Cell Adhesion & MigrationPub Date : 2019-12-01Epub Date: 2018-08-30DOI: 10.1080/19336918.2018.1506652
Andrea A Villanueva, Sofía Puvogel, Pablo Lois, Ernesto Muñoz-Palma, Manuel Ramírez Orellana, Fabiana Lubieniecki, Fernando Casco Claro, Iván Gallegos, Javier García-Castro, Pilar Sanchez-Gomez, Vicente A Torres, Verónica Palma
{"title":"The Netrin-4/Laminin γ1/Neogenin-1 complex mediates migration in SK-N-SH neuroblastoma cells.","authors":"Andrea A Villanueva, Sofía Puvogel, Pablo Lois, Ernesto Muñoz-Palma, Manuel Ramírez Orellana, Fabiana Lubieniecki, Fernando Casco Claro, Iván Gallegos, Javier García-Castro, Pilar Sanchez-Gomez, Vicente A Torres, Verónica Palma","doi":"10.1080/19336918.2018.1506652","DOIUrl":"https://doi.org/10.1080/19336918.2018.1506652","url":null,"abstract":"<p><p>Neuroblastoma (NB) is the most common pediatric extracranial solid tumor. It arises during development of the sympathetic nervous system. Netrin-4 (NTN4), a laminin-related protein, has been proposed as a key factor to target NB metastasis, although there is controversy about its function. Here, we show that NTN4 is broadly expressed in tumor, stroma and blood vessels of NB patient samples. Furthermore, NTN4 was shown to act as a cell adhesion molecule required for the migration induced by Neogenin-1 (NEO1) in SK-N-SH neuroblastoma cells. Therefore, we propose that NTN4, by forming a ternary complex with Laminin γ1 (LMγ1) and NEO1, acts as an essential extracellular matrix component, which induces the migration of SK-N-SH cells.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"33-40"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1506652","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36443601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2019-12-01Epub Date: 2019-02-08DOI: 10.1080/19336918.2019.1568140
Zeinab Al-Rekabi, Adriane M Fura, Ilsa Juhlin, Alaa Yassin, Tracy E Popowics, Nathan J Sniadecki
{"title":"Hyaluronan-CD44 interactions mediate contractility and migration in periodontal ligament cells.","authors":"Zeinab Al-Rekabi, Adriane M Fura, Ilsa Juhlin, Alaa Yassin, Tracy E Popowics, Nathan J Sniadecki","doi":"10.1080/19336918.2019.1568140","DOIUrl":"https://doi.org/10.1080/19336918.2019.1568140","url":null,"abstract":"<p><p>The role of hyaluronan (HA) in periodontal healing has been speculated via its interaction with the CD44 receptor. While HA-CD44 interactions have previously been implicated in numerous cell types; effect and mechanism of exogenous HA on periodontal ligament (PDL) cells is less clear. Herein, we examine the effect of exogenous HA on contractility and migration in human and murine PDL cells using arrays of microposts and time-lapse microscopy. Our findings observed HA-treated human PDL cells as more contractile and less migratory than untreated cells. Moreover, the effect of HA on contractility and focal adhesion area was abrogated when PDL cells were treated with Y27632, an inhibitor of rho-dependent kinase, but not when these cells were treated with ML-7, an inhibitor of myosin light chain kinase. Our results provide insight into the mechanobiology of PDL cells, which may contribute towards the development of therapeutic strategies for periodontal healing and tissue regeneration.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"138-150"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1568140","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36881879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Weimin Wang, Dan Li, Liangliang Xiang, Mengying Lv, Li Tao, Tengyang Ni, Jianliang Deng, Xiancheng Gu, Sunagawa Masatara, Yanqing Liu, Yan Zhou
