S. Cejkova, H. Kubátová, F. Thieme, L. Janousek, J. Fronek, R. Poledne, I. Králová Lesná
{"title":"The effect of cytokines produced by human adipose tissue on monocyte adhesion to the endothelium","authors":"S. Cejkova, H. Kubátová, F. Thieme, L. Janousek, J. Fronek, R. Poledne, I. Králová Lesná","doi":"10.1080/19336918.2019.1644856","DOIUrl":"https://doi.org/10.1080/19336918.2019.1644856","url":null,"abstract":"ABSTRACT Visceral adipose tissue (VAT) may play a critical role in atherosclerotic cardiovascular disease. The goal of this study was to determine the effect of human VAT-released pro‑inflammatory cytokines on monocyte adhesion to the endothelium. The cytokine effects on monocyte adhesion to the endothelial cells (ECs) were tested using adipose tissue-conditioned media (ATCM) prepared by culturing human VAT. The cytokines concentrations in ATCM, the cytokines expression and adhesion molecules in stimulated ECs were measured. The concentrations of IL-1β,TNF-α,MCP-1,IL-10,and RANTES measured in ATCM correlated positively with monocyte adhesiveness to ECs. Additionally, ATCM increased the adhesion molecules (ICAM-1, VCAM-1) gene expression. Selective inhibitors highlighted the importance of IL-1β and TNF-α in the process by a significant decrease in monocyte adhesion compared to ATCM preconditioning without inhibitors. Human VAT significantly increased monocyte adhesion to ECs. It was significantly influenced by IL-1β, TNF-α, MCP-1, IL-10, and RANTES, with IL-1β and TNF‑α having the strongest impact.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1644856","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43935771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Splicing factor-modulated generation of mechano growth factor regulates physiological processes in osteoblasts under mechanical stimuli","authors":"Qian Yi, Huan Liu, Jianguo Feng, Yanjiao Wu, Weichao Sun, Mengting Ou, Liling Tang","doi":"10.1080/19336918.2019.1686103","DOIUrl":"https://doi.org/10.1080/19336918.2019.1686103","url":null,"abstract":"ABSTRACT Mechanical stimuli influence various physiological processes in osteoblasts. We previously showed that mechano-growth factor (MGF), a splicing variant of insulin-like growth factor 1, is highly expressed in osteoblasts in response to mechanical stimuli. This study aims to explore the systemic functions of MGF in osteoblasts, and the mechanisms by which mechanical stress regulates the alternative splicing of Igf1 to generate MGF. We found that MGF promoted the proliferation and migration of osteoblasts, while it inhibited their differentiation via Erk1/2 pathway. Furthermore, cyclic stretching upregulated the expression of ASF/SF2, which in turn regulated the expression of MGF. Our findings indicate that mechanical stimuli influence the physiological responses of osteoblasts by increasing the expression of MGF, which is regulated by splicing factors.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1686103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41395646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. B. Mangukiya, H. Negi, S. B. Merugu, Qudsia Sehar, D. S. Mashausi, F. Yunus, Zhenghua Wu, Dawei Li
{"title":"Paracrine signalling of AGR2 stimulates RhoA function in fibroblasts and modulates cell elongation and migration","authors":"H. B. Mangukiya, H. Negi, S. B. Merugu, Qudsia Sehar, D. S. Mashausi, F. Yunus, Zhenghua Wu, Dawei Li","doi":"10.1080/19336918.2019.1685928","DOIUrl":"https://doi.org/10.1080/19336918.2019.1685928","url":null,"abstract":"ABSTRACT The most prominent cancer-associated fibroblasts (CAFs) in tumor stroma is known to form a protective structure to support tumor growth. Anterior gradient-2 (AGR2), a tumor secretory protein is believed to play a pivotal role during tumor microenvironment (TME) development. Here, we report that extracellular AGR2 enhances fibroblasts elongation and migration significantly. The early stimulation of RhoA showed the association of AGR2 by upregulation of G1-S phase-regulatory protein cyclin D1 and FAK phosphorylation through fibroblasts growth factor receptor (FGFR) and vascular endothelial growth factor receptor (VEGFR). Our finding indicates that secretory AGR2 alters fibroblasts elongation, migration, and organization suggesting the secretory AGR2 as a potential molecular target that might be responsible to alter fibroblasts infiltration to support tumor growth.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1685928","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47123853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Melville B Vaughan, Gang Xu, Tracy L. Morris, Pratiksha Kshetri, Jing X Herwig
