Gap junction-mediated regulation of endothelial cellular stiffness

Abstract Endothelial monolayers have shown the ability to signal each other through gap junctions. Gap junction-mediated cell-cell interactions have been implicated in the modulation of endothelial cell functions during vascular inflammation. Inflammatory mediators alter the mechanical properties of...

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Autores principales:	Takayuki Okamoto, Eiji Kawamoto, Yoshimi Takagi, Nobuyuki Akita, Tatsuya Hayashi, Eun Jeong Park, Koji Suzuki, Motomu Shimaoka
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/836b92d19bc04c53b5c9c8d3c69f61d0
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spelling	oai:doaj.org-article:836b92d19bc04c53b5c9c8d3c69f61d02021-12-02T12:30:54ZGap junction-mediated regulation of endothelial cellular stiffness10.1038/s41598-017-06463-x2045-2322https://doaj.org/article/836b92d19bc04c53b5c9c8d3c69f61d02017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06463-xhttps://doaj.org/toc/2045-2322Abstract Endothelial monolayers have shown the ability to signal each other through gap junctions. Gap junction-mediated cell-cell interactions have been implicated in the modulation of endothelial cell functions during vascular inflammation. Inflammatory mediators alter the mechanical properties of endothelial cells, although the exact role of gap junctions in this process remains unclear. Here, we sought to study the role of gap junctions in the regulation of endothelial stiffness, an important physical feature that is associated with many vascular pathologies. The endothelial cellular stiffness of living endothelial cells was determined by using atomic force microscopy. We found that tumor necrosis factor-α transiently increased endothelial cellular stiffness, which is regulated by cytoskeletal rearrangement and cell-cell interactions. We explored the role of gap junctions in endothelial cellular stiffening by utilizing gap junction blockers, carbenoxolone, inhibitory anti-connexin 32 antibody or anti-connexin 43 antibody. Blockade of gap junctions induced the cellular stiffening associated with focal adhesion formation and cytoskeletal rearrangement, and prolonged tumor necrosis factor-α-induced endothelial cellular stiffening. These results suggest that gap junction-mediated cell-cell interactions play an important role in the regulation of endothelial cellular stiffness.Takayuki OkamotoEiji KawamotoYoshimi TakagiNobuyuki AkitaTatsuya HayashiEun Jeong ParkKoji SuzukiMotomu ShimaokaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Takayuki Okamoto Eiji Kawamoto Yoshimi Takagi Nobuyuki Akita Tatsuya Hayashi Eun Jeong Park Koji Suzuki Motomu Shimaoka Gap junction-mediated regulation of endothelial cellular stiffness
description	Abstract Endothelial monolayers have shown the ability to signal each other through gap junctions. Gap junction-mediated cell-cell interactions have been implicated in the modulation of endothelial cell functions during vascular inflammation. Inflammatory mediators alter the mechanical properties of endothelial cells, although the exact role of gap junctions in this process remains unclear. Here, we sought to study the role of gap junctions in the regulation of endothelial stiffness, an important physical feature that is associated with many vascular pathologies. The endothelial cellular stiffness of living endothelial cells was determined by using atomic force microscopy. We found that tumor necrosis factor-α transiently increased endothelial cellular stiffness, which is regulated by cytoskeletal rearrangement and cell-cell interactions. We explored the role of gap junctions in endothelial cellular stiffening by utilizing gap junction blockers, carbenoxolone, inhibitory anti-connexin 32 antibody or anti-connexin 43 antibody. Blockade of gap junctions induced the cellular stiffening associated with focal adhesion formation and cytoskeletal rearrangement, and prolonged tumor necrosis factor-α-induced endothelial cellular stiffening. These results suggest that gap junction-mediated cell-cell interactions play an important role in the regulation of endothelial cellular stiffness.
format	article
author	Takayuki Okamoto Eiji Kawamoto Yoshimi Takagi Nobuyuki Akita Tatsuya Hayashi Eun Jeong Park Koji Suzuki Motomu Shimaoka
author_facet	Takayuki Okamoto Eiji Kawamoto Yoshimi Takagi Nobuyuki Akita Tatsuya Hayashi Eun Jeong Park Koji Suzuki Motomu Shimaoka
author_sort	Takayuki Okamoto
title	Gap junction-mediated regulation of endothelial cellular stiffness
title_short	Gap junction-mediated regulation of endothelial cellular stiffness
title_full	Gap junction-mediated regulation of endothelial cellular stiffness
title_fullStr	Gap junction-mediated regulation of endothelial cellular stiffness
title_full_unstemmed	Gap junction-mediated regulation of endothelial cellular stiffness
title_sort	gap junction-mediated regulation of endothelial cellular stiffness
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/836b92d19bc04c53b5c9c8d3c69f61d0
work_keys_str_mv	AT takayukiokamoto gapjunctionmediatedregulationofendothelialcellularstiffness AT eijikawamoto gapjunctionmediatedregulationofendothelialcellularstiffness AT yoshimitakagi gapjunctionmediatedregulationofendothelialcellularstiffness AT nobuyukiakita gapjunctionmediatedregulationofendothelialcellularstiffness AT tatsuyahayashi gapjunctionmediatedregulationofendothelialcellularstiffness AT eunjeongpark gapjunctionmediatedregulationofendothelialcellularstiffness AT kojisuzuki gapjunctionmediatedregulationofendothelialcellularstiffness AT motomushimaoka gapjunctionmediatedregulationofendothelialcellularstiffness
_version_	1718394288765665280

Gap junction-mediated regulation of endothelial cellular stiffness

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