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Knockout of PERK protects rat Müller glial cells against OGD-induced endoplasmic reticulum stress-related apoptosis
The pathological basis for many retinal diseases, retinal ischemia is also one of the most common causes of visual impairment. Numerous ocular diseases have been linked to Endoplasmic reticulum(ER)stress. However, there is still no clear understanding of the relationship between ER stress and Müller...
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Published in: | BMC ophthalmology 2023-06, Vol.23 (1), p.286-286, Article 286 |
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description | The pathological basis for many retinal diseases, retinal ischemia is also one of the most common causes of visual impairment. Numerous ocular diseases have been linked to Endoplasmic reticulum(ER)stress. However, there is still no clear understanding of the relationship between ER stress and Müller glial cells during retinal ischemia and hypoxia. This study examined the effects of ER stress on autophagy and apoptosis-related proteins, as well as the microtubule-related protein tau in rMC-1 cells.
rMC-1 cells were cultured in vitro. RT-PCR、immunofluorescence and Western blotting revealed the expression levels of associated mRNAs and proteins, and the CCK-8 and flow cytometry assays detected cell apoptosis.
The results showed that under OGD(Oxygen-glucose deprivation) conditions, the number of rMC-1 cells was decreased, the PERK/eIF2a pathway was activated, and the expressions of p-tau, LC3、Beclin1 and Caspase-12 proteins were increased. After the PERK knockout, the expression of the above proteins was decreased, and the apoptosis was also decreased.
According to the findings of this study, specific downregulation of PERK expression had an anti-apoptotic effect on OGD-conditioned rMC-1 cells. There is a possibility that this is one of the mechanisms of MG cell apoptosis during retinal ischemic injury. |
doi_str_mv | 10.1186/s12886-023-03022-z |
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rMC-1 cells were cultured in vitro. RT-PCR、immunofluorescence and Western blotting revealed the expression levels of associated mRNAs and proteins, and the CCK-8 and flow cytometry assays detected cell apoptosis.
The results showed that under OGD(Oxygen-glucose deprivation) conditions, the number of rMC-1 cells was decreased, the PERK/eIF2a pathway was activated, and the expressions of p-tau, LC3、Beclin1 and Caspase-12 proteins were increased. After the PERK knockout, the expression of the above proteins was decreased, and the apoptosis was also decreased.
According to the findings of this study, specific downregulation of PERK expression had an anti-apoptotic effect on OGD-conditioned rMC-1 cells. There is a possibility that this is one of the mechanisms of MG cell apoptosis during retinal ischemic injury.</description><identifier>ISSN: 1471-2415</identifier><identifier>EISSN: 1471-2415</identifier><identifier>DOI: 10.1186/s12886-023-03022-z</identifier><identifier>PMID: 37353739</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Alzheimer's disease ; Animals ; Apoptosis ; Autophagy ; Caspase-12 ; Cells ; Cholecystokinin ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress ; Ependymoglial Cells ; Eye diseases ; Flow cytometry ; Glial cells ; Glucose ; Homeostasis ; Hypoxia ; Immunofluorescence ; Initiation factor eIF-2 ; Ischemia ; Metabolism ; Mueller cells ; Müller glia ; Ophthalmology ; Oxygen ; Oxygen-glucose deprivation ; Pathogenesis ; Protein synthesis ; Proteins ; Rats ; Rats, Sprague-Dawley ; Reagents ; Retina ; Signal Transduction ; Tau protein ; Western blotting</subject><ispartof>BMC ophthalmology, 2023-06, Vol.23 (1), p.286-286, Article 286</ispartof><rights>2023. The Author(s).</rights><rights>COPYRIGHT 2023 BioMed Central Ltd.</rights><rights>2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c515t-342238138c70cbf2f595f42a11d7f5903412c9bef1253e5a5b424c3bde03988b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10290337/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2838768730?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37353739$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xiaorui</creatorcontrib><creatorcontrib>Zhu, Xinxing</creatorcontrib><creatorcontrib>Huang, Guangqian</creatorcontrib><creatorcontrib>Wu, Lili</creatorcontrib><creatorcontrib>Meng, Zhiyong</creatorcontrib><creatorcontrib>Wu, Yuyu</creatorcontrib><title>Knockout of PERK protects rat Müller glial cells against OGD-induced endoplasmic reticulum stress-related apoptosis</title><title>BMC ophthalmology</title><addtitle>BMC Ophthalmol</addtitle><description>The pathological basis for many retinal diseases, retinal ischemia is also one of the most common causes of visual impairment. Numerous ocular diseases have been linked to Endoplasmic reticulum(ER)stress. However, there is still no clear understanding of the relationship between ER stress and Müller glial cells during retinal ischemia and hypoxia. This study examined the effects of ER stress on autophagy and apoptosis-related proteins, as well as the microtubule-related protein tau in rMC-1 cells.
