miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice
Ischemic stroke is a common disease of the central nervous system, and ischemic brain injury (IBI) is its main manifestation. Recently, extracellular vesicles (EVs) have been strongly related to the diagnosis and treatment of IBI. However, the underlying mechanism of their effects remains enigmatic....
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2022, Vol.2022, p.8603427-21 |
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| creator | Yang, Zhang Shi, Xiaofang Gao, Zidan Chu, Lan |
| description | Ischemic stroke is a common disease of the central nervous system, and ischemic brain injury (IBI) is its main manifestation. Recently, extracellular vesicles (EVs) have been strongly related to the diagnosis and treatment of IBI. However, the underlying mechanism of their effects remains enigmatic. In the present study, we aimed to study how miR-155-5p plays a role in choroid plexus epithelial (CPE) cell-derived EVs in IBI pathology. We found that miR-155-5p expression was enriched in CPE cell-derived EVs, which were subsequently internalized by neurons, enabling the delivery of miR-155-5p into neurons. An inducible oxygen and glucose deprivation and reoxygenation (OGD/R) cell model was developed to mimic ischemic neuronal injury in vitro. miR-155-5p overexpression led to reduced neuron viability, promoted apoptosis, elevated autophagic proteins’ expression, and activated NLR family pyrin domain-containing 3- (NLRP3-) related inflammasomes, thereby aggravating OGD-induced neuronal injury. A dual-luciferase reporter assay exhibited that miR-155-5p could inhibit the Ras homolog enriched in brain (Rheb) expression, a mechanism critical for miR-155-5p-mediated neuronal injury. Furthermore, a mouse IBI model was developed using the transient middle cerebral artery occlusion (tMCAO) method. Animal experiments verified that miR-155p delivery via CPE cell-derived EVs aggravated IBI by suppressing Rheb expression. In conclusion, miR-155-5p in CPE-derived EVs can aggravate IBI pathology by suppressing Rheb expression and promoting NLRP3-mediated inflammasomes, suggesting its role as a potential therapeutic target in IBI. |
| doi_str_mv | 10.1155/2022/8603427 |
| format | Article |
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Recently, extracellular vesicles (EVs) have been strongly related to the diagnosis and treatment of IBI. However, the underlying mechanism of their effects remains enigmatic. In the present study, we aimed to study how miR-155-5p plays a role in choroid plexus epithelial (CPE) cell-derived EVs in IBI pathology. We found that miR-155-5p expression was enriched in CPE cell-derived EVs, which were subsequently internalized by neurons, enabling the delivery of miR-155-5p into neurons. An inducible oxygen and glucose deprivation and reoxygenation (OGD/R) cell model was developed to mimic ischemic neuronal injury in vitro. miR-155-5p overexpression led to reduced neuron viability, promoted apoptosis, elevated autophagic proteins’ expression, and activated NLR family pyrin domain-containing 3- (NLRP3-) related inflammasomes, thereby aggravating OGD-induced neuronal injury. A dual-luciferase reporter assay exhibited that miR-155-5p could inhibit the Ras homolog enriched in brain (Rheb) expression, a mechanism critical for miR-155-5p-mediated neuronal injury. Furthermore, a mouse IBI model was developed using the transient middle cerebral artery occlusion (tMCAO) method. Animal experiments verified that miR-155p delivery via CPE cell-derived EVs aggravated IBI by suppressing Rheb expression. In conclusion, miR-155-5p in CPE-derived EVs can aggravate IBI pathology by suppressing Rheb expression and promoting NLRP3-mediated inflammasomes, suggesting its role as a potential therapeutic target in IBI.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2022/8603427</identifier><identifier>PMID: 35222806</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Animal research ; Animals ; Antibodies ; Apoptosis ; Autophagy ; Brain damage ; Brain Ischemia - genetics ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Cell culture ; Choroid Plexus - metabolism ; Cloning ; Enzymes ; Epithelial Cells - metabolism ; Extracellular vesicles ; Extracellular Vesicles - genetics ; Extracellular Vesicles - metabolism ; Gene expression ; Glucose ; Infarction, Middle Cerebral Artery - genetics ; Infarction, Middle Cerebral Artery - metabolism ; Infarction, Middle Cerebral Artery - pathology ; Inflammasomes - metabolism ; Inflammation ; Ischemia ; Kinases ; Mice ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Neurons ; Neurons - metabolism ; Neurons - pathology ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Pathology ; Proteins ; Ras Homolog Enriched in Brain Protein - genetics ; Ras Homolog Enriched in Brain Protein - metabolism ; Signal Transduction ; Stroke ; Traumatic brain injury</subject><ispartof>Oxidative medicine and cellular longevity, 2022, Vol.2022, p.8603427-21</ispartof><rights>Copyright © 2022 Zhang Yang et al.