Cell adhesion and communication最新文献

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Wistar Furth rat megakaryocytes lack dense compartments and intercellular plaques, membranous structures rich in cytoskeletal proteins. Wistar Furth大鼠巨核细胞缺乏密集的室室和细胞间斑块,即富含细胞骨架蛋白的膜状结构。
Cell adhesion and communication Pub Date : 1998-07-01 DOI: 10.3109/15419069809010784
P E Stenberg, J H Beckstead, C W Jackson
{"title":"Wistar Furth rat megakaryocytes lack dense compartments and intercellular plaques, membranous structures rich in cytoskeletal proteins.","authors":"P E Stenberg,&nbsp;J H Beckstead,&nbsp;C W Jackson","doi":"10.3109/15419069809010784","DOIUrl":"https://doi.org/10.3109/15419069809010784","url":null,"abstract":"<p><p>Wistar Furth (WF) rats have an abnormal thrombopoietic phenotype with morphologically aberrant megakaryocytes, larger than normal mean platelet volume, and platelet alpha-granule protein deficiency. Here, ultrastructural comparisons of WF rat megakaryocytes to those of rats (Wistar) with normal platelet formation during stimulated megakaryocytopoiesis following 5-fluorouracil administration, have revealed a previously unrecognized membrane structure in normal rat megakaryocytes, and two additional abnormalities in WF megakaryocytes. The novel structures were zones of electron density on the cytoplasmic face of apposed plasma membranes of adjoining normal megakaryocytes. These modified focal adhesion-type contacts were distributed at intervals between adjacent megakaryocytes, and were spaced by deposits of extracellular material. These structures also were present between apposed plasma membranes of Wistar rat megakaryocytes in unperturbed marrows, but were absent between megakaryocytes of WF rats. The second WF rat megakaryocyte abnormality is the absence of cytoplasmic dense compartments, another specialized membranous structure that is continuous with the megakaryocyte demarcation membrane system. Both the intercellular plaques and dense compartments of Wistar rat megakaryocytes were found to be rich in cytoskeletal proteins including actin, alpha-actinin, talin, and vinculin as indicated by ultrastructural immunogold labeling. We hypothesize that an abnormality in cytoskeletal protein function may be responsible for the lack of these structures in the WF rat.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"5 5","pages":"397-407"},"PeriodicalIF":0.0,"publicationDate":"1998-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809010784","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20701647","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: 3
Role of PECAM-1 in the adherence of PMN to hypoxic endothelial cells. PECAM-1在PMN粘附于缺氧内皮细胞中的作用。
Cell adhesion and communication Pub Date : 1998-07-01 DOI: 10.3109/15419069809010782
C Michiels, T Arnould, J Remacle
{"title":"Role of PECAM-1 in the adherence of PMN to hypoxic endothelial cells.","authors":"C Michiels,&nbsp;T Arnould,&nbsp;J Remacle","doi":"10.3109/15419069809010782","DOIUrl":"https://doi.org/10.3109/15419069809010782","url":null,"abstract":"<p><p>Hypoxia induces an increase in PMN adherence to endothelial cells for which an interaction between ICAM-1 and CD18/CD11b has been demonstrated. Since PECAM-1 has been shown to be involved in PMN transmigration through the endothelium and to increase the binding capacity of leukocyte CD18/CD11b, the role of this molecule in the hypoxia-induced PMN adherence was investigated. Hypoxia did not change the total surface expression of PECAM-1 on HUVEC and did not change the cell-cell border localization of this molecule as TNF-alpha did. In addition, blocking anti-PECAM-1 antibodies could not inhibit the increased adherence of unstimulated human PMN to hypoxia-incubated HUVEC while anti-ICAM-1 partially inhibited this process. These results indicate that PECAM-1 is probably not involved in the hypoxia-induced PMN adherence to endothelial cells.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"5 5","pages":"367-74"},"PeriodicalIF":0.0,"publicationDate":"1998-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809010782","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20701645","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: 13
The leukointegrin alpha d/beta 2 (alpha d/CD18): specific changes in surface expression in patients on hemodialysis. 白细胞整合素α d/ β 2 (α d/CD18):血液透析患者表面表达的特异性变化。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809069757
H Rabb, S J Agosti, S Hakala, P Hoffman, W M Gallatin, G Ramirez