{"title":"TIMP-2 inhibits metastasis and predicts prognosis of colorectal cancer via regulating MMP-9.","authors":"Weimin Wang, Dan Li, Liangliang Xiang, Mengying Lv, Li Tao, Tengyang Ni, Jianliang Deng, Xiancheng Gu, Sunagawa Masatara, Yanqing Liu, Yan Zhou","doi":"10.1080/19336918.2019.1639303","DOIUrl":"https://doi.org/10.1080/19336918.2019.1639303","url":null,"abstract":"<p><p>Colorectal cancer has a common cause of morbidity and mortality. Therefore, it is urgent to detect reliable biomarkers to predict prognosis in CRC. Here, we determined the expression of TIMP-2 and MMP-9 in a CRC tissue microarray by immunohistochemistry. We found that lower TIMP-2 or/and higher MMP-9 expression in cancer tissues was correlated with poorer overall survival (OS). TIMP-2 or MMP-9 expression was independent prognostic factors for CRC. Furthermore, TIMP-2 and MMP-9 expression had a synergistic role as efficient prognostic indicators for CRC patients. In vitro and in vivo, TIMP-2 could inhibit HCT 116 cells invasion and migration by regulating MMP-9. In sum, a combined expression of TIMP-2 and MMP-9 as efficient prognostic indicators was found for the first time.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"273-284"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1639303","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37134835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2019-12-01Epub Date: 2018-09-27DOI: 10.1080/19336918.2018.1506654
Alexandra Sneider, Jungwon Hah, Denis Wirtz, Dong-Hwee Kim
{"title":"Recapitulation of molecular regulators of nuclear motion during cell migration.","authors":"Alexandra Sneider, Jungwon Hah, Denis Wirtz, Dong-Hwee Kim","doi":"10.1080/19336918.2018.1506654","DOIUrl":"10.1080/19336918.2018.1506654","url":null,"abstract":"<p><p>Cell migration is a highly orchestrated cellular event that involves physical interactions of diverse subcellular components. The nucleus as the largest and stiffest organelle in the cell not only maintains genetic functionality, but also actively changes its morphology and translocates through dynamic formation of nucleus-bound contractile stress fibers. Nuclear motion is an active and essential process for successful cell migration and nucleus self-repairs in response to compression and extension forces in complex cell microenvironment. This review recapitulates molecular regulators that are crucial for nuclear motility during cell migration and highlights recent advances in nuclear deformation-mediated rupture and repair processes in a migrating cell.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"50-62"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1506654","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36530139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2019-12-01Epub Date: 2018-10-08DOI: 10.1080/19336918.2018.1526612
Christian Mayr, Marlena Beyreis, Heidemarie Dobias, Martin Gaisberger, Julia Fuchs, Martin Pichler, Markus Ritter, Martin Jakab, Katharina Helm, Daniel Neureiter, Tobias Kiesslich
{"title":"Continuous, label-free, 96-well-based determination of cell migration using confluence measurement.","authors":"Christian Mayr, Marlena Beyreis, Heidemarie Dobias, Martin Gaisberger, Julia Fuchs, Martin Pichler, Markus Ritter, Martin Jakab, Katharina Helm, Daniel Neureiter, Tobias Kiesslich","doi":"10.1080/19336918.2018.1526612","DOIUrl":"https://doi.org/10.1080/19336918.2018.1526612","url":null,"abstract":"<p><p>Cellular migration is essential in diverse physiological and pathophysiological processes. Here, we present a protocol for quantitative analysis of migration using confluence detection allowing continuous, non-endpoint measurement with minimal hands-on time under cell incubator conditions. Applicability was tested using substances which enhance (EGF) or inhibit (cytochalasin D, ouabain) migration. Using a gap-closure assay we demonstrate that automated confluence detection monitors cellular migration in the 96-well microplate format. Quantification by % confluence, % cell free-area or % confluence in cell-free area against time, allows detailed analysis of cellular migration. The study describes a practicable approach for continuous, non-endpoint measurement of migration in 96-well microplates and for detailed data analysis, which allows for medium/high-throughput analysis of cellular migration in vitro.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"76-82"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1526612","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36554311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stav Kozlovski, Ofir Atrakchi, Sara W Feigelson, Ziv Shulman, Ronen Alon