{"title":"Predictable fibroblast tension generation by measuring compaction of anchored collagen matrices using microscopy and optical coherence tomography","authors":"Melville B Vaughan, Gang Xu, Tracy L. Morris, Pratiksha Kshetri, Jing X Herwig","doi":"10.1080/19336918.2019.1644855","DOIUrl":"https://doi.org/10.1080/19336918.2019.1644855","url":null,"abstract":"ABSTRACT The anchored fibroblast-populated collagen matrix (aFPCM) is an appropriate model to study fibrocontractive disease mechanisms. Our goal was to determine if aFPCM height reduction (compaction) during development is sufficient to predict tension generation. Compaction was quantified daily by both traditional light microscopy and an optical coherence tomography (OCT) system. Contraction in aFPCM was revealed by releasing them from anchorage. We found that aFPCM contraction increase was correlated to the compaction increase. Cytochalasin D treatment reversibly inhibited compaction. Therefore, we demonstrated that aFPCM height reduction efficiently measures compaction, contraction, and relative maturity of the collagen matrix during development or treatment. In addition, we showed that OCT is suitable for effectively imaging the cross-sectional morphology of the aFPCM in culture. This study will pave the way for more efficient studies on the mechanisms of (and treatments that target) migration and contraction in wound healing and Dupuytren’s contracture in a tissue environment.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1644855","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45978409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mathematical Models of Specific Cell Adhesion Phenomena","authors":"M. Hjortso, J. Roos","doi":"10.1201/9781315138954-2","DOIUrl":"https://doi.org/10.1201/9781315138954-2","url":null,"abstract":"","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2018-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90907012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Kinetics of Ligand-Receptor Bond Formation","authors":"J. Roos, M. Hjortso","doi":"10.1201/9781315138954-1","DOIUrl":"https://doi.org/10.1201/9781315138954-1","url":null,"abstract":"","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2018-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74333357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Adhesion & MigrationPub Date : 2018-05-04Epub Date: 2017-08-18DOI: 10.1080/19336918.2017.1344796
Pavla Röselová, Adam Obr, Aleš Holoubek, Dana Grebeňová, Kateřina Kuželová
{"title":"Adhesion structures in leukemia cells and their regulation by Src family kinases.","authors":"Pavla Röselová, Adam Obr, Aleš Holoubek, Dana Grebeňová, Kateřina Kuželová","doi":"10.1080/19336918.2017.1344796","DOIUrl":"https://doi.org/10.1080/19336918.2017.1344796","url":null,"abstract":"<p><p>Interaction of leukemia blasts with the bone marrow extracellular matrix often results in protection of leukemia cells from chemotherapy and in persistence of the residual disease which is on the basis of subsequent relapses. The adhesion signaling pathways have been extensively studied in adherent cells as well as in mature haematopoietic cells, but the adhesion structures and signaling in haematopoietic stem and progenitor cells, either normal or malignant, are much less explored. We analyzed the interaction of leukemia cells with fibronectin (FN) using interference reflection microscopy, immunofluorescence, measurement of adherent cell fraction, real-time microimpedance measurement and live cell imaging. We found that leukemia cells form very dynamic adhesion structures similar to early stages of focal adhesions. In contrast to adherent cells, where Src family kinases (SFK) belong to important regulators of focal adhesion dynamics, we observed only minor effects of SFK inhibitor dasatinib on leukemia cell binding to FN. The relatively weak involvement of SFK in adhesion structure regulation might be associated with the lack of cytoskeletal mechanical tension in leukemia cells. On the other hand, active Lyn kinase was found to specifically localize to leukemia cell adhesion structures and a less firm cell attachment to FN was often associated with higher Lyn activity (this unexpectedly occurred also after cell treatment with the inhibitor SKI-1). Lyn thus may be important for signaling from integrin-associated complexes to other processes in leukemia cells.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2018-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2017.1344796","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35143574","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 : 2018-05-04Epub Date: 2017-11-13DOI: 10.1080/19336918.2017.1385713
M Rampichová, E Košt'áková Kuželová, E Filová, J Chvojka, J Šafka, M Pelcl, J Daňková, E Prosecká, M Buzgo, M Plencner, D Lukáš, E Amler
