr to induce GPHα expression in somatic cell hybrids between HeLa SR3<sub>hyg</sub> and JEG-3<sub>neo</sub>. The hybrid cells, pooled clones resistant to both hygromycin B and G418 sulfate, have been named JELA and were indistinguishable from the SR3 parent with regard to induction of the GPHα gene. The effects of NaBtr on cell proliferation were also similar in HeLa and JELA but different from those in JEG-3. The GPHα gene could be induced by NaBtr in the JEG-3 parent only when they were simultaneously treated with cycloheximide (CHX). The ability of NaBtr to induce GPHα in CHX-treated JEG-3 cells occurred concomitantly with a change in the electrophoretic mobility of enhancer binding proteins as determined in gel shift assays. The DNA–protein complexes generated between a trophoblast specific element (TSE) and nuclear proteins in HeLa SR3 and JELA migrated significantly more slowly than the complex generated by JEG-3 nuclear proteins. However, when nuclear extracts were prepared from CHX-treated JEG-3 cells, the complex generated with the TSE oligonucleotide migrated more slowly than the complex from untreated JEG-3 cells and coincident with the complexes produced with nuclear extracts from HeLa SR3 and JELA cells. Together, these data demonstrate that inducibility of the GPHα gene by NaBtr in JELA cell hybrids resembles that of the HeLa SR3 parent and that its inducibility in the JEG-3 parent parallels the status of an enhancer binding protein (TSEB) as judged from changes in electrophoretic mobility. The results are consistent with a model in which the status of TSEB has a profound influence on the gene's response to NaBtr.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 329-337"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862841","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}
Samuel Rahbar , Kiran Kumar Yerneni , Stephen Scott , Noe Gonzales , Iraj Lalezari
{"title":"Novel Inhibitors of Advanced Glycation Endproducts (Part II)","authors":"Samuel Rahbar , Kiran Kumar Yerneni , Stephen Scott , Noe Gonzales , Iraj Lalezari","doi":"10.1006/mcbr.2000.0239","DOIUrl":"10.1006/mcbr.2000.0239","url":null,"abstract":"<div><p>Enhanced formation and accumulation of advanced glycation endproducts (AGEs), have been implicated as a major pathogenesis process leading to diabetic complications, normal aging, atherosclerosis, and Alzheimer's Disease. Several potential drug candidates as AGE inhibitors have been reported recently. The aim of this study was to develop classes of novel inhibitors of glycation, AGE formation, and AGE-crosslinking and to investigate their effects through <em>in vitro</em> chemical and immunochemical assays. A total of 92 compounds were designed and synthesized. The first 63 compounds were reported before. Nearly half of the 29 novel inhibitors reported here are benzoic acid derivatives and related molecules, and found to be potent inhibitors of multistage glycation, AGE formation, and AGE-protein crosslinking. All 29 compounds show some degrees of inhibitory activities as detected by the four assay methods, 9 compounds demonstrated high percent inhibition (PI) in all tests, 30 to 40 times stronger than aminoguanidine.</p></div>","PeriodicalId":80086,"journal":{"name":"Molecular cell biology research communications : MCBRC","volume":"3 6","pages":"Pages 360-366"},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/mcbr.2000.0239","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21862845","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}