Dynamic microtubules drive fibroblast spreading

Tvorogova, Anna; Saidova, Aleena A.; Смирнова, Т. А.; Vorobjev, Ivan A.

doi:10.1242/bio.038968

“…The aim of this study was to create a nanofibrous scaffold suitable for the efficient cell adhesion, spreading and functional activity of fibroblasts. The normal cell adhesion and spreading on the substrate surface affect the later stages of the cell functional activity [14,15,16,17]. Therefore, the study of cell spreading is vital in the scaffold’s screening for the purpose of regenerative medicine.…”

Section: Discussionmentioning

confidence: 99%

“…The effectiveness of cell matrices depends on the functional activity of the cells used, which in turn depends on the initial processes of adhesion and spreading on the matrix. Cell adhesion to a functionally well-founded substrate is characterized by a well-defined time, as well as mechanical and energy-dependent processes, determining further cell proliferation, cell migration, cell differentiation, and gene expression [14,15,16,17]. It should be noted that the spreading of cells on the surface of substrates is a complex process and it is controlled by the matrix–integrin interactions that form adhesion sites [15,18,19,20,21].…”

Section: Introductionmentioning

confidence: 99%

Plasma-Coated Polycaprolactone Nanofibers with Covalently Bonded Platelet-Rich Plasma Enhance Adhesion and Growth of Human Fibroblasts

Miroshnichenko

¹

,

Timofeeva

²

,

Permykova

³

et al. 2019

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Biodegradable nanofibers are extensively employed in different areas of biology and medicine, particularly in tissue engineering. The electrospun polycaprolactone (PCL) nanofibers are attracting growing interest due to their good mechanical properties and a low-cost structure similar to the extracellular matrix. However, the unmodified PCL nanofibers exhibit an inert surface, hindering cell adhesion and negatively affecting their further fate. The employment of PCL nanofibrous scaffolds for wound healing requires a certain modification of the PCL surface. In this work, the morphology of PCL nanofibers is optimized by the careful tuning of electrospinning parameters. It is shown that the modification of the PCL nanofibers with the COOH plasma polymers and the subsequent binding of NH2 groups of protein molecules is a rather simple and technologically accessible procedure allowing the adhesion, early spreading, and growth of human fibroblasts to be boosted. The behavior of fibroblasts on the modified PCL surface was found to be very different when compared to the previously studied cultivation of mesenchymal stem cells on the PCL nanofibrous meshes. It is demonstrated by X-ray photoelectron spectroscopy (XPS) that the freeze–thawed platelet-rich plasma (PRP) immobilization can be performed via covalent and non-covalent bonding and that it does not affect biological activity. The covalently bound components of PRP considerably reduce the fibroblast apoptosis and increase the cell proliferation in comparison to the unmodified PCL nanofibers or the PCL nanofibers with non-covalent bonding of PRP. The reported research findings reveal the potential of PCL matrices for application in tissue engineering, while the plasma modification with COOH groups and their subsequent covalent binding with proteins expand this potential even further. The use of such matrices with covalently immobilized PRP for wound healing leads to prolonged biological activity of the immobilized molecules and protects these biomolecules from the aggressive media of the wound.

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“…Interestingly, microtubules drive the spreading response in fibroblasts, where the rapid growth of microtubules toward the cell borders is essential for isotropic spreading ( Tvorogova et al, 2018 ). In our study, we found that Ecm29-silenced B cells displayed a highly symmetric IS, which resembles an isotropic spreading response.…”

Section: Discussionmentioning

confidence: 99%

Ecm29-Dependent Proteasome Localization Regulates Cytoskeleton Remodeling at the Immune Synapse

Ibañez-Vega

¹

,

Valle

²

,

Sáez

³

et al. 2021

Front. Cell Dev. Biol.

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The formation of an immune synapse (IS) enables B cells to capture membrane-tethered antigens, where cortical actin cytoskeleton remodeling regulates cell spreading and depletion of F-actin at the centrosome promotes the recruitment of lysosomes to facilitate antigen extraction. How B cells regulate both pools of actin, remains poorly understood. We report here that decreased F-actin at the centrosome and IS relies on the distribution of the proteasome, regulated by Ecm29. Silencing Ecm29 decreases the proteasome pool associated to the centrosome of B cells and shifts its accumulation to the cell cortex and IS. Accordingly, Ecm29-silenced B cells display increased F-actin at the centrosome, impaired centrosome and lysosome repositioning to the IS and defective antigen extraction and presentation. Ecm29-silenced B cells, which accumulate higher levels of proteasome at the cell cortex, display decreased actin retrograde flow in lamellipodia and enhanced spreading responses. Our findings support a model where B the asymmetric distribution of the proteasome, mediated by Ecm29, coordinates actin dynamics at the centrosome and the IS, promoting lysosome recruitment and cell spreading.

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“…Interestingly, microtubules drive the spreading response in fibroblasts, where the rapid growth of microtubules toward the cell borders is essential for isotropic spreading (Tvorogova et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Ecm29-dependent proteasome localization regulates cytoskeleton remodeling at the immune synapse

Ibañez-Vega

¹

,

Batalla

²

,

Sáez

³

et al. 2020

Preprint

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The formation of an immune synapse (IS) enables B cells to capture membrane-tethered antigens, where cortical actin cytoskeleton remodeling regulates cell spreading and depletion of F-actin at the centrosome promotes the recruitment of lysosomes to facilitate antigen extraction. How B cells regulate both pools of actin, remains poorly understood. We report here that decreased F-actin at the centrosome and IS relies on the distribution of the proteasome, regulated by Ecm29. Silencing Ecm29 decreases the proteasome pool associated to the centrosome of B cells and shifts its accumulation to the cell cortex and IS. Accordingly, Ecm29-silenced B cells display increased F-actin at the centrosome, impaired centrosome and lysosome repositioning to the IS and defective antigen extraction and presentation. Ecm29-silenced B cells, which accumulate higher levels of proteasome at the cell cortex, display decreased actin retrograde flow in lamellipodia and enhanced spreading responses. Our findings support a model where B the asymmetric distribution of the proteasome, mediated by Ecm29, coordinates actin dynamics at the centrosome and the IS, promoting lysosome recruitment and cell spreading.

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Dynamic microtubules drive fibroblast spreading

Cited by 5 publications

References 69 publications

Plasma-Coated Polycaprolactone Nanofibers with Covalently Bonded Platelet-Rich Plasma Enhance Adhesion and Growth of Human Fibroblasts

Plasma-Coated Polycaprolactone Nanofibers with Covalently Bonded Platelet-Rich Plasma Enhance Adhesion and Growth of Human Fibroblasts

Ecm29-Dependent Proteasome Localization Regulates Cytoskeleton Remodeling at the Immune Synapse

Ecm29-dependent proteasome localization regulates cytoskeleton remodeling at the immune synapse

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