Cell Adhesion & Migration最新文献_第8页

Platelet endothelial aggregation receptor-1 regulates bovine muscle satellite cell migration and differentiation via integrin beta-1 and focal adhesion kinase. 血小板内皮聚集受体-1通过整合素-1和局灶黏附激酶调控牛肌肉卫星细胞的迁移和分化。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1619434

Yusheng Pang, Ziheng Zhang, Zhao Wang, Yuxin Wang, Yunqin Yan, Shufeng Li, Huili Tong

引用次数: 8

Decreased expression of circ_0020397 in intracranial aneurysms may be contributing to decreased vascular smooth muscle cell proliferation via increased expression of miR-138 and subsequent decreased KDR expression. circ_0020397在颅内动脉瘤中的表达减少可能通过miR-138的表达增加和随后的KDR表达减少导致血管平滑肌细胞增殖减少。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1619432

Yushe Wang, Yong Wang, Yu Li, Bin Wang, Zhuang Miao, Xianzhi Liu, Yuanyuan Ma

{"title":"Decreased expression of circ_0020397 in intracranial aneurysms may be contributing to decreased vascular smooth muscle cell proliferation via increased expression of miR-138 and subsequent decreased KDR expression.","authors":"Yushe Wang, Yong Wang, Yu Li, Bin Wang, Zhuang Miao, Xianzhi Liu, Yuanyuan Ma","doi":"10.1080/19336918.2019.1619432","DOIUrl":"https://doi.org/10.1080/19336918.2019.1619432","url":null,"abstract":"Dysfunction of vascular smooth muscle cells (VSMCs) mediates intracranial aneurysm (IA). KDR is reported to alleviate IA progression via promoting VSMC proliferation, while the upstream regulators are still unclear. Arterial wall tissues at the aneurysm site from 12 patients were obtained. The real-time PCR result indicated that circRNA_0020397 was down-regulated, but miR-138 was up-regulated in artery wall tissues and cells of IA. Overexpressed circRNA_0020397 promoted proliferation of human umbilical artery SMCs. MiR-138 negatively regulated KDR via binding with 3'UTR of KDR mRNA. The expression of circRNA_0020397 was negatively correlated with miR-138. In conclusion, our findings demonstrated that decreased expression of circRNA_0020397 in IA may contribute to the decreased VSMC proliferation via increasing miR-138 expression and subsequently decreasing KDR expression.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"220-228"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1619432","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37421594","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}

引用次数: 27

BECN1 promotes the migration of NSCLC cells through regulating the ubiquitination of Vimentin. BECN1通过调控Vimentin泛素化促进NSCLC细胞的迁移。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1638690

Zhujun Cheng, Hongbo Xin, Tianyu Han

引用次数: 15

Fluid shear stress induces cell migration and invasion via activating autophagy in HepG2 cells. 流体剪切应力通过激活HepG2细胞的自噬诱导细胞迁移和侵袭。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2019-01-31 DOI: 10.1080/19336918.2019.1568141

Zhiping Yan, Guanyue Su, Wenbo Gao, Jia He, Yang Shen, Ye Zeng, Xiaoheng Liu

引用次数: 25

N3ICD with the transmembrane domain can effectively inhibit EMT by correcting the position of tight/adherens junctions. 具有跨膜结构域的N3ICD可以通过纠正紧密/粘附连接的位置有效地抑制EMT。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1619958

Junyu Tan, Xixun Zhang, Wenjun Xiao, Xiong Liu, Chun Li, Yuxian Guo, Wei Xiong, Yaochen Li

