T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells

Background. Activation of endothelial cells by inflammatory mediators secreted by CD4+ T lymphocytes plays a key role in the inflammatory response. Exosomes represent a specific class of signaling cues transporting a mixture of proteins, nucleic acids, and other biomolecules. So far, the impact of e...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Oxidative medicine and cellular longevity 2022-09, Vol.2022, p.1-17
Hauptverfasser: Rolski, Filip, Czepiel, Marcin, Tkacz, Karolina, Fryt, Katarzyna, Siedlar, Maciej, Kania, Gabriela, Błyszczuk, Przemysław
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 17
container_issue
container_start_page 1
container_title Oxidative medicine and cellular longevity
container_volume 2022
creator Rolski, Filip
Czepiel, Marcin
Tkacz, Karolina
Fryt, Katarzyna
Siedlar, Maciej
Kania, Gabriela
Błyszczuk, Przemysław
description Background. Activation of endothelial cells by inflammatory mediators secreted by CD4+ T lymphocytes plays a key role in the inflammatory response. Exosomes represent a specific class of signaling cues transporting a mixture of proteins, nucleic acids, and other biomolecules. So far, the impact of exosomes shed by T lymphocytes on cardiac endothelial cells remained unknown. Methods and Results. Supernatants of CD4+ T cells activated with anti-CD3/CD28 beads were used to isolate exosomes by differential centrifugation. Activation of CD4+ T cells enhanced exosome production, and these exosomes (CD4-exosomes) induced oxidative stress in cardiac microvascular endothelial cells (cMVECs) without affecting their adhesive properties. Furthermore, CD4-exosome treatment aggravated the generation of mitochondrial reactive oxygen species (ROS), reduced nitric oxide (NO) levels, and enhanced the proliferation of cMVECs. These effects were reversed by adding the antioxidant apocynin. On the molecular level, CD4-exosomes increased NOX2, NOX4, ERK1/2, and MEK1/2 in cMVECs, and ERK1/2 and MEK1/2 proteins were found in CD4-exosomes. Inhibition of either MEK/ERK with U0126 or ERK with FR180204 successfully protected cMVECs from increased ROS levels and reduced NO bioavailability. Treatment with NOX1/4 inhibitor GKT136901 effectively blocked excessive ROS and superoxide production, reversed impaired NO levels, and reversed enhanced cMVEC proliferation triggered by CD4-exosomes. The siRNA-mediated silencing of Nox4 in cMVECs confirmed the key role of NOX4 in CD4-exosome-induced oxidative stress. To address the properties of exosomes under inflammatory conditions, we used the mouse model of CD4+ T cell-dependent experimental autoimmune myocarditis. In contrast to exosomes obtained from control hearts, exosomes obtained from inflamed hearts upregulated NOX2, NOX4, ERK1/2, MEK1/2, increased ROS and superoxide levels, and reduced NO bioavailability in treated cMVECs, and these changes were reversed by apocynin. Conclusion. Our results point to exosomes as a novel class of bioactive factors secreted by CD4+ T cells in immune response and represent potential important triggers of NOX4-dependent endothelial dysfunction. Neutralization of the prooxidative aspect of CD4-exosomes could open perspectives for the development of new therapeutic strategies in inflammatory cardiovascular diseases.
