Collagen‐I/silk‐fibroin biocomposite exhibits microscalar confinement of cells and induces anisotropic morphology and migration of embedded fibroblasts

2020 ◽  
Vol 108 (5) ◽  
pp. 2368-2377
Author(s):  
Subhajit Konar ◽  
Privita Edwina ◽  
Vaibavi Ramanujam ◽  
Arockiarajan Arunachalakasi ◽  
Saumendra Kumar Bajpai
Keyword(s):  
Silk Fibroin ◽  
Collagen I ◽  
Anisotropic Morphology ◽  
And Migration

In Vitro Evaluation of the Growth and Migration of Schwann Cells on Electrospun Silk Fibroin Nanofibers

2011 ◽  
Vol 175-176 ◽  
pp. 220-223 ◽  
Author(s):  
Ai Jun Hu ◽  
Bao Qi Zuo ◽  
Feng Zhang ◽  
Qing Lan ◽  
Huan Xiang Zhang
Keyword(s):  
Tissue Engineering ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Schwann Cells ◽  
Silk Fibroin ◽  
Nerve Tissue ◽  
Nerve Tissue Engineering ◽  
And Migration ◽  
Silk Fibroin Nanofibers

Schwann cells (SCs) are primary structural and functional cells in peripheral nervous system and play a crucial role in peripheral nerve regeneration. Current challenge in peripheral nerve tissue engineering is to produce an implantable scaffold capable of bridging long nerve gaps and assist Scs in directing the growth of regenerating axons in nerve injury recovery. Electrospun silk fibroin nanofibers, fabricated for the cell culture in vitro, can provide such experiment support. Silk fibroin scaffolds (SFS) were fabricated with formic acid (FA), and the average fiber diameter was 305 ± 24 nm. The data from microscopic, immunohistochemical and scanning electron micrograph confirmed that the scaffold was beneficial to the adherence, proliferation and migration of SCs without exerting any significant cytotoxic effects on their phenotype. Thus, providing an experimental foundation accelerated the formation of bands of Bünger to enhance nerve regeneration. 305 nm SFS could be a candidate material for nerve tissue engineering.

Guidance of Olfactory Ensheathing Cell Growth and Migration on Electrospun Silk Fibroin Scaffolds

2010 ◽  
Vol 19 (2) ◽  
pp. 147-158 ◽  
Author(s):  
Yixin Shen ◽  
Yuqiang Qian ◽  
Huanxiang Zhang ◽  
Baoqi Zuo ◽  
Zhenfeng Lu ◽  
...  
Keyword(s):  
Cell Growth ◽  
Silk Fibroin ◽  
Olfactory Ensheathing Cell ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals CXCL12 Modulates Prostate Cancer Cell Adhesion by Altering the Levels or Activities ofβ1-Containing Integrins

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Mehdi Dehghani ◽  
Sedigheh Kianpour ◽  
Ana Zangeneh ◽  
Zohreh Mostafavi-Pour
Keyword(s):  
Prostate Cancer ◽  
Cell Adhesion ◽  
Collagen I ◽  
Integrin Receptors ◽  
High Concentration ◽  
Kinase Activation ◽  
Potential Biomarker ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Recombinant Fragments

The mechanisms by which prostate cancer (PCa) cell adhesion and migration are controlled during metastasis are not well understood. Here, we studied the effect of CXCL12 in PCa cell adhesion and spreading in DU145 and PC3 cell lines using as substrates collagen I, fibronectin (FN), and their recombinant fragments. CXCL12 treatment increasedβ1 integrin-dependent PC3 cell adhesion on FN which correlated with increased focal adhesion kinase activation. However neitherα5β1 norα4β1 subunits were involved in this adhesion. By contrast, CXCL12 decreased DU145 adhesion and spreading on FN by downregulatingα5 andβ1 integrin expression. To demonstrate the clinical relevance of CXCL12 in PCa, we measured CXCL12 levels in plasma by using ELISA and found that the chemokine is elevated in PCa patients when compared to controls. The high concentration of CXCL12 in patients suffering from PCa in comparison to those with benign disease or healthy individuals implicates CXCL12 as a potential biomarker for PCa. In addition these data show that CXCL12 may be crucial in controlling PCa cell adhesion on fibronectin and collagen I, possibly via crosstalk with integrin receptors and/or altering the expression levels of integrin subunits.

scholarly journals Gα12 Inhibits α2β1 Integrin–mediated Madin-Darby Canine Kidney Cell Attachment and Migration on Collagen-I and Blocks Tubulogenesis