{"title":"The leukointegrin alpha d/beta 2 (alpha d/CD18): specific changes in surface expression in patients on hemodialysis.","authors":"H Rabb,&nbsp;S J Agosti,&nbsp;S Hakala,&nbsp;P Hoffman,&nbsp;W M Gallatin,&nbsp;G Ramirez","doi":"10.3109/15419069809069757","DOIUrl":"https://doi.org/10.3109/15419069809069757","url":null,"abstract":"<p><p>Alpha d/CD18 is a newly discovered leukocyte adhesion molecule with sequence homology to CD11a, b and c of the beta 2 integrin family. Little is known about alpha d expression in vivo, particularly how it compares with the other beta 2 integrins. Previous studies have demonstrated that beta 2 integrin expression, particularly CD11b, is upregulated in vivo during hemodialysis (HD) with complement activating membranes. These changes may contribute to the immunologic abnormalities seen in HD patients. Given the well described changes of beta 2 integrins in these patients, we hypothesized that alpha d expression could also be altered by HD. Using flow cytometry with two specific antibodies to alpha d, alpha d expression in healthy adults (n = 16) was compared on macrophages (MO) > polymorphonuclear cells (PMNs) > lymphocytes (LY). Phorbol ester treatment of leukocytes in vitro significantly increased expression on MO and PMN, but not LY. Chronic HD patients at baseline (n = 15) had elevated (P < 0.05) alpha d mean channel fluorescence (MCF) on MOs, PMNs and LYs compared to normals. PMN alpha d MCF increased at 15 min into HD, but then returned to baseline levels at 180 min. Alpha d MCF for LYs decreased at 180 min, while MOs levels were unchanged. Alpha d expression is increased in chronic renal failure and further regulated by hemodialysis, but with unique characteristics compared to the other beta 2 integrins. Alpha d may be important in abnormal cell-cell contacts in renal failure.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"6 1","pages":"13-20"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809069757","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20672800","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: 3
Cadherin/catenin complexes in murine epidermal keratinocytes: E-cadherin complexes containing either beta-catenin or plakoglobin contribute to stable cell-cell contacts. 小鼠表皮角质形成细胞中的钙粘蛋白/连环蛋白复合物:含有β -连环蛋白或血小板红蛋白的e -钙粘蛋白复合物有助于稳定细胞-细胞接触。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809069760
E Lozano, A Cano
{"title":"Cadherin/catenin complexes in murine epidermal keratinocytes: E-cadherin complexes containing either beta-catenin or plakoglobin contribute to stable cell-cell contacts.","authors":"E Lozano,&nbsp;A Cano","doi":"10.3109/15419069809069760","DOIUrl":"https://doi.org/10.3109/15419069809069760","url":null,"abstract":"<p><p>The cadherin/catenin complexes expressed by a murine epidermal keratinocyte cell line PDV, expressing E- and P-cadherin, have been analysed using a combination of biochemical and confocal microscopy analysis. Two types of E-cadherin complexes, containing beta-catenin or plakoglobin and alpha-catenin, were detected in PDV cells as in other cell types, while P-cadherin was mainly detected in complexes containing beta-catenin and alpha-catenin in PDV and other murine epidermal keratinocytes. Biotin-labelling studies have shown that both types of E-cadherin complexes are present at the surface of confluent cells. Furthermore, confocal microscopy analysis indicated that E-cadherin/plakoglobin complexes are located in stable cell-cell contacts at the middle lateral membranes and associated with alpha-catenin and the actin cytoskeleton, with a similar distribution to that to the E-cadherin/beta-catenin complexes. In addition, E-cadherin/plakoglobin complexes not associated with alpha-catenin or the actin cytoskeleton were detected in lower planes of the lateral contacting membranes as well as E-cadherin non-associated with catenins in the more basal planes. These studies support that in murine epidermal keratinocytes both beta-catenin- and plakoglobin-containing E-cadherin complexes contribute to the maintenance of stable cell-cell contacts and suggest a differential role of the plakoglobin containing complexes in different epithelial cell types.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"6 1","pages":"51-67"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809069760","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20672632","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: 15
Expression of cell adhesion molecules and cytokines in murine antigen-induced arthritis. 小鼠抗原性关节炎中细胞粘附分子和细胞因子的表达。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809069761
G H Hersmann, J Kriegsmann, J Simon, C Hüttich, R Bräuer