rMC-1 cells were cultured in vitro. RT-PCR、immunofluorescence and Western blotting revealed the expression levels of associated mRNAs and proteins, and the CCK-8 and flow cytometry assays detected cell apoptosis.
The results showed that under OGD(Oxygen-glucose deprivation) conditions, the number of rMC-1 cells was decreased, the PERK/eIF2a pathway was activated, and the expressions of p-tau, LC3、Beclin1 and Caspase-12 proteins were increased. After the PERK knockout, the expression of the above proteins was decreased, and the apoptosis was also decreased.
According to the findings of this study, specific downregulation of PERK expression had an anti-apoptotic effect on OGD-conditioned rMC-1 cells. There is a possibility that this is one of the mechanisms of MG cell apoptosis during retinal ischemic injury.</description><subject>Alzheimer's disease</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Caspase-12</subject><subject>Cells</subject><subject>Cholecystokinin</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress</subject><subject>Ependymoglial Cells</subject><subject>Eye diseases</subject><subject>Flow cytometry</subject><subject>Glial cells</subject><subject>Glucose</subject><subject>Homeostasis</subject><subject>Hypoxia</subject><subject>Immunofluorescence</subject><subject>Initiation factor eIF-2</subject><subject>Ischemia</subject><subject>Metabolism</subject><subject>Mueller cells</subject><subject>Müller glia</subject><subject>Ophthalmology</subject><subject>Oxygen</subject><subject>Oxygen-glucose deprivation</subject><subject>Pathogenesis</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reagents</subject><subject>Retina</subject><subject>Signal Transduction</subject><subject>Tau protein</subject><subject>Western blotting</subject><issn>1471-2415</issn><issn>1471-2415</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCIloU_wAFZ4sIlxZ8b54SqUkrVoiIEZ8txxosXb5zaDhL9bdz4Yzjdfi1CluXR-L3nmfGrqpcEHxAil28ToVIua0xZjRmmtL56VO0T3pCaciIeP4j3qmcprTGmmDP5tNpjDRNlt_tVPhuC-RGmjIJFn4-_nKExhgwmJxR1Rp_-_PYeIlp5pz0y4H1CeqXdkDK6OHlfu6GfDPQIhj6MXqeNMyhCdmby0walHCGlOoLXuYD0GMYckkvPqydW-wQvbs5F9e3D8dejj_X5xcnp0eF5bQQRuWacUiYJk6bBprPUilZYTjUhfVNizDihpu3AEioYCC06TrlhXQ-YtVJ2bFGdbnX7oNdqjG6j4y8VtFPXiRBXSsdSrAe15I20WEigpISi67BtOeG9lbNkL4vWu63WOHUb6A0MOWq_I7p7M7jvahV-KoJpKbVMe1G9uVGI4XKClNXGpXmkeoAwJUUlbTltlmKGvv4Hug5THMqsCorJZikbhu9RK106cIMN5WEzi6rDRnDeCt6Sgjr4D6qsHspvhQGsK_kdAt0STAwpRbB3TRKsZuOprfFUMZ66Np66KqRXD8dzR7l1GvsLCV3Tiw</recordid><startdate>20230623</startdate><enddate>20230623</enddate><creator>Wang, Xiaorui</creator><creator>Zhu, Xinxing</creator><creator>Huang, Guangqian</creator><creator>Wu, Lili</creator><creator>Meng, Zhiyong</creator><creator>Wu, Yuyu</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><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>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20230623</creationdate><title>Knockout of PERK protects rat Müller glial cells against OGD-induced endoplasmic reticulum stress-related apoptosis</title><author>Wang, Xiaorui ; Zhu, Xinxing ; Huang, Guangqian ; Wu, Lili ; Meng, Zhiyong ; Wu, Yuyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-342238138c70cbf2f595f42a11d7f5903412c9bef1253e5a5b424c3bde03988b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Alzheimer's disease</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Caspase-12</topic><topic>Cells</topic><topic>Cholecystokinin</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress</topic><topic>Ependymoglial Cells</topic><topic>Eye diseases</topic><topic>Flow cytometry</topic><topic>Glial cells</topic><topic>Glucose</topic><topic>Homeostasis</topic><topic>Hypoxia</topic><topic>Immunofluorescence</topic><topic>Initiation