{"title":"Stable contacts of naïve CD4 T cells with migratory dendritic cells are ICAM-1-dependent but dispensable for proliferation in vivo.","authors":"Stav Kozlovski, Ofir Atrakchi, Sara W Feigelson, Ziv Shulman, Ronen Alon","doi":"10.1080/19336918.2019.1644857","DOIUrl":"10.1080/19336918.2019.1644857","url":null,"abstract":"<p><p>It is unclear if naïve T cells require dendritic cell ICAMs to proliferate inside lymph nodes. To check if and when CD4 lymphocytes use ICAMs on migratory DCs, wild-type and ICAM-1 and 2 double knock out bone marrow-derived DCs pulsed with saturating levels of an OT-II transgene-specific ovalbumin-derived peptide were co-transferred into skin-draining lymph nodes. Intravital imaging of OT-II lymphocytes entering these lymph nodes revealed that ICAM-1 and -2 deficient migratory DCs formed fewer stable conjugates with OT-II lymphocytes but promoted normal T cell proliferation. DC ICAMs were also not required for unstable TCR-dependent lymphocyte arrests on antigen presenting migratory DCs. Thus, rare antigen-stimulated ICAM-stabilized T-DC conjugates are dispensable for CD4 lymphocyte proliferation inside lymph nodes.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"315-321"},"PeriodicalIF":3.3,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6682365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48937918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Runjing Cao, Shiping Li, Junxiang Yin, Li Guo, Jiong Shi
{"title":"Sirtuin 3 promotes microglia migration by upregulating CX3CR1.","authors":"Runjing Cao, Shiping Li, Junxiang Yin, Li Guo, Jiong Shi","doi":"10.1080/19336918.2019.1629224","DOIUrl":"https://doi.org/10.1080/19336918.2019.1629224","url":null,"abstract":"<p><p>We studied the role of Sirtuin 3 (SIRT3) in microglial cell migration in ischemic stroke. We used a middle cerebral artery occlusion (MCAO) model of focal ischemia. We then applied lentivirus-packaged SIRT3 overexpression and knock down in microglial N9 cells to investigate the underlying mechanism driving microglial cell migration. More microglial cells appeared in the ischemic lesion side after MCAO. The levels of SIRT3 were increased in macrophages, the main source of microglia, after ischemia. CX3CR1 levels were increased with SIRT3 overexpression. SIRT3 promoted microglial N9 cells migration by upregulating CX3CR1 in both normal and glucose deprived culture media. These effects were G protein-dependent. Our study for the first time shows that SIRT3 promotes microglia migration by upregulating CX3CR1.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"229-235"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1629224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37336453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Caffeine inhibits hypoxia-induced renal fibroblast activation by antioxidant mechanism.","authors":"Angkhana Nilnumkhum, Rattiyaporn Kanlaya, Sunisa Yoodee, Visith Thongboonkerd","doi":"10.1080/19336918.2019.1638691","DOIUrl":"https://doi.org/10.1080/19336918.2019.1638691","url":null,"abstract":"<p><p>Caffeine has been demonstrated to possess anti-fibrotic activity against liver fibrosis. However, its role in renal fibrosis remained unclear. This study investigated the effects of caffeine on renal fibroblast activation induced by hypoxia (one of the inducers for renal fibrosis). BHK-21 fibroblasts were cultured under normoxia or hypoxia with or without caffeine treatment. Hypoxia increased levels of fibronectin, α-smooth muscle actin, actin stress fibers, intracellular reactive oxygen species (ROS), and oxidized proteins. However, caffeine successfully preserved all these activated fibroblast markers to their basal levels. Cellular catalase activity was dropped under hypoxic condition but could be reactivated by caffeine. <i>Hif1a</i> gene and stress-responsive Nrf2 signaling molecule were elevated/activated by hypoxia, but only Nrf2 could be partially recovered by caffeine. These data suggest that caffeine exhibits anti-fibrotic effect against hypoxia-induced renal fibroblast activation through its antioxidant property to eliminate intracellular ROS, at least in part, via downstream catalase and Nrf2 mechanisms.