Modulation of cell behaviors by electrochemically active polyelectrolyte multilayers

e-Polymers ◽  
2014 ◽  
Vol 14 (5) ◽  
pp. 297-304
Author(s):  
Guo-xun Chang ◽  
Ke-feng Ren ◽  
Yi-xiu Zhao ◽  
Yi-xin Sun ◽  
Jian Ji
Keyword(s):  
Mechanical Properties ◽  
Chemical Properties ◽  
Fibroblast Cell ◽  
Electrochemical Treatment ◽  
Cell Behaviors ◽  
Cellular Processes ◽  
Tunable Mechanical Properties ◽  
And Migration ◽  
Nih 3T3 ◽  
Proliferation And Migration

AbstractIn addition to the topographical features and chemical properties of substrates, the mechanical properties are known as a vital regulator of cellular processes such as adhesion, proliferation, and migration, and have received considerable attention in recent years. In this work, electrochemical redox multilayers made of ferrocene-modified poly(ethylenimine) (PEI-Fc) and deoxyribonucleic acid (DNA) with controlled stiffness were used to investigate the effects of the mechanical properties of multilayers on fibroblast cell (NIH/3T3) behaviors. Redox PEI-Fc plays an essential role in inducing swelling in multilayers under an electrochemical stimulus, resulting in distinct changes in the stiffness of the multilayers. The Young’s modulus varied from 2.05 to 1.07 MPa for the (PEI-Fc/DNA) multilayers by changing the oxidation time of the electrochemical treatment. We demonstrated that the adhesion, proliferation, and migration of fibroblast cells depended on the multilayers’ stiffness. These results indicate that cell behaviors can be precisely controlled by electrochemical treatment, which provides a new way to prepare thin films with tunable mechanical properties with potential biomedical applications.

scholarly journals MicroRNA-27a-3p promotes proliferation and migration by up-regulation of perlecan in murine fibroblast cell line NIH/3T3

2021 ◽  
Author(s):  
Jin Wang ◽  
Qingyue Ma ◽  
Wenquan Pang ◽  
Shangzhi Li ◽  
Yunwen Zou ◽  
...  
Keyword(s):  
Cell Viability ◽  
Fibroblast Cell ◽  
3T3 Cells ◽  
Expression Levels ◽  
Gene Assay ◽  
And Migration ◽  
Skin Scar ◽  
Nih 3T3 ◽  
Proliferation And Migration ◽  
Nih 3T3 Cells

IntroductionSkin scar is a common cutaneous complication, the outcome of which is unpleasant. Several microRNAs (miRs) participate in the process of skin scar formation. We aimed to explore the role of miR-27a-3p in NIH/3T3 mouse fibroblasts as well as the downstream protein and signaling cascades.Material and methodsmiR-27a-3p was aberrantly expressed in NIH/3T3 cells, followed by measurements of cell viability, migration and expressions of proteins related to proliferation and migration. Perlecan expression in cells aberrantly expressing miR-27a-3p was examined by Western blot analysis. Reporter gene assay was conducted to assess the relationship between miR-27a-3p and perlecan. Then, whether miR-27a-3p affected NIH/3T3 cells through regulating perlecan was ascertained. The effects of aberrantly expressed miR-27a-3p and perlecan on expression levels of VEGF, bFGF and key kinases in the MAPK/ERK and the PI3K/AKT pathways were detected.ResultsCell viability and migration were enhanced and protein expression levels of Cyclin D1, MMP-2 and MMP-9 were up-regulated by miR-27a-3p overexpression in NIH/3T3 cells. Then, we found that perlecan was positively correlated with miR-27a-3p expression, and its knockdown abrogated the effects of miR-27a-3p overexpression on NIH/3T3 cells. Finally, we found that the expression levels of VEGF and bFGF as well as phosphorylated levels of MAPK, ERK, PI3K and AKT were increased by miR-27a-3p overexpression, and those increases were reversed by perlecan knockdown.ConclusionsmiR-27a-3p promotes proliferation and migration of NIH/3T3 cells through up-regulating perlecan expression. Meanwhile, miR-27a-3p up-regulates expression levels of VEGF and bFGF, and activates MAPK/ERK and PI3K/AKT pathways through up-regulating perlecan expression.

scholarly journals High shear stress suppresses proliferation and migration but promotes apoptosis of endothelial cells co-cultured with vascular smooth muscle cells via down-regulating MAPK pathway