{"title":"N3ICD with the transmembrane domain can effectively inhibit EMT by correcting the position of tight/adherens junctions.","authors":"Junyu Tan, Xixun Zhang, Wenjun Xiao, Xiong Liu, Chun Li, Yuxian Guo, Wei Xiong, Yaochen Li","doi":"10.1080/19336918.2019.1619958","DOIUrl":"https://doi.org/10.1080/19336918.2019.1619958","url":null,"abstract":"EMT allows a polarized epithelium to lose epithelial integrity and acquire mesenchymal characteristics. Previously, we found that overexpression of the intracellular domain of Notch3 (N3ICD) can inhibit EMT in breast cancer cells. In this study, we aimed to elucidate the influence of N3ICD or N3ICD combined with the transmembrane domain (TD+N3ICD) on the expression and distribution of TJs/AJs and polar molecules. We found that although N3ICD can upregulate the expression levels of the above-mentioned molecules, TD+N3ICD can inhibit EMT more effectively than N3ICD alone. TD+N3ICD overexpression upregulated the expression of endogenous full-length Notch3 and contributed to correcting the position of TJs/AJs molecules and better acinar structures formation. Co-immunoprecipitation results showed that the upregulated endogenous full-length Notch3 could physically interact with E-ca in MDA-MB-231/pCMV-(TD+N3ICD) cells. Collectively, our data indicate that overexpression of TD+N3ICD can effectively inhibit EMT, resulting in better positioning of TJs/AJs molecules and cell-cell adhesion in breast cancer cells. Abbreviations: EMT: Epithelial-mesenchymal transition; TJs: Tight junctions; AJs: Adherens junctions; aPKC: Atypical protein kinase C; Crb: Crumbs; Lgl: Lethal (2) giant larvae; LLGL2: lethal giant larvae homolog 2; PAR: Partitioning defective; PATJ: Pals1-associated TJ protein.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"203-218"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1619958","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37421597","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}

引用次数: 5

Gradient fluid shear stress regulates migration of osteoclast precursors. 梯度流体剪切应力调节破骨细胞前体的迁移。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1619433

Yan Gao, Taiyang Li, Qing Sun, Bo Huo

{"title":"Gradient fluid shear stress regulates migration of osteoclast precursors.","authors":"Yan Gao, Taiyang Li, Qing Sun, Bo Huo","doi":"10.1080/19336918.2019.1619433","DOIUrl":"https://doi.org/10.1080/19336918.2019.1619433","url":null,"abstract":"Cell migration is highly sensitive to fluid shear stress (FSS) in blood flow or interstitial fluid flow. However, whether the FSS gradient can regulate the migration of cells remains unclear. In this work, we constructed a parallel-plate flow chamber with different FSS gradients and verified the gradient flow field by particle image velocimetry measurements and finite element analyses. We then investigated the effect of FSS magnitudes and gradients on the migration of osteoclast precursor RAW264.7 cells. Results showed that the cells sensed the FSS gradient and migrated toward the low-FSS region. This FSS gradient-induced migration tended to occur in low-FSS magnitudes and high gradients, e.g., the migration angle relative to flow direction was approximately 90° for 0.1 Pa FSS and 0.2 Pa mm-1 FSS gradient. When chemically inhibiting the calcium signaling pathways of the mechanosensitive cation channel, endoplasmic reticulum, phospholipase C, and extracellular calcium, the cell migration toward the low-FSS region was significantly reduced. This study may provide insights into the mechanism of the recruitment of osteoclast precursors at the site of bone resorption and of mechanical stimulation-induced bone remodeling.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"183-191"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1619433","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37277687","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}

引用次数: 13

A biophysically-defined hyaluronic acid-based compound accelerates migration and stimulates the production of keratinocyte-derived neuromodulators. 一种生物物理定义的透明质酸化合物加速迁移并刺激角化细胞衍生的神经调节剂的产生。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-08-19 DOI: 10.1080/19336918.2018.1494997

Annalisa La Gatta, Antonella D'Agostino, Chiara Schiraldi, Giuseppe Colella, Nicola Cirillo

{"title":"A biophysically-defined hyaluronic acid-based compound accelerates migration and stimulates the production of keratinocyte-derived neuromodulators.","authors":"Annalisa La Gatta, Antonella D'Agostino, Chiara Schiraldi, Giuseppe Colella, Nicola Cirillo","doi":"10.1080/19336918.2018.1494997","DOIUrl":"https://doi.org/10.1080/19336918.2018.1494997","url":null,"abstract":"Hyaluronic acid (HA) preparations are widely used in clinical practice and recent data suggest that commercially available HA-based compounds promote ulcer re-epithelialization and induce pain relief. However, the pathophysiological basis of these effects remains poorly understood. In the present study, we investigated the biophysical, biomolecular and functional properties of a HA preparation combined with a pool of collagen precursor synthetic aminoacids, namely l-proline, l-leucine, l-lysine and glycine (Aminogam®). Hydrodynamic characterization of Aminogam® by size exclusion chromatography-triple detector array (SEC-TDA) revealed an average molecular weight in the range of 700-1700 kDa. Rheological measurements of the 1700kDa Mw lot showed a pseoudoplastic behaviour with a zero-shear viscosity (η0) equal to 90 ± 9 Pa∙s at 25°C and 55 ± 6 Pa∙s at 37°C. Automated time-lapse videomicroscopy studies in a fibroblast-free system demonstrated that 1% (v/v) Aminogam® significantly reduced the healing time of wounded keratinocyte monolayers. In AKGOS assays, Aminogam® stimulated cellular locomotion (chemokinesis) and directional migration (chemotaxis) of keratinocytes. Analysis of microarray data suggested that keratinocytes had a functional neuroendocrine machinery, and this was confirmed by testing the secretion of six neuroactive molecules by ELISA, namely α-MSH, β-endorphins, melatonin, substance P, cortisol, and neurotensin. Interestingly, Aminogam® regulated the production of several neuropeptides, including β-endorphins. In conclusion, our data shed light on the epithelial-dependent mechanisms that underlie the efficacy of Aminogam®, particularly in reference to wound healing and nociception.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"23-32"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2018.1494997","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36273752","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}