doi_str_mv 10.1155/2022/2457687
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9534701</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2722971734</sourcerecordid><originalsourceid>FETCH-LOGICAL-c425t-e5c4baaa354aaec2f80ef92490e9400b6dc955c0cc49608c43752e2ca30c21ec3</originalsourceid><addsrcrecordid>eNp9kcFuEzEQhleISpSWGw9giQsSLLG9dja-IKEQ2oqUSBAkbtbEnhBXu_bW3g3NU_DKOEoUqT1wmpHmm1_zz18Urxn9wJiUI045H3Eh6_GkflacMyV4SZUSz089pS-KlyndUTquuGDnxd8lme_abhPMrsfyM0a3RUtmDyGFFhNZRvCpC7Ent7OvbMQJ-Dz9fmpvvB0Mkm-LXyIvd-gt-p4sHpyFPiuRH33ElIjzZArROjDk1pkYtpDM0EAkM29Dv8HGQUOm2DTpsjhbQ5Pw1bFeFD-_zJbT63K-uLqZfpqXRnDZlyiNWAFAJQUAGr6eUFwrLhRFJShdja1RUhpqjFBjOjGiqiVHbqCihjM01UXx8aDbDasWrclnR2h0F10LcacDOP144t1G_w5brWQlasqywNujQAz3A6Zety6ZbAE8hiFpXvNKTKRiKqNvnqB3YYg-29tTXNWsrkSm3h-o_J-UIq5PxzCq9_Hqfbz6GG_G3x3wjfMW_rj_0_8AVg-lZA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2722971734</pqid></control><display><type>article</type><title>T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells</title><source>Wiley Online Library Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>PubMed Central Open Access</source><creator>Rolski, Filip ; Czepiel, Marcin ; Tkacz, Karolina ; Fryt, Katarzyna ; Siedlar, Maciej ; Kania, Gabriela ; Błyszczuk, Przemysław</creator><contributor>J L, Franco</contributor><creatorcontrib>Rolski, Filip ; Czepiel, Marcin ; Tkacz, Karolina ; Fryt, Katarzyna ; Siedlar, Maciej ; Kania, Gabriela ; Błyszczuk, Przemysław ; J L, Franco</creatorcontrib><description>Background. Activation of endothelial cells by inflammatory mediators secreted by CD4+ T lymphocytes plays a key role in the inflammatory response. Exosomes represent a specific class of signaling cues transporting a mixture of proteins, nucleic acids, and other biomolecules. So far, the impact of exosomes shed by T lymphocytes on cardiac endothelial cells remained unknown. Methods and Results. Supernatants of CD4+ T cells activated with anti-CD3/CD28 beads were used to isolate exosomes by differential centrifugation. Activation of CD4+ T cells enhanced exosome production, and these exosomes (CD4-exosomes) induced oxidative stress in cardiac microvascular endothelial cells (cMVECs) without affecting their adhesive properties. Furthermore, CD4-exosome treatment aggravated the generation of mitochondrial reactive oxygen species (ROS), reduced nitric oxide (NO) levels, and enhanced the proliferation of cMVECs. These effects were reversed by adding the antioxidant apocynin. On the molecular level, CD4-exosomes increased NOX2, NOX4, ERK1/2, and MEK1/2 in cMVECs, and ERK1/2 and MEK1/2 proteins were found in CD4-exosomes. Inhibition of either MEK/ERK with U0126 or ERK with FR180204 successfully protected cMVECs from increased ROS levels and reduced NO bioavailability. Treatment with NOX1/4 inhibitor GKT136901 effectively blocked excessive ROS and superoxide production, reversed impaired NO levels, and reversed enhanced cMVEC proliferation triggered by CD4-exosomes. The siRNA-mediated silencing of Nox4 in cMVECs confirmed the key role of NOX4 in CD4-exosome-induced oxidative stress. To address the properties of exosomes under inflammatory conditions, we used the mouse model of CD4+ T cell-dependent experimental autoimmune myocarditis. In contrast to exosomes obtained from control hearts, exosomes obtained from inflamed hearts upregulated NOX2, NOX4, ERK1/2, MEK1/2, increased ROS and superoxide levels, and reduced NO bioavailability in treated cMVECs, and these changes were reversed by apocynin. Conclusion. Our results point to exosomes as a novel class of bioactive factors secreted by CD4+ T cells in immune response and represent potential important triggers of NOX4-dependent endothelial dysfunction. Neutralization of the prooxidative aspect of CD4-exosomes could open perspectives for the development of new therapeutic strategies in inflammatory cardiovascular diseases.