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Qiang Ji ◽  
Yu Lin Wang ◽  
Li Min Xia ◽  
Ye Yang ◽  
Chun Sheng Wang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Culture System ◽  
Stress Condition ◽  
Mapk Pathway ◽  
High Shear ◽  
High Shear Stress ◽  
Cellular Processes ◽  
Mapk Pathways ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Early neointimal hyperplasia of vein graft may be ameliorated via enhancing intravenous surface shear stress. Cellular processes including proliferation, apoptosis and migration of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) may play very important roles in the process of neointimal hyperplasia of vein graft; and mitogen-activated protein kinase (MAPK) pathways including extracellular signal-regulated kinase (ERK1/2) and p38 pathways play vital roles in regulating a large variety of cellular processes. This study evaluated the impacts of shear stress and MAPK pathways on cellular processes of ECs in a co-culture system with VSMCs, and aimed to test the hypothesis that high shear stress suppresses proliferation and migration but promotes apoptosis of ECs co-cultured with VSMCs via down-regulating MAPK pathway. Methods Primary ECs and VSMCs derived from porcine great saphenous vein were collected, respectively. 4–7 generation of cells were used as work cells. ECs and VSMCs were co-cultured and synchronized under high and low shear stress using Parallel-Plate Flow Chamber system. And then, ECs co-cultured with VSMCs were incubated with U0126 (ERK1/2 inhibitor) or PD98059 (p38 inhibitor) under different shear stress. Proliferation, apoptosis and migration of ECs in a co-culture system with VSMCs were detected by 4,5-dimethyl-2-thiazolyl (MTT) assay and bromodeoxyuridine (BrdU) assay, fluorescent-activated cell sorting (FACS) technique, and Transwell assay separately. Each test repeated 3 times. Additionally, protein expressions of ERK1/2 and p38 MAPK were detected by using Western blot, respectively. Results Under higher level of shear stress condition, proliferation and migration of ECs co-cultured with VSMCs were suppressed, while cell apoptosis was promoted. And blocking ERK1/2 pathway by U0126 or blocking p38 pathway by PD98059, proliferation and migration of ECs co-cultured with VSMCs were further suppressed, while cell apoptosis was further promoted. Additionally, protein expressions of phosphorylation of ERK1/2 and p38MAPK were decreased under higher level of shear stress condition, and were further reduced by blocking ERK1/2 or p38 pathway under shear stress condition. Conclusions High shear stress may suppress proliferation and apoptosis of ECs in a co-culture system with VSMCs but promote cell migration via down-regulating ERK1/2 and p38 MAPK pathways.

scholarly journals Wound Healing Potential of Spirulina Protein on CCD-986sk Cells

Marine Drugs ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. 130
Author(s):  
Ping Liu ◽  
Jeong-Wook Choi ◽  
Min-Kyeong Lee ◽  
Youn-Hee Choi ◽  
Taek-Jeong Nam
Keyword(s):  
Wound Healing ◽  
Dermal Fibroblast ◽  
Fibroblast Cell ◽  
Underlying Mechanism ◽  
Human Dermal Fibroblast ◽  
Dermal Fibroblasts ◽  
Cyclin Dependent Kinase ◽  
Pi3k Inhibitor Ly294002 ◽  
And Migration ◽  
Proliferation And Migration

Wound healing is a dynamic and complex process. The proliferation and migration of dermal fibroblasts are crucial for wound healing. Recent studies have indicated that the extracts from Spirulina platensis have a positive potential for wound healing. However, its underlying mechanism is not fully understood. Our previous study showed that spirulina crude protein (SPCP) promoted the viability of human dermal fibroblast cell line (CCD-986sk cells). In this study, we further investigated the wound healing effect and corresponding mechanisms of SPCP on CCD-986sk cells. Bromodeoxyuridine (BrdU) assay showed that SPCP promoted the proliferation of CCD-986sk cells. The wound healing assay showed that SPCP promoted the migration of CCD-986sk cells. Furthermore, cell cycle analysis demonstrated that SPCP promoted CCD-986sk cells to enter S and G2/M phases from G0/G1 phase. Western blot results showed that SPCP significantly upregulated the expression of cyclin D1, cyclin E, cyclin-dependent kinase 2 (Cdk2), cyclin-dependent kinase 4 (Cdk4), and cyclin-dependent kinase 6 (Cdk6), as well as inhibited the expression of CDK inhibitors p21 and p27 in CCD-986sk cells. In the meanwhile, SPCP promoted the phosphorylation and activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt). However, the phosphorylation of Akt was significantly blocked by PI3K inhibitor (LY294002), which in turn reduced the SPCP-induced proliferation and migration of CCD-986sk cells. Therefore, the results presenting in this study suggested that SPCP can promote the proliferation and migration of CCD-986sk cells; the PI3K/Akt signaling pathway play a positive and important role in these processes.