{"title":"Expression of cell adhesion molecules and cytokines in murine antigen-induced arthritis.","authors":"G H Hersmann,&nbsp;J Kriegsmann,&nbsp;J Simon,&nbsp;C Hüttich,&nbsp;R Bräuer","doi":"10.3109/15419069809069761","DOIUrl":"https://doi.org/10.3109/15419069809069761","url":null,"abstract":"<p><p>Adhesion molecules and cytokines are important in chronic inflammatory conditions such as rheumatoid arthritis (RA) by virtue of their role in cell activation and emigration. Using immunohistochemical techniques we studied the expression of adhesion molecules and cytokines in cryopreserved sections of murine knee joint in the course of antigen-induced arthritis, an animal model of human RA. Various adhesion molecules and cytokines are expressed in the arthritic joint tissue. LFA-1, Mac-1, CD44, ICAM-1 and P-selectin were strongly expressed in the acute phase and to a lesser degree in the chronic phase of arthritis. VLA-4 and VCAM-1 appeared to be moderately expressed on day 1, L-selectin between days 1 and 3. LFA-1, Mac-1, CD44, alpha 4-integrin, ICAM-1 and the selectins were found expressed on cells of the synovial infiltrate, LFA-1, Mac-1 and ICAM-1 on the synovial lining layer, and VCAM-1 and P-selectin on endothelial cells. Expression of E-selectin could be demonstrated throughout the experiment at a low level in cells of the acute cell infiltrate. Cytokines, especially IL-2, IL-4, IL-6, TNF, and IFN-gamma, were heavily expressed during the acute phase of arthritis in cellular infiltrate. Taken together these data demonstrate that cytokines and their activation of adhesion molecules contribute to cell infiltration and activation during the initial phase of arthritis and to the induction and progression of tissue destruction in arthritic joints. These molecules might be potential targets for novel therapeutic strategies in inflammatory and arthritic disorders.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"6 1","pages":"69-82"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809069761","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20672633","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: 34
Abnormal interactions of embryonic mouse trisomy 16 heart fibroblasts with extracellular matrix components in vitro. 胚胎小鼠16三体心脏成纤维细胞与细胞外基质组分的异常相互作用。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809069756
W Carver
{"title":"Abnormal interactions of embryonic mouse trisomy 16 heart fibroblasts with extracellular matrix components in vitro.","authors":"W Carver","doi":"10.3109/15419069809069756","DOIUrl":"https://doi.org/10.3109/15419069809069756","url":null,"abstract":"<p><p>Trisomy 16 mice have cardiovascular abnormalities thought to arise from altered development and maturation of the cardiac cushions. Cell-cell and cell-extracellular matrix (ECM) interactions play critical roles in heart morphogenesis. To begin to examine the potential involvement of cell-ECM interactions in abnormal trisomy 16 heart development, fibroblasts were isolated from normal and trisomy 16 embryonic mouse hearts. Behavior of these cells was compared in bioassays involving cell-ECM interactions including cell attachment and collagen gel contraction. Significant differences in cell-ECM interactions were found between fibroblasts isolated from normal and trisomy 16 embryonic hearts. Trisomy 16 cells attached poorly to collagen and laminin compared to normal fibroblasts. Trisomy 16 heart fibroblasts also contracted collagen gels less effectively than normal heart fibroblasts. Cell-ECM interactions are largely mediated by ECM receptors of the integrin family. Expression of beta 1 integrins was examined at the mRNA and protein levels in normal and trisomy 16 fibroblasts. Analyses of integrin expression indicated the pattern of integrins produced by normal and trisomy 16 fibroblasts to be similar. These results indicate that fibroblasts isolated from embryonic trisomy 16 mouse hearts interact with several ECM components including collagen and laminin less efficiently than fibroblasts from normal mouse embryos. As cell-ECM interactions play significant roles in cardiac cushion development, abnormal interactions may contribute to defective atrioventricular septal morphogenesis in the trisomy 16 mouse.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"6 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809069756","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20672799","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: 6
Adhesive interactions of human multiple myeloma cell lines with different extracellular matrix molecules. 人多发性骨髓瘤细胞系与不同细胞外基质分子的粘附相互作用。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809040300
C Kibler, F Schermutzki, H D Waller, R Timpl, C A Müller, G Klein