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2022/2457687</identifier><language>eng</language><publisher>New York: Hindawi</publisher><subject>Antigens ; Atherosclerosis ; Cardiovascular disease ; Experiments ; Growth factors ; Heart ; Inflammation ; Lymphocytes ; Nitric oxide ; Oxidative stress ; Proteins ; Reactive oxygen species ; T cell receptors</subject><ispartof>Oxidative medicine and cellular longevity, 2022-09, Vol.2022, p.1-17</ispartof><rights>Copyright © 2022 Filip Rolski et al.</rights><rights>Copyright © 2022 Filip Rolski et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Filip Rolski et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-e5c4baaa354aaec2f80ef92490e9400b6dc955c0cc49608c43752e2ca30c21ec3</citedby><cites>FETCH-LOGICAL-c425t-e5c4baaa354aaec2f80ef92490e9400b6dc955c0cc49608c43752e2ca30c21ec3</cites><orcidid>0000-0002-3904-5412 ; 0000-0003-2521-3232 ; 0000-0003-4402-1738 ; 0000-0003-4106-1224 ; 0000-0001-9159-6169 ; 0000-0003-4707-9126 ; 0000-0003-3788-4594</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9534701/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9534701/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><contributor>J L, Franco</contributor><creatorcontrib>Rolski, Filip</creatorcontrib><creatorcontrib>Czepiel, Marcin</creatorcontrib><creatorcontrib>Tkacz, Karolina</creatorcontrib><creatorcontrib>Fryt, Katarzyna</creatorcontrib><creatorcontrib>Siedlar, Maciej</creatorcontrib><creatorcontrib>Kania, Gabriela</creatorcontrib><creatorcontrib>Błyszczuk, Przemysław</creatorcontrib><title>T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells</title><title>Oxidative medicine and cellular longevity</title><description>Background. Activation of endothelial cells by inflammatory mediators secreted by CD4+ T lymphocytes plays a key role in the inflammatory response. Exosomes represent a specific class of signaling cues transporting a mixture of proteins, nucleic acids, and other biomolecules. So far, the impact of exosomes shed by T lymphocytes on cardiac endothelial cells remained unknown. Methods and Results. Supernatants of CD4+ T cells activated with anti-CD3/CD28 beads were used to isolate exosomes by differential centrifugation. Activation of CD4+ T cells enhanced exosome production, and these exosomes (CD4-exosomes) induced oxidative stress in cardiac microvascular endothelial cells (cMVECs) without affecting their adhesive properties. Furthermore, CD4-exosome treatment aggravated the generation of mitochondrial reactive oxygen species (ROS), reduced nitric oxide (NO) levels, and enhanced the proliferation of cMVECs. These effects were reversed by adding the antioxidant apocynin. On the molecular level, CD4-exosomes increased NOX2, NOX4, ERK1/2, and MEK1/2 in cMVECs, and ERK1/2 and MEK1/2 proteins were found in CD4-exosomes. Inhibition of either MEK/ERK with U0126 or ERK with FR180204 successfully protected cMVECs from increased ROS levels and reduced NO bioavailability. Treatment with NOX1/4 inhibitor GKT136901 effectively blocked excessive ROS and superoxide production, reversed impaired NO levels, and reversed enhanced cMVEC proliferation triggered by CD4-exosomes. The siRNA-mediated silencing of Nox4 in cMVECs confirmed the key role of NOX4 in CD4-exosome-induced oxidative stress. To address the properties of exosomes under inflammatory conditions, we used the mouse model of CD4+ T cell-dependent experimental autoimmune myocarditis. In contrast to exosomes obtained from control hearts, exosomes obtained from inflamed hearts upregulated NOX2, NOX4, ERK1/2, MEK1/2, increased ROS and superoxide levels, and reduced NO bioavailability in treated cMVECs, and these changes were reversed by apocynin. Conclusion. Our results point to exosomes as a novel class of bioactive factors secreted by CD4+ T cells in immune response and represent potential important triggers of NOX4-dependent endothelial dysfunction. Neutralization of the prooxidative aspect of CD4-exosomes could open perspectives for the development of new therapeutic strategies in inflammatory cardiovascular diseases.