Electrospun PLGA/SF Modified with Electrosprayed Microparticles: A Novel Biomimetic Composite Scaffold for Vascular Tissue Engineering

2014 ◽  
Vol 1015 ◽  
pp. 336-339 ◽  
Author(s):  
Li Yu ◽  
Xue Fang Hao ◽  
Qian Li ◽  
Chang Can Shi ◽  
Ya Kai Feng
Keyword(s):  
Mechanical Properties ◽  
Vascular Tissue ◽  
Composite Scaffold ◽  
Weight Ratio ◽  
Electrospinning Technique ◽  
Electrospun Scaffolds ◽  
Biomimetic Scaffold ◽  
Ea.Hy926 Cells ◽  
And Migration ◽  
Proliferation And Migration

Here, a novel biomimetic scaffold with controlled diameters and mechanical properties was prepared from negatively charged silk fiber (SF) and poly (lactide-co-glycolide) (PLGA) by electrospinning technique. The fiber diameters and mechanical properties of the scaffolds were controlled by varying the weight ratio of PLGA/SF. Furthermore, in order to promote endothelialization on the scaffolds, pEGFP-ZNF580 loaded microparticles (MPs) were used to modify the surface of the electrospun scaffolds via electrospraying technique. Results showed that the composite scaffolds with these MPs could promote proliferation and migration of EA.hy926 cells significantly.

scholarly journals The role of RelA (p65) threonine 505 phosphorylation in the regulation of cell growth, survival, and migration

2011 ◽  
Vol 22 (17) ◽  
pp. 3032-3040 ◽  
Author(s):  
Aichi Msaki ◽  
Ana M. Sánchez ◽  
Li Fang Koh ◽  
Benjamin Barré ◽  
Sonia Rocha ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Cellular Migration ◽  
Negative Regulator ◽  
Drug Induced ◽  
Conserved Residues ◽  
Cellular Processes ◽  
And Migration ◽  
Induced Apoptosis ◽  
Proliferation And Migration

The NF-κB family of transcription factors is a well-established regulator of the immune and inflammatory responses and also plays a key role in other cellular processes, including cell death, proliferation, and migration. Conserved residues in the trans-activation domain of RelA, which can be posttranslationally modified, regulate divergent NF-κB functions in response to different cellular stimuli. Using rela−/−mouse embryonic fibroblasts reconstituted with RelA, we find that mutation of the threonine 505 (T505) phospho site to alanine has wide-ranging effects on NF-κB function. These include previously described effects on chemotherapeutic drug-induced apoptosis, as well as new roles for this modification in autophagy, cell proliferation, and migration. This last effect was associated with alterations in the actin cytoskeleton and expression of cellular migration–associated genes such as WAVE3 and α-actinin 4. We also define a new component of cisplatin-induced, RelA T505–dependent apoptosis, involving induction of NOXA gene expression, an effect explained at least in part through induction of the p53 homologue, p73. Therefore, in contrast to other RelA phosphorylation events, which positively regulate NF-κB function, we identified RelA T505 phosphorylation as a negative regulator of its ability to induce diverse cellular processes such as apoptosis, autophagy, proliferation, and migration.

X-RAY IRRADIATION AFFECTS MORPHOLOGY, PROLIFERATION AND MIGRATION RATE OF HEALTHY AND CANCER CELLS

2015 ◽  
Vol 15 (02) ◽  
pp. 1540022 ◽  
Author(s):  
VALERIA PANZETTA ◽  
MARTA DE MENNA ◽  
DEBORA BUCCI ◽  
VITTORIA GIOVANNINI ◽  
MARIAGABRIELLA PUGLIESE ◽  
...  
Keyword(s):  
Simian Virus 40 ◽  
Simian Virus ◽  
Cell Phenotype ◽  
X Rays ◽  
X Ray ◽  
Cellular Processes ◽  
And Migration ◽  
Normalization Effect ◽  
Different Doses ◽  
Proliferation And Migration