{"title":"Adhesive interactions of human multiple myeloma cell lines with different extracellular matrix molecules.","authors":"C Kibler,&nbsp;F Schermutzki,&nbsp;H D Waller,&nbsp;R Timpl,&nbsp;C A Müller,&nbsp;G Klein","doi":"10.3109/15419069809040300","DOIUrl":"https://doi.org/10.3109/15419069809040300","url":null,"abstract":"<p><p>Multiple myeloma represents a human B cell malignancy which is characterized by a predominant localization of the malignant cell clone within the bone marrow. With the exception of the terminal stage of the disease the myeloma tumor cells do not circulate in the peripheral blood. The bone marrow microenvironment is believed to play an important role in homing, proliferation and terminal differentiation of myeloma cells. Here we have studied the expression of several extracellular matrix (ECM) molecules in the bone marrow of multiple myeloma patients and analyzed their adhesive capacities with four different human myeloma-derived cell lines. All ECM molecules analyzed (tenascin, laminin, fibronectin, collagen types I, III, V and VI) could be detected in bone marrow cryostat sections of multiple myeloma patients. Adhesion assays showed that only laminin, the microfibrillar collagen type VI and fibronectin were strong adhesive components for the myeloma cell lines U266, IM-9, OPM-2 and NCI-H929. Tenascin and collagen type I were only weak adhesive substrates for these myeloma cells. Adhesion to laminin and fibronectin was beta 1-integrin-mediated since addition of anti-beta 1-integrin antibodies could inhibit the binding of the four different cell types to both matrix molecules. In contrast, integrins do not seem to be involved in binding of the myeloma cells to collagen type VI. Instead, inhibition of binding by heparin suggested that membrane-bound heparan sulfate proteoglycans are responsible ligands for binding to collagen type VI. Adhesion assays with several B-cell lines resembling earlier differentiation stages revealed only weak interactions with tenascin and no interactions with collagen type VI, laminin or fibronectin. In summary, the interactions of human myeloma cells with the extracellular matrix may explain the specific retention of the plasma cells within the bone marrow.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"5 4","pages":"307-23"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809040300","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20676082","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: 37
Engagement of variant CD44 confers resistance to anti-integrin antibody-mediated apoptosis in a colon carcinoma cell line. 在结肠癌细胞系中,变体CD44的参与赋予抗整合素抗体介导的细胞凋亡的抗性。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809069758
R C Bates, C A Elith, R F Thorne, G F Burns
{"title":"Engagement of variant CD44 confers resistance to anti-integrin antibody-mediated apoptosis in a colon carcinoma cell line.","authors":"R C Bates,&nbsp;C A Elith,&nbsp;R F Thorne,&nbsp;G F Burns","doi":"10.3109/15419069809069758","DOIUrl":"https://doi.org/10.3109/15419069809069758","url":null,"abstract":"<p><p>The LIM 1863 colon carcinoma cell line grows as structured organoids around a central lumen, and we have previously demonstrated that the three-dimensional arrangement protects the individual cells from apoptosis induced by an anti-alpha v integrin antibody, 23C6 (Bates et al., 1994). Here we show that the intercellular forces which drive spheroid formation can be overcome by exposure of the cells to a collagen substrate, or more specifically through ligation of the CD44 receptor by a monoclonal antibody. Binding to immobilized anti-CD44 antibody induced a monolayer morphology which is accompanied by fibronectin production and secretion, and expression of the integrin alpha v beta 6. Significantly, the cells of the monolayer acquired resistance to 23C6 antibody-mediated apoptosis over time and this property was sustained even after removal from the monolayer. We provide data to show that this resistance is not dependent on monolayer morphology, constant engagement of the CD44 receptor, loss of the 23C6 antigen, or elevation of Bcl-2 or Bcl-XL protein. The CD44 expressed by LIM 1863 is shown to be the metastatic variant of the molecule therefore these results provide a possible explanation for the selective advantages conferred by expression of this variant for metastasizing colon cancer cells. Overall, the findings of this study support a model for the development of malignancy through the production of specific survival and growth signals as a direct consequence of a signaling event induced by stimulation of an epithelial variant of CD44.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"6 1","pages":"21-38"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809069758","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20672630","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: 31