</rights><rights>Copyright © 2022 Zhang Yang 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 Zhang Yang et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-aad5a9cea47148765df32213176fe915349edcb5cc59df0fd71ba27badba9f43</citedby><cites>FETCH-LOGICAL-c448t-aad5a9cea47148765df32213176fe915349edcb5cc59df0fd71ba27badba9f43</cites><orcidid>0000-0003-2797-7535 ; 0000-0002-1004-0300</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/PMC8865969/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8865969/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35222806$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Caner, Basak</contributor><creatorcontrib>Yang, Zhang</creatorcontrib><creatorcontrib>Shi, Xiaofang</creatorcontrib><creatorcontrib>Gao, Zidan</creatorcontrib><creatorcontrib>Chu, Lan</creatorcontrib><title>miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Ischemic stroke is a common disease of the central nervous system, and ischemic brain injury (IBI) is its main manifestation. Recently, extracellular vesicles (EVs) have been strongly related to the diagnosis and treatment of IBI. However, the underlying mechanism of their effects remains enigmatic. In the present study, we aimed to study how miR-155-5p plays a role in choroid plexus epithelial (CPE) cell-derived EVs in IBI pathology. We found that miR-155-5p expression was enriched in CPE cell-derived EVs, which were subsequently internalized by neurons, enabling the delivery of miR-155-5p into neurons. An inducible oxygen and glucose deprivation and reoxygenation (OGD/R) cell model was developed to mimic ischemic neuronal injury in vitro. miR-155-5p overexpression led to reduced neuron viability, promoted apoptosis, elevated autophagic proteins’ expression, and activated NLR family pyrin domain-containing 3- (NLRP3-) related inflammasomes, thereby aggravating OGD-induced neuronal injury. A dual-luciferase reporter assay exhibited that miR-155-5p could inhibit the Ras homolog enriched in brain (Rheb) expression, a mechanism critical for miR-155-5p-mediated neuronal injury. Furthermore, a mouse IBI model was developed using the transient middle cerebral artery occlusion (tMCAO) method. Animal experiments verified that miR-155p delivery via CPE cell-derived EVs aggravated IBI by suppressing Rheb expression. In conclusion, miR-155-5p in CPE-derived EVs can aggravate IBI pathology by suppressing Rheb expression and promoting NLRP3-mediated inflammasomes, suggesting its role as a potential therapeutic target in IBI.</description><subject>Animal research</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Brain damage</subject><subject>Brain Ischemia - genetics</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Cell culture</subject><subject>Choroid Plexus - metabolism</subject><subject>Cloning</subject><subject>Enzymes</subject><subject>Epithelial Cells - metabolism</subject><subject>Extracellular vesicles</subject><subject>Extracellular Vesicles - genetics</subject><subject>Extracellular Vesicles - metabolism</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Infarction, Middle Cerebral Artery - genetics</subject><subject>Infarction, Middle Cerebral Artery - metabolism</subject><subject>Infarction, Middle Cerebral Artery - pathology</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Mice</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Neurons</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Pathology</subject><subject>Proteins</subject><subject>Ras Homolog Enriched in Brain Protein - genetics</subject><subject>Ras Homolog Enriched in Brain Protein - metabolism</subject><subject>Signal Transduction</subject><subject>Stroke</subject><subject>Traumatic brain injury</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>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kU2P0zAQhiMEYj_gxhlZ4oK0hLUdOx8XpFIKVFrECq24WhPHaVw5dtZOyvbf8FNx1FIBB04z0jzz6p15k-QFwW8J4fyaYkqvyxxnjBaPknNSMZriqmKPTz3GZ8lFCFuM84wy8jQ5yziltMT5efKz19_SKJPyAWmLVg-jB6mMmQx49F0FLY0K6IPyeqca1HrXo2XnvNMNujXqYQpoNeixU0aDQcu4GNBthNwYtxbT6IYONnsEtkFr2xroexi1s2h0aLHZeNjBqNA6yE71WqL3HqKHtd1Ofj-7-aKlepY8acEE9fxYL5O7j6u75ef05uun9XJxk0rGyjEFaDhUUgErCCuLnDdtRinJSJG3qiI8Y5VqZM2l5FXT4rYpSA20qKGpoWpZdpm8O8gOU91HUtn4CCMGr3vwe-FAi78nVndi43aiLHNe5VUUeH0U8O5-UmEUvQ7zJ8EqNwVB84xxHAPhEX31D7p1k7fxupnKeB7R2dGbAyW9C8Gr9mSGYDEnL-bkxTH5iL_884AT_DvqCFwdgE7bBn7o_8v9AtUKuH0</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Yang, Zhang</creator><creator>Shi, Xiaofang</creator><creator>Gao, Zidan</creator><creator>Chu, Lan</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</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>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/0000-0003-2797-7535</orcidid><orcidid>https://orcid.org/0000-0002-1004-0300</orcidid></search><sort><creationdate>2022</creationdate><title>miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice</title><author>Yang, Zhang ; Shi, Xiaofang ; Gao, Zidan ; Chu, Lan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-aad5a9cea47148765df32213176fe915349edcb5cc59df0fd71ba27badba9f43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animal research</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Brain damage</topic><topic>Brain Ischemia - genetics</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Cell culture</topic><topic>Choroid Plexus - metabolism</topic><topic>Cloning</topic><topic>Enzymes</topic><topic>Epithelial Cells - metabolism</topic><topic>Extracellular vesicles</topic><topic>Extracellular Vesicles - genetics</topic><topic>Extracellular Vesicles - metabolism</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>Infarction, Middle Cerebral Artery - genetics</topic><topic>Infarction, Middle Cerebral Artery - metabolism</topic><topic>Infarction, Middle Cerebral Artery - pathology</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Mice</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Neurons</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Pathology</topic><topic>Proteins</topic><topic>Ras Homolog Enriched in Brain Protein - genetics</topic><topic>Ras Homolog Enriched in Brain Protein - metabolism</topic><topic>Signal Transduction</topic><topic>Stroke</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Zhang</creatorcontrib><creatorcontrib>Shi, Xiaofang</creatorcontrib><creatorcontrib>Gao, Zidan</creatorcontrib><creatorcontrib>Chu, Lan</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & 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>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 & Medical Complete (Alumni)</collection><collection>Health & 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>Yang, Zhang</au><au>Shi, Xiaofang</au><au>Gao, Zidan</au><au>Chu, Lan</au><au>Caner, Basak</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2022</date><risdate>2022</risdate><volume>2022</volume><spage>8603427</spage><epage>21</epage><pages>8603427-21</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Ischemic stroke is a common disease of the central nervous system, and ischemic brain injury (IBI) is its main manifestation. Recently, extracellular vesicles (EVs) have been strongly related to the diagnosis and treatment of IBI. However, the underlying mechanism of their effects remains enigmatic. In the present study, we aimed to study how miR-155-5p plays a role in choroid plexus epithelial (CPE) cell-derived EVs in IBI pathology. We found that miR-155-5p expression was enriched in CPE cell-derived EVs, which were subsequently internalized by neurons, enabling the delivery of miR-155-5p into neurons. An inducible oxygen and glucose deprivation and reoxygenation (OGD/R) cell model was developed to mimic ischemic neuronal injury in vitro. miR-155-5p overexpression led to reduced neuron viability, promoted apoptosis, elevated autophagic proteins’ expression, and activated NLR family pyrin domain-containing 3- (NLRP3-) related inflammasomes, thereby aggravating OGD-induced neuronal injury. A dual-luciferase reporter assay exhibited that miR-155-5p could inhibit the Ras homolog enriched in brain (Rheb) expression, a mechanism critical for miR-155-5p-mediated neuronal injury. Furthermore, a mouse IBI model was developed using the transient middle cerebral artery occlusion (tMCAO) method. Animal experiments verified that miR-155p delivery via CPE cell-derived EVs aggravated IBI by suppressing Rheb expression. In conclusion, miR-155-5p in CPE-derived EVs can aggravate IBI pathology by suppressing Rheb expression and promoting NLRP3-mediated inflammasomes, suggesting its role as a potential therapeutic target in IBI.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>35222806</pmid><doi>10.1155/2022/8603427</doi><tpages>21</tpages><orcidid>https://orcid.org/0000-0003-2797-7535</orcidid><orcidid>https://orcid.org/0000-0002-1004-0300</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animal research Animals Antibodies Apoptosis Autophagy Brain damage Brain Ischemia - genetics Brain Ischemia - metabolism Brain Ischemia - pathology Cell culture Choroid Plexus - metabolism Cloning Enzymes Epithelial Cells - metabolism Extracellular vesicles Extracellular Vesicles - genetics Extracellular Vesicles - metabolism Gene expression Glucose Infarction, Middle Cerebral Artery - genetics Infarction, Middle Cerebral Artery - metabolism Infarction, Middle Cerebral Artery - pathology Inflammasomes - metabolism Inflammation Ischemia Kinases Mice MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Neurons Neurons - metabolism Neurons - pathology NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Pathology Proteins Ras Homolog Enriched in Brain Protein - genetics Ras Homolog Enriched in Brain Protein - metabolism Signal Transduction Stroke Traumatic brain injury |
| title | miR-155-5p in Extracellular Vesicles Derived from Choroid Plexus Epithelial Cells Promotes Autophagy and Inflammation to Aggravate Ischemic Brain Injury in Mice |
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