Exosomes derived from HeLa cells break down vascular integrity by triggering endoplasmic reticulum stress in endothelial cells
Identifieur interne : 000156 ( an2020/Analysis ); précédent : 000155; suivant : 000157Exosomes derived from HeLa cells break down vascular integrity by triggering endoplasmic reticulum stress in endothelial cells
Auteurs : Yinuo Lin [République populaire de Chine] ; Chi Zhang [République populaire de Chine] ; Pingping Xiang [République populaire de Chine] ; Jian Shen [République populaire de Chine] ; Weijian Sun [République populaire de Chine] ; Hong Yu [République populaire de Chine]Source :
- Journal of Extracellular Vesicles [ 2001-3078 ] ; 2020.
Abstract
Exosomes play a critical role in intercellular communication since they contain signalling molecules and genetic materials. During tumorigenesis, tumour-derived exosomes have been demonstrated to promote tumour angiogenesis and metastasis. However, how the exosomes facilitate tumour metastasis is not clear. Here we explored the effect of HeLa cell-derived exosomes (ExoHeLa) on endothelial tight junctions (TJ) and the related mechanisms. After human umbilical vein endothelial cells (HUVEC) were treated with ExoHeLa, TJ proteins zonula occludens-1 (ZO-1) and Claudin-5 in HUVEC were significantly reduced as compared with that treated with exosomes from human cervical epithelial cells, while mRNA levels of ZO-1 and Claudin-5 remained unchanged. Consequently, permeability of endothelial monolayer was increased after the treatment with ExoHeLa. Injection of ExoHeLa into mice also increased vascular permeability and tumour metastasis
Url:
DOI: 10.1080/20013078.2020.1722385
PubMed: 32128072
PubMed Central: 7034510
Affiliations:
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first="Yinuo" last="Lin">Yinuo Lin</name><affiliation wicri:level="1"><nlm:aff id="AFF0001"><institution>Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF0002"><institution>Provincial Key Cardiovascular Research Laboratory, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF0003"><institution>Department of Cardiology, The First Affiliated Hospital, Wenzhou Medical University</institution>, Wenzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Zhang, Chi" sort="Zhang, Chi" uniqKey="Zhang C" first="Chi" last="Zhang">Chi Zhang</name><affiliation wicri:level="1"><nlm:aff id="AFF0001"><institution>Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF0002"><institution>Provincial Key Cardiovascular Research Laboratory, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Xiang, Pingping" sort="Xiang, Pingping" uniqKey="Xiang P" first="Pingping" last="Xiang">Pingping Xiang</name><affiliation wicri:level="1"><nlm:aff id="AFF0001"><institution>Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF0002"><institution>Provincial Key Cardiovascular Research Laboratory, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Shen, Jian" sort="Shen, Jian" uniqKey="Shen J" first="Jian" last="Shen">Jian Shen</name><affiliation wicri:level="1"><nlm:aff id="AFF0001"><institution>Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF0002"><institution>Provincial Key Cardiovascular Research Laboratory, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Sun, Weijian" sort="Sun, Weijian" uniqKey="Sun W" first="Weijian" last="Sun">Weijian Sun</name><affiliation wicri:level="1"><nlm:aff id="AFF0004"><institution>Department of Surgery, The Second Affiliated Hospital and Yuying Children’s Hospital, Wenzhou Medical University</institution>, Wenzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Yu, Hong" sort="Yu, Hong" uniqKey="Yu H" first="Hong" last="Yu">Hong Yu</name><affiliation wicri:level="1"><nlm:aff id="AFF0001"><institution>Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="AFF0002"><institution>Provincial Key Cardiovascular Research Laboratory, The Second Affiliated Hospital, Zhejiang University School of Medicine</institution>, Hangzhou, Zhejiang,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Journal of Extracellular Vesicles</title><idno type="eISSN">2001-3078</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>ABSTRACT</title><p>Exosomes play a critical role in intercellular communication since they contain signalling molecules and genetic materials. During tumorigenesis, tumour-derived exosomes have been demonstrated to promote tumour angiogenesis and metastasis. However, how the exosomes facilitate tumour metastasis is not clear. Here we explored the effect of HeLa cell-derived exosomes (Exo<sup>HeLa</sup>) on endothelial tight junctions (TJ) and the related mechanisms. After human umbilical vein endothelial cells (HUVEC) were treated with Exo<sup>HeLa</sup>, TJ proteins zonula occludens-1 (ZO-1) and Claudin-5 in HUVEC were significantly reduced as compared with that treated with exosomes from human cervical epithelial cells, while mRNA levels of ZO-1 and Claudin-5 remained unchanged. Consequently, permeability of endothelial monolayer was increased after the treatment with Exo<sup>HeLa</sup>. Injection of Exo<sup>HeLa</sup> into mice also increased vascular permeability and tumour metastasis <italic>in vivo</italic>. Neither knocking down of Dicer nor use of inhibitors of microRNAs targeting at mRNAs of ZO-1 and Claudin-5 could block the inhibitory effect of Exo<sup>HeLa</sup> on ZO-1 and Claudin-5. The expression of genes involved in endoplasmic reticulum (ER) stress was significantly increased in HUVECs after treated with Exo<sup>HeLa</sup>. Inhibition of ER stress by knocking down protein kinase RNA-like endoplasmic reticulum kinase prevented the down-regulation of ZO-1 and Claudin-5 by Exo<sup>HeLa</sup>. Our study found that HeLa cell-derived exosomes promote metastasis by triggering ER stress in endothelial cells and break down endothelial integrity. Such effect of exosomes is microRNA-independent.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Egeblad, M" uniqKey="Egeblad M">M Egeblad</name></author><author><name sortKey="Nakasone, E" uniqKey="Nakasone E">E Nakasone</name></author><author><name sortKey="Werb, Z" uniqKey="Werb Z">Z. 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sort="Sun, Weijian" uniqKey="Sun W" first="Weijian" last="Sun">Weijian Sun</name><name sortKey="Xiang, Pingping" sort="Xiang, Pingping" uniqKey="Xiang P" first="Pingping" last="Xiang">Pingping Xiang</name><name sortKey="Xiang, Pingping" sort="Xiang, Pingping" uniqKey="Xiang P" first="Pingping" last="Xiang">Pingping Xiang</name><name sortKey="Yu, Hong" sort="Yu, Hong" uniqKey="Yu H" first="Hong" last="Yu">Hong Yu</name><name sortKey="Yu, Hong" sort="Yu, Hong" uniqKey="Yu H" first="Hong" last="Yu">Hong Yu</name><name sortKey="Zhang, Chi" sort="Zhang, Chi" uniqKey="Zhang C" first="Chi" last="Zhang">Chi Zhang</name><name sortKey="Zhang, Chi" sort="Zhang, Chi" uniqKey="Zhang C" first="Chi" last="Zhang">Chi Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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