Cytoskeleton plays a central role in many cellular processes, such as migration, adhesion and proliferation. Alterations of its structural properties are commonly associated with different diseases (malignancy, cardiac hypertrophy, etc.). In this work, we studied the effects of X-radiations on cytoskeleton architecture of two cell lines: BALBc/3T3 and Simian virus 40-transformed BALBc/3T3 (SVT2) cells. In agreement with the current literature, we observed reduced adhesion and increased motility of SVT2 cells respect to non-transformed BALBc/3T3. In addition, we showed that two different doses of X-rays (1 and 2 Gy) increased cell-dish adhesiveness and reduced cell proliferation and cell motility of transformed cells, whereas minor effects were measured on the normal counterpart. These results suggested that low doses or fractioning of X-rays may have a normalization effect on the investigated parameters for the transformed cell phenotype.

scholarly journals Long non-coding RNAs: novel regulators of cellular physiology and function

2021 ◽  
Author(s):  
James A. Oo ◽  
Ralf P. Brandes ◽  
Matthias S. Leisegang
Keyword(s):  
Damage Control ◽  
Regulation Of Gene Expression ◽  
Cellular Processes ◽  
Current Thinking ◽  
Physiological Relevance ◽  
Non Coding Rnas ◽  
And Migration ◽  
And Function ◽  
Rna And Dna ◽  
Proliferation And Migration

AbstractLong non-coding RNAs were once considered as “junk” RNA produced by aberrant DNA transcription. They are now understood to play central roles in diverse cellular processes from proliferation and migration to differentiation, senescence and DNA damage control. LncRNAs are classed as transcripts longer than 200 nucleotides that do not encode a peptide. They are relevant to many physiological and pathophysiological processes through their control of fundamental molecular functions. This review summarises the recent progress in lncRNA research and highlights the far-reaching physiological relevance of lncRNAs. The main areas of lncRNA research encompassing their characterisation, classification and mechanisms of action will be discussed. In particular, the regulation of gene expression and chromatin landscape through lncRNA control of proteins, DNA and other RNAs will be introduced. This will be exemplified with a selected number of lncRNAs that have been described in numerous physiological contexts and that should be largely representative of the tens-of-thousands of mammalian lncRNAs. To some extent, these lncRNAs have inspired the current thinking on the central dogmas of epigenetics, RNA and DNA mechanisms.

scholarly journals LINC01232 exerts oncogenic activities in pancreatic adenocarcinoma via regulation of TM9SF2

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Qian Li ◽  
Chengbin Lei ◽  
Changliang Lu ◽  
Jingye Wang ◽  
Min Gao ◽  
...  
Keyword(s):  
Pancreatic Adenocarcinoma ◽  
Transcriptional Activation ◽  
Digestive System ◽  
Malignant Tumors ◽  
Loss Of Function ◽  
Protein Coding ◽  
Cellular Processes ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Pancreatic adenocarcinoma (PAAD), one of the most prevailing malignant tumors in digestive system, is identified as one of the main culprits of cancer-associated mortality. Despite long intergenic non-protein coding RNA 1232 (LINC01232) is found to be upregulated in TCGA PAAD tissues and associated with poor prognosis, the potential of LINC01232 in PAAD progression still needs more explorations. In this study, LINC01232 was chosen to be the research object in PAAD cellular processes. Functionally, loss-of function assays were carried out and the experimental results indicated that suppression of LINC01232 hindered the deterioration of PAAD by affecting cell proliferation and migration. Furthermore, relationship between LINC01232 and its nearby gene transmembrane 9 superfamily member 2 (TM9SF2) was investigated. The same expression pattern of TM9SF2 in TCGA PAAD samples was observed. It was found that upregulation of LINC01232 could be a crucial factor for the dysregulation of TM9SF2. Mechanistically, LINC01232 recruited EIF4A3 to boost TM9SF2 mRNA stability. Besides, our findings demonstrated that the transcriptional activation of LINC01232 and TM9SF2 was mediated by SP1. Therefore, we concluded that LINC01232 executed carcinogenic properties in PAAD progression via regulation of TM9SF2. In conclusion, this study was the first to unveil the role and molecular mechanism of LINC01232, suggesting LINC01232 as a promising molecular target for pancreatic cancer treatment.

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