2009 ◽  
Vol 20 (21) ◽  
pp. 4596-4610 ◽  
Author(s):  
Tianqing Kong ◽  
Daosong Xu ◽  
Wanfeng Yu ◽  
Ayumi Takakura ◽  
Ilene Boucher ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Focal Adhesion ◽  
Cell Attachment ◽  
Mdck Cells ◽  
Rho Kinase ◽  
Focal Adhesions ◽  
Collagen I ◽  
Partial Recovery ◽  
And Migration ◽  
Α2β1 Integrin

Regulation of epithelial cell attachment and migration are essential for normal development and maintenance of numerous tissues. G proteins and integrins are critical signaling proteins regulating these processes, yet in polarized cells little is known about the interaction of these pathways. Herein, we demonstrate that Gα12 inhibits interaction of MDCK cells with collagen-I, the major ligand for α2β1 integrin. Activating Gα12 (QL point mutation or stimulating endogenous Gα12 with thrombin) inhibited focal adhesions and lamellipodia formation and led to impaired cell migration. Consistent with Gα12-regulated attachment to collagen-I, Gα12-silenced MDCK cells revealed a more adherent phenotype. Inhibiting Rho kinase completely restored normal attachment in Gα12-activated cells, and there was partial recovery with inhibition of Src and protein phosphatase pathways. Gα12 activation led to decreased phosphorylation of focal adhesion kinase and paxillin with displacement of α2 integrin from the focal adhesion protein complex. Using the MDCK cell 3D-tubulogenesis assay, activated Gα12 inhibited tubulogenesis and led to the formation of cyst-like structures. Furthermore, Gα12-silenced MDCK cells were resistant to thrombin-stimulated cyst development. Taken together, these studies provide direct evidence for Gα12–integrin regulation of epithelial cell spreading and migration necessary for normal tubulogenesis.

scholarly journals Multilayer Membranes of Glycosaminoglycans and Collagen I Biomaterials Modulate the Function and Microvesicle Release of Endothelial Progenitor Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Bingyan Dai ◽  
Qunwen Pan ◽  
Zhanghua Li ◽  
Mingyan Zhao ◽  
Xiaorong Liao ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Composite Membranes ◽  
Collagen I ◽  
Layer By Layer ◽  
Multilayer Composite ◽  
Endothelial Progenitor ◽  
Multilayer Membranes ◽  
Novel Strategy ◽  
And Migration

Multilayer composite membrane of biomaterials can increase the function of adipose stem cells or osteoprogenitor cells. Recent evidence indicates endothelial progenitor cells (EPCs) and EPCs released microvesicles (MVs) play important roles in angiogenesis and vascular repair. Here, we investigated the effects of biomaterial multilayer membranes of hyaluronic acid (HA) or chondroitin sulfate (CS) and Collagen I (Col I) on the functions and MVs release of EPCs. Layer-by-layer (LBL) technology was applied to construct the multilayer composite membranes. Four types of the membranes constructed by adsorbing either HA or CS and Col I alternatively with different top layers were studied. The results showed that all four types of multilayer composite membranes could promote EPCs proliferation and migration and inhibit cell senility, apoptosis, and the expression of activated caspase-3. Interestingly, these biomaterials increased the release and the miR-126 level of EPCs-MVs. Moreover, the CS-Col I membrane with CS on the top layer showed the most effects on promoting EPCs proliferation, EPCs-MV release, and miR-126 level in EPCs-MVs. In conclusion, HA/CS and Collagen I composed multilayer composite membranes can promote EPCs functions and release of miR-126 riched EPCs-MVs, which provides a novel strategy for tissue repair treatment.

scholarly journals MicroRNA-223 Regulates Cardiac Fibrosis After Myocardial Infarction by Targeting RASA1

2018 ◽  
Vol 46 (4) ◽  
pp. 1439-1454 ◽  
Author(s):  
Xiaoxiao Liu ◽  
Yifeng Xu ◽  
Yunfei Deng ◽  
Hongli Li
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Cardiac Fibrosis ◽  
Collagen I ◽  
Cell Proliferation And Migration ◽  
Collagen Iii ◽  
And Migration ◽  
Tgf Β1 ◽  
Proliferation And Migration