引用次数: 4

The role of cellular contact and TGF-beta signaling in the activation of the epithelial mesenchymal transition (EMT). 细胞接触和 TGF-beta 信号在激活上皮间质转化（EMT）中的作用。

IF 3.3 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2018-10-08 DOI: 10.1080/19336918.2018.1526597

Kelsey Gasior, Nikki J Wagner, Jhon Cores, Rose Caspar, Alyson Wilson, Sudin Bhattacharya, Marlene L Hauck

引用次数: 0

ARHGEF4-mediates the actin cytoskeleton reorganization of hepatic stellate cells in 3-dimensional collagen matrices. arhgef4介导三维胶原基质中肝星状细胞的肌动蛋白细胞骨架重组。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 Epub Date: 2019-03-24 DOI: 10.1080/19336918.2019.1594497

Xiaowei Zhang, Lan Sun, Wei Chen, Shanna Wu, Yanmeng Li, Xiaojin Li, Bei Zhang, Jingyi Yao, Huan Wang, Anjian Xu

{"title":"ARHGEF4-mediates the actin cytoskeleton reorganization of hepatic stellate cells in 3-dimensional collagen matrices.","authors":"Xiaowei Zhang, Lan Sun, Wei Chen, Shanna Wu, Yanmeng Li, Xiaojin Li, Bei Zhang, Jingyi Yao, Huan Wang, Anjian Xu","doi":"10.1080/19336918.2019.1594497","DOIUrl":"https://doi.org/10.1080/19336918.2019.1594497","url":null,"abstract":"The actin cytoskeleton of hepatic stellate cells (HSCs) is reorganized when they are cultured in 3D collagen matrices. Here, we investigated the molecular mechanism of actin cytoskeleton reorganization in HSCs cultured in 3D floating collagen matrices (FCM) compared to those on 2D polystyrene surfaces (PS). First, we found that the generation of dendritic cellular processes was controlled by Rac1. Next, we examined the differential gene expression of HSCs cultured on 2D PS and in 3D FCM by RNA-Seq and focused on the changes of actin cytoskeleton reorganization-related molecular components and guanine nucleotide exchange factors (GEFs). The results showed that the expression of genes associated with actin cytoskeleton reorganization-related cellular components, filopodia and lamellipodia, were significantly decreased, but podosome-related genes was significantly increased in 3D FCM. Furthermore, we found that a Rac1-specific GEF, ARHGEF4, played roles in morphological changes, migration and podosome-related gene expression in HSCs cultured in 3D FCM. Abbreviations: 2D PS: 2-dimensional polystyrene surface; 3D FCM: 3-dimensional floating collagen matrices; ARHGEF4: Rho guanine nucleotide exchange factor 4; ARHGEF6: Rho guanine nucleotide exchange factor 6; GEF: guanine nucleotide exchange factor; HSC: hepatic stellate cell.","PeriodicalId":9680,"journal":{"name":"Cell Adhesion & Migration","volume":"13 1","pages":"169-181"},"PeriodicalIF":3.2,"publicationDate":"2019-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/19336918.2019.1594497","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37055881","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}

引用次数: 0

Snail2 induced E-cadherin suppression and metastasis in lung carcinoma facilitated by G9a and HDACs. Snail2诱导G9a和hdac促进肺癌E-cadherin抑制和转移。

IF 3.2 3区生物学

Cell Adhesion & Migration Pub Date : 2019-12-01 DOI: 10.1080/19336918.2019.1638689

Yue Hu, Yayuan Zheng, Mingrui Dai, Jiaxin Wu, Bin Yu, Haihong Zhang, Wei Kong, Hui Wu, Xianghui Yu

引用次数: 23