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"260-272"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1638691","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37393611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2019-12-01Epub Date: 2018-10-29DOI: 10.1080/19336918.2018.1540903
Svetlana I Galkina, Natalia V Fedorova, Alexander L Ksenofontov, Vladimir I Stadnichuk, Ludmila A Baratova, Galina F Sud'Ina
{"title":"Neutrophils as a source of branched-chain, aromatic and positively charged free amino acids.","authors":"Svetlana I Galkina, Natalia V Fedorova, Alexander L Ksenofontov, Vladimir I Stadnichuk, Ludmila A Baratova, Galina F Sud'Ina","doi":"10.1080/19336918.2018.1540903","DOIUrl":"https://doi.org/10.1080/19336918.2018.1540903","url":null,"abstract":"<p><p>Neutrophils release branched-chain (valine, isoleucine, leucine), aromatic (tyrosine, phenylalanine) and positively charged free amino acids (arginine, ornithine, lysine, hydroxylysine, histidine) when adhere and spread onto fibronectin. In the presence of agents that impair cell spreading or adhesion (cytochalasin D, fMLP, nonadhesive substrate), neutrophils release the same amino acids, except for a sharp decrease in hydroxylysine and an increase in phenylalanine, indicating their special connection with cell adhesion. Plasma of patients with diabetes is characterized by an increased content of branched-chain and aromatic amino acids and a reduced ratio of arginine/ornithine compared to healthy human plasma. Our data showed that the secretion of neutrophils, regardless of their adhesion state, can contribute to this shift in the amino acid content. Abbreviations: BCAAs: branched-chain amino acids; Е2: 17β-estradiol; LPS: lipopolysaccharide from Salmonella enterica serovar Typhimurium; fMLP: N-formylmethionyl-leucyl-phenylalanine.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"98-105"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1540903","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36605785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Small G protein signalling modulator 2 (SGSM2) is involved in oestrogen receptor-positive breast cancer metastasis through enhancement of migratory cell adhesion via interaction with E-cadherin.","authors":"Juo-Han Lin, Wen-Jui Lee, Han-Chung Wu, Chih-Hsiung Wu, Li-Ching Chen, Chi-Cheng Huang, Hang-Lung Chang, Tzu-Chun Cheng, Hui-Wen Chang, Chi-Tang Ho, Shih-Hsin Tu, Yuan-Soon Ho","doi":"10.1080/19336918.2019.1568139","DOIUrl":"https://doi.org/10.1080/19336918.2019.1568139","url":null,"abstract":"<p><p>The function of small G protein signalling modulators (SGSM1/2/3) in cancer remains unknown. Our findings demonstrated that SGSM2 is a plasma membrane protein that strongly interacted with E-cadherin/β-catenin. SGSM2 downregulation enhanced the phosphorylation of focal adhesion kinase (FAK; Y576/577), decreased the expression of epithelial markers such as E-cadherin, β-catenin, and Paxillin, and increased the expression of Snail and Twist-1, which reduced cell adhesion and promoted cancer cell migration. Oestrogen and fibronectin treatment was found to promote the colocalization of SGSM2 at the leading edge with phospho-FAK (Y397). The BioGRID database showed that SGSM2 potentially interacts with cytoskeleton remodelling and cell-cell junction proteins. These evidences suggest that SGSM2 plays a role in modulating cell adhesion and cytoskeleton dynamics during cancer migration.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"120-137"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1568139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36545940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}