Background/Aims: Percutaneous coronary intervention reduces acute myocardial infarction (MI)-induced mortality to a great extent, but effective treatments for MI-induced cardiac fibrosis and heart failure are still lacking. MicroRNAs (miRNAs) play a variety of roles in cells and have thus been investigated extensively. MicroRNA-223 (miR-223) expression has been reported to be altered in post-MI heart failure in humans; however, the roles of miR-223 in MI remain unknown. Our study aimed to elucidate the roles of miR-223 in cardiac fibrosis. Methods: Cultured cardiac fibroblasts (CFs) were activated by TGF-β1 stimulation. Gain and loss of miR-223 and RAS p21 protein activator 1 (RASA1) knockdown in CFs were achieved by transfecting the cells with miR-223 mimics and inhibitors, as well as small interfering RNA-RASA1 (siRASA1), respectively. Quantitative real-time reverse transcriptase-polymerase chain reactions (qRT-PCR) was used to determine miR-223-3p and RASA1 expression levels, and Cell Counting Kit-8 (CCK-8), transwell migration and scratch assays were performed to assess CFs viability and migration, respectively. Western blotting was used to detect collagen I, collagen III, alpha-smooth muscle actin (a-SMA), RASA1, p-Akt/t-Akt, p-MEK1/2/t-MEK1/2, and p-ERK1/2/t-ERK1/2 protein expressions, and immunofluorescence assays were used to detect the expression of α-actin, vimentin and α-SMA. Luciferase assays were carried out to determine whether miR-223 binds to RASA1. Rat models of MI were established by the ligation of the left anterior descending (LAD) coronary artery. MiR-223 inhibition in vivo was achieved via intramyocardial injections of the miR-223 sponge carried by adeno-associated virus 9 (AAV9). The cardiac function was detected by echocardiography, and cardiac fibrosis was shown by Masson’s trichrome staining. Results: miR-223 was increased in CFs compared to cardiomypcytes, and TGF-β1 treatment increased miR-223 expression in CFs. The miR-223 mimics enhanced cell proliferation and migration and collagen I, collagen III, and α-SMA protein expression in CFs, while the miR-223 inhibitors had contrasting effects and partially prevented the promoting effects of TGF-β1. qRT-PCR and western blotting revealed that miR-223 negatively regulated RASA1 expression, and the luciferase assays showed that miR-223 suppressed the luciferase activity of the RASA1 3’ untranslated region (3'UTR), indicating that miR-223 binds directly to RASA1. Similar to transfection with the miR-223 mimics, RASA1 knockdown enhanced cell proliferation and migration and collagen I, collagen III, and α-SMA protein expression in CFs. Moreover, RASA1 knockdown partially reversed the inhibitory effects of the miR-223 inhibitor on cell proliferation and migration and collagen I, collagen III, and α-SMA protein expression, indicating that the effects of miR-223 in CFs are partially mediated by the regulation of RASA1 expression. Further exploration showed that miR-223 mimics and siRASA1 promoted MEK1/2, ERK1/2 and AKT phosphorylation, while the miR-223 inhibitors had contrasting effects. The in vivo experiments confirmed the results of the in vitro experiments and showed that miR-223 inhibition prevented cardiac functional deterioration and cardiac fibrosis. Conclusions: miR-223 enhanced cell proliferation, migration, and differentiation in CFs, thus mediated cardiac fibrosis after MI partially via the involvement of RASA1.

Neovascularization of Porous Silk Fibroin Films(PSFFs) as Dermis Substitutes Implanted in Rats

2009 ◽  
Vol 610-613 ◽  
pp. 1113-1119 ◽  
Author(s):  
Guo Ping Guan ◽  
Lun Bai ◽  
Bao Qi Zuo ◽  
Ming Zhong Li ◽  
Zi Lin Sun ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cells ◽  
Connective Tissue ◽  
Silk Fibroin ◽  
Loose Connective Tissue ◽  
Normal Tissues ◽  
Subcutaneous Tissues ◽  
And Migration ◽  
New Formation ◽  
Proliferation And Migration

Neovascularization in biomaterials plays a key role in wound healing. In this paper, porous silk fibroin films (PSFFs) whose structure was optimized, as dermis substitutes, were implanted in the back skin of rats for recovery of dermis loss. Results showed that a thin layer of loose connective tissue had formed at the interface between PSFFs and subcutaneous tissues, in which abundant blood vessels could be observed at 24 h after surgery. Whereafter the newly formed connective tissue thickened and the number of microvessels in the tissue increased. Furthermore, a few microvessels could be seen in PSFFs at day 5, most of which were capillaries. By day 10, the density of microvessels in PSFFs increased to a peak while the percentage of capillary decreased. At day 23, both the density of microvessels and the percentage of capillary was almost equal to those of normal tissues. In summary, wound healing with PSFFs as dermis substitutes is the neovascularization process of PSFFs. The process includes three major steps: (1) new formation and growth of loose connective tissue into the pores of PSFFs, (2) proliferation and migration of fibroblasts and endothelial cells, and (3) formation of functional microvessels and their networks.

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