{"title":"Composite 3D printed scaffold with structured electrospun nanofibers promotes chondrocyte adhesion and infiltration.","authors":"M Rampichová, E Košt'áková Kuželová, E Filová, J Chvojka, J Šafka, M Pelcl, J Daňková, E Prosecká, M Buzgo, M Plencner, D Lukáš, E Amler","doi":"10.1080/19336918.2017.1385713","DOIUrl":"https://doi.org/10.1080/19336918.2017.1385713","url":null,"abstract":"<p><p>Additive manufacturing, also called 3D printing, is an effective method for preparing scaffolds with defined structure and porosity. The disadvantage of the technique is the excessive smoothness of the printed fibers, which does not support cell adhesion. In the present study, a 3D printed scaffold was combined with electrospun classic or structured nanofibers to promote cell adhesion. Structured nanofibers were used to improve the infiltration of cells into the scaffold. Electrospun layers were connected to 3D printed fibers by gluing, thus enabling the fabrication of scaffolds with unlimited thickness. The composite 3D printed/nanofibrous scaffolds were seeded with primary chondrocytes and tested in vitro for cell adhesion, proliferation and differentiation. The experiment showed excellent cell infiltration, viability, and good cell proliferation. On the other hand, partial chondrocyte dedifferentiation was shown. Other materials supporting chondrogenic differentiation will be investigated in future studies.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2018-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2017.1385713","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35248371","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 : 2018-05-04Epub Date: 2017-11-02DOI: 10.1080/19336918.2017.1379634
Hongyu Zhu, Mingming Gao, Xiangdong Gao, Yue Tong
{"title":"Vascular endothelial growth factor-B: Impact on physiology and pathology.","authors":"Hongyu Zhu, Mingming Gao, Xiangdong Gao, Yue Tong","doi":"10.1080/19336918.2017.1379634","DOIUrl":"https://doi.org/10.1080/19336918.2017.1379634","url":null,"abstract":"<p><p>Angiogenesis plays an important role in controlling tissue development and maintaining normal tissue function. Dysregulated angiogenesis is implicated in the pathogenesis of a variety of diseases, particularly diabetes, cancers, and neurodegenerative disorders. As the major regulator of angiogenesis, the vascular endothelial growth factor (VEGF) family is composed of a group of crucial members including VEGF-B. While the physiological roles of VEGF-B remain debatable, increasing evidence suggests that this protein is able to protect certain type of cells from apoptosis under pathological conditions. More importantly, recent studies reveal that VEGF-B is involved in lipid transport and energy metabolism, implicating this protein in obesity, diabetes and related metabolic complications. This article summarizes the current knowledge and understanding of VEGF-B in physiology and pathology, and shed light on the therapeutic potential of this crucial protein.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2018-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2017.1379634","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35515180","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 : 2018-05-04Epub Date: 2017-11-06DOI: 10.1080/19336918.2017.1377388
Pablo A Mendoza, Patricio Silva, Jorge Díaz, Cecilia Arriagada, Jimena Canales, Oscar Cerda, Vicente A Torres
{"title":"Calpain2 mediates Rab5-driven focal adhesion disassembly and cell migration.","authors":"Pablo A Mendoza, Patricio Silva, Jorge Díaz, Cecilia Arriagada, Jimena Canales, Oscar Cerda, Vicente A Torres","doi":"10.1080/19336918.2017.1377388","DOIUrl":"https://doi.org/10.1080/19336918.2017.1377388","url":null,"abstract":"<p><p>The early endosome protein Rab5 was recently shown to promote cell migration by enhancing focal adhesion disassembly through mechanisms that remain elusive. Focal adhesion disassembly is associated to proteolysis of talin, in a process that requires calpain2. Since calpain2 has been found at vesicles and endosomal compartments, we hypothesized that Rab5 stimulates calpain2 activity, leading to enhanced focal adhesion disassembly in migrating cells. We observed that calpain2 co-localizes with EEA1-positive early endosomes and co-immunoprecipitates with EEA1 and Rab5 in A549 lung carcinoma cells undergoing spreading, whereas Rab5 knock-down decreased the accumulation of calpain2 at early endosomal-enriched fractions. In addition, Rab5 silencing decreased calpain2 activity, as shown by cleavage of the fluorogenic substrate tBOC-LM-CMAC and the endogenous substrate talin. Accordingly, Rab5 promoted focal adhesion disassembly in a calpain2-dependent manner, as expression of GFP-Rab5 accelerated focal adhesion disassembly in nocodazole-synchronized cells, whereas pharmacological inhibition of calpain2 with N-acetyl-Leu-Leu-Met prevented both focal adhesion disassembly and cell migration induced by Rab5. In summary, these data uncover Rab5 as a novel regulator of calpain2 activity and focal adhesion proteolysis leading to cell migration.</p>","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2018-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2017.1377388","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35518804","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}