</description><subject>Antigens</subject><subject>Atherosclerosis</subject><subject>Cardiovascular disease</subject><subject>Experiments</subject><subject>Growth factors</subject><subject>Heart</subject><subject>Inflammation</subject><subject>Lymphocytes</subject><subject>Nitric oxide</subject><subject>Oxidative stress</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>T cell receptors</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kcFuEzEQhleISpSWGw9giQsSLLG9dja-IKEQ2oqUSBAkbtbEnhBXu_bW3g3NU_DKOEoUqT1wmpHmm1_zz18Urxn9wJiUI045H3Eh6_GkflacMyV4SZUSz089pS-KlyndUTquuGDnxd8lme_abhPMrsfyM0a3RUtmDyGFFhNZRvCpC7Ent7OvbMQJ-Dz9fmpvvB0Mkm-LXyIvd-gt-p4sHpyFPiuRH33ElIjzZArROjDk1pkYtpDM0EAkM29Dv8HGQUOm2DTpsjhbQ5Pw1bFeFD-_zJbT63K-uLqZfpqXRnDZlyiNWAFAJQUAGr6eUFwrLhRFJShdja1RUhpqjFBjOjGiqiVHbqCihjM01UXx8aDbDasWrclnR2h0F10LcacDOP144t1G_w5brWQlasqywNujQAz3A6Zety6ZbAE8hiFpXvNKTKRiKqNvnqB3YYg-29tTXNWsrkSm3h-o_J-UIq5PxzCq9_Hqfbz6GG_G3x3wjfMW_rj_0_8AVg-lZA</recordid><startdate>20220928</startdate><enddate>20220928</enddate><creator>Rolski, Filip</creator><creator>Czepiel, Marcin</creator><creator>Tkacz, Karolina</creator><creator>Fryt, Katarzyna</creator><creator>Siedlar, Maciej</creator><creator>Kania, Gabriela</creator><creator>Błyszczuk, Przemysław</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3904-5412</orcidid><orcidid>https://orcid.org/0000-0003-2521-3232</orcidid><orcidid>https://orcid.org/0000-0003-4402-1738</orcidid><orcidid>https://orcid.org/0000-0003-4106-1224</orcidid><orcidid>https://orcid.org/0000-0001-9159-6169</orcidid><orcidid>https://orcid.org/0000-0003-4707-9126</orcidid><orcidid>https://orcid.org/0000-0003-3788-4594</orcidid></search><sort><creationdate>20220928</creationdate><title>T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells</title><author>Rolski, Filip ; Czepiel, Marcin ; Tkacz, Karolina ; Fryt, Katarzyna ; Siedlar, Maciej ; Kania, Gabriela ; Błyszczuk, Przemysław</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-e5c4baaa354aaec2f80ef92490e9400b6dc955c0cc49608c43752e2ca30c21ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Antigens</topic><topic>Atherosclerosis</topic><topic>Cardiovascular disease</topic><topic>Experiments</topic><topic>Growth factors</topic><topic>Heart</topic><topic>Inflammation</topic><topic>Lymphocytes</topic><topic>Nitric oxide</topic><topic>Oxidative stress</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>T cell receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rolski, Filip</creatorcontrib><creatorcontrib>Czepiel, Marcin</creatorcontrib><creatorcontrib>Tkacz, Karolina</creatorcontrib><creatorcontrib>Fryt, Katarzyna</creatorcontrib><creatorcontrib>Siedlar, Maciej</creatorcontrib><creatorcontrib>Kania, Gabriela</creatorcontrib><creatorcontrib>Błyszczuk, Przemysław</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rolski, Filip</au><au>Czepiel, Marcin</au><au>Tkacz, Karolina</au><au>Fryt, Katarzyna</au><au>Siedlar, Maciej</au><au>Kania, Gabriela</au><au>Błyszczuk, Przemysław</au><au>J L, Franco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><date>2022-09-28</date><risdate>2022</risdate><volume>2022</volume><spage>1</spage><epage>17</epage><pages>1-17</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Background. Activation of endothelial cells by inflammatory mediators secreted by CD4+ T lymphocytes plays a key role in the inflammatory response. Exosomes represent a specific class of signaling cues transporting a mixture of proteins, nucleic acids, and other biomolecules. So far, the impact of exosomes shed by T lymphocytes