Aggregation independent of N-cadherin and neural cell adhesion molecule on quail myoblasts transformed with temperature-sensitive Rous sarcoma virus. 温度敏感型劳斯肉瘤病毒转化鹌鹑成肌细胞中不依赖n -钙粘蛋白和神经细胞粘附分子的聚集。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809069759
T Adachi, T Takahashi, J Kim
{"title":"Aggregation independent of N-cadherin and neural cell adhesion molecule on quail myoblasts transformed with temperature-sensitive Rous sarcoma virus.","authors":"T Adachi,&nbsp;T Takahashi,&nbsp;J Kim","doi":"10.3109/15419069809069759","DOIUrl":"https://doi.org/10.3109/15419069809069759","url":null,"abstract":"<p><p>Quail myoblasts transformed with the temperature-sensitive mutant of Rous sarcoma virus (QM-RSV cells) differentiate temperature-sensitively. At 41 degrees C, the cells begin to fuse after about 15-18 h and form multinucleated myotubes, whereas, at 35.5 degrees C, the cells proliferate. Tyrosine-phosphorylation relates to this temperature-sensitive differentiation. In the course of the investigation of QM-RSV cells, when QM-RSV cells were dissociated with EDTA and shaken in DMEM, the aggregation activity was detected. This activity was expressed on the cells cultured at 41 degrees C, but not at 35.5 degrees C. For detailed characterization of the aggregation, cells from which cadherin and/or neural cell adhesion molecule (NCAM) were removed by trypsin treatment were used. It was then observed that temperature-sensitive and calcium-dependent aggregation activity was expressed on the cells treated with trypsin and EDTA (TE-cells), although the TE-cells did not retain either aggregation molecule. The aggregation activity began to be expressed at 2-4 h after temperature shift and increased with the differentiation. The expression of the activity related to the tyrosine-phosphorylation of some protein. The aggregation of TE-cells was completely inhibited by D(+)-mannose, D(+)-glucose, and N-acetyl-D-glucosamine, but D(+)-galactose did not affect the aggregation. Thus, the present results suggest that the aggregation of mannose specific C-type animal lectin recognized on TE-cells relates to the early stage of the differentiation of QM-RSV cells.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"6 1","pages":"39-50"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809069759","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20672631","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: 1
Microtubule depolymerization induces stress fibers, focal adhesions, and DNA synthesis via the GTP-binding protein Rho. 微管解聚通过gtp结合蛋白Rho诱导应力纤维、黏附和DNA合成。
Cell adhesion and communication Pub Date : 1998-06-01 DOI: 10.3109/15419069809040295
B P Liu, M Chrzanowska-Wodnicka, K Burridge
{"title":"Microtubule depolymerization induces stress fibers, focal adhesions, and DNA synthesis via the GTP-binding protein Rho.","authors":"B P Liu,&nbsp;M Chrzanowska-Wodnicka,&nbsp;K Burridge","doi":"10.3109/15419069809040295","DOIUrl":"https://doi.org/10.3109/15419069809040295","url":null,"abstract":"<p><p>Microtubule depolymerization has multiple consequences that include actin stress fiber and focal adhesion assembly, increased tyrosine phosphorylation and DNA synthesis. Similar effects induced by serum, or agents such as lysophosphatidic acid, have previously been shown to be mediated by the GTP-binding protein Rho. We have investigated whether the effects of microtubule depolymerization are similarly mediated by Rho and show that they are blocked by the specific Rho inhibitor, C3 transferase. Because microtubule depolymerization induces these effects in quiescent cells, in which Rho is largely inactive, we conclude that microtubule depolymerization leads to activation of Rho. The activation of Rho in response to microtubule depolymerization and the consequent stimulation of contractility suggest a mechanism by which microtubules may regulate microfilament function in various motile phenomena. These range from growth cone extension to the development of the contractile ring during cytokinesis, in which there are interactions between the microtubule and microfilament systems.</p>","PeriodicalId":79325,"journal":{"name":"Cell adhesion and communication","volume":"5 4","pages":"249-55"},"PeriodicalIF":0.0,"publicationDate":"1998-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419069809040295","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20676077","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: 190
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