on cardiac endothelial cells remained unknown. Methods and Results. Supernatants of CD4+ T cells activated with anti-CD3/CD28 beads were used to isolate exosomes by differential centrifugation. Activation of CD4+ T cells enhanced exosome production, and these exosomes (CD4-exosomes) induced oxidative stress in cardiac microvascular endothelial cells (cMVECs) without affecting their adhesive properties. Furthermore, CD4-exosome treatment aggravated the generation of mitochondrial reactive oxygen species (ROS), reduced nitric oxide (NO) levels, and enhanced the proliferation of cMVECs. These effects were reversed by adding the antioxidant apocynin. On the molecular level, CD4-exosomes increased NOX2, NOX4, ERK1/2, and MEK1/2 in cMVECs, and ERK1/2 and MEK1/2 proteins were found in CD4-exosomes. Inhibition of either MEK/ERK with U0126 or ERK with FR180204 successfully protected cMVECs from increased ROS levels and reduced NO bioavailability. Treatment with NOX1/4 inhibitor GKT136901 effectively blocked excessive ROS and superoxide production, reversed impaired NO levels, and reversed enhanced cMVEC proliferation triggered by CD4-exosomes. The siRNA-mediated silencing of Nox4 in cMVECs confirmed the key role of NOX4 in CD4-exosome-induced oxidative stress. To address the properties of exosomes under inflammatory conditions, we used the mouse model of CD4+ T cell-dependent experimental autoimmune myocarditis. In contrast to exosomes obtained from control hearts, exosomes obtained from inflamed hearts upregulated NOX2, NOX4, ERK1/2, MEK1/2, increased ROS and superoxide levels, and reduced NO bioavailability in treated cMVECs, and these changes were reversed by apocynin. Conclusion. Our results point to exosomes as a novel class of bioactive factors secreted by CD4+ T cells in immune response and represent potential important triggers of NOX4-dependent endothelial dysfunction. Neutralization of the prooxidative aspect of CD4-exosomes could open perspectives for the development of new therapeutic strategies in inflammatory cardiovascular diseases.</abstract><cop>New York</cop><pub>Hindawi</pub><doi>10.1155/2022/2457687</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0002-3904-5412</orcidid><orcidid>https://orcid.org/0000-0003-2521-3232</orcidid><orcidid>https://orcid.org/0000-0003-4402-1738</orcidid><orcidid>https://orcid.org/0000-0003-4106-1224</orcidid><orcidid>https://orcid.org/0000-0001-9159-6169</orcidid><orcidid>https://orcid.org/0000-0003-4707-9126</orcidid><orcidid>https://orcid.org/0000-0003-3788-4594</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1942-0900
ispartof Oxidative medicine and cellular longevity, 2022-09, Vol.2022, p.1-17
issn 1942-0900
1942-0994
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9534701
source Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access
subjects Antigens
Atherosclerosis
Cardiovascular disease
Experiments
Growth factors
Heart
Inflammation
Lymphocytes
Nitric oxide
Oxidative stress
Proteins
Reactive oxygen species
T cell receptors
title T Lymphocyte-Derived Exosomes Transport MEK1/2 and ERK1/2 and Induce NOX4-Dependent Oxidative Stress in Cardiac Microvascular Endothelial Cells
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T02%3A35%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=T%20Lymphocyte-Derived%20Exosomes%20Transport%20MEK1/2%20and%20ERK1/2%20and%20Induce%20NOX4-Dependent%20Oxidative%20Stress%20in%20Cardiac%20Microvascular%20Endothelial%20Cells&rft.jtitle=Oxidative%20medicine%20and%20cellular%20longevity&rft.au=Rolski,%20Filip&rft.date=2022-09-28&rft.volume=2022&rft.spage=1&rft.epage=17&rft.pages=1-17&rft.issn=1942-0900&rft.eissn=1942-0994&rft_id=info:doi/10.1155/2022/2457687&rft_dat=%3Cproquest_pubme%3E2722971734%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2722971734&rft_id=info:pmid/&rfr_iscdi=true