factor eIF-2</topic><topic>Ischemia</topic><topic>Metabolism</topic><topic>Mueller cells</topic><topic>Müller glia</topic><topic>Ophthalmology</topic><topic>Oxygen</topic><topic>Oxygen-glucose deprivation</topic><topic>Pathogenesis</topic><topic>Protein synthesis</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reagents</topic><topic>Retina</topic><topic>Signal Transduction</topic><topic>Tau protein</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xiaorui</creatorcontrib><creatorcontrib>Zhu, Xinxing</creatorcontrib><creatorcontrib>Huang, Guangqian</creatorcontrib><creatorcontrib>Wu, Lili</creatorcontrib><creatorcontrib>Meng, Zhiyong</creatorcontrib><creatorcontrib>Wu, Yuyu</creatorcontrib><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>Neurosciences Abstracts</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>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: 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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>BMC ophthalmology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xiaorui</au><au>Zhu, Xinxing</au><au>Huang, Guangqian</au><au>Wu, Lili</au><au>Meng, Zhiyong</au><au>Wu, Yuyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Knockout of PERK protects rat Müller glial cells against OGD-induced endoplasmic reticulum stress-related apoptosis</atitle><jtitle>BMC ophthalmology</jtitle><addtitle>BMC Ophthalmol</addtitle><date>2023-06-23</date><risdate>2023</risdate><volume>23</volume><issue>1</issue><spage>286</spage><epage>286</epage><pages>286-286</pages><artnum>286</artnum><issn>1471-2415</issn><eissn>1471-2415</eissn><abstract>The pathological basis for many retinal diseases, retinal ischemia is also one of the most common causes of visual impairment. Numerous ocular diseases have been linked to Endoplasmic reticulum(ER)stress. However, there is still no clear understanding of the relationship between ER stress and Müller glial cells during retinal ischemia and hypoxia. This study examined the effects of ER stress on autophagy and apoptosis-related proteins, as well as the microtubule-related protein tau in rMC-1 cells.
rMC-1 cells were cultured in vitro. RT-PCR、immunofluorescence and Western blotting revealed the expression levels of associated mRNAs and proteins, and the CCK-8 and flow cytometry assays detected cell apoptosis.
The results showed that under OGD(Oxygen-glucose deprivation) conditions, the number of rMC-1 cells was decreased, the PERK/eIF2a pathway was activated, and the expressions of p-tau, LC3、Beclin1 and Caspase-12 proteins were increased. After the PERK knockout, the expression of the above proteins was decreased, and the apoptosis was also decreased.
According to the findings of this study, specific downregulation of PERK expression had an anti-apoptotic effect on OGD-conditioned rMC-1 cells. There is a possibility that this is one of the mechanisms of MG cell apoptosis during retinal ischemic injury.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>37353739</pmid><doi>10.1186/s12886-023-03022-z</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alzheimer's disease Animals Apoptosis Autophagy Caspase-12 Cells Cholecystokinin Endoplasmic reticulum Endoplasmic Reticulum Stress Ependymoglial Cells Eye diseases Flow cytometry Glial cells Glucose Homeostasis Hypoxia Immunofluorescence Initiation factor eIF-2 Ischemia Metabolism Mueller cells Müller glia Ophthalmology Oxygen Oxygen-glucose deprivation Pathogenesis Protein synthesis Proteins Rats Rats, Sprague-Dawley Reagents Retina Signal Transduction Tau protein Western blotting |
title | Knockout of PERK protects rat Müller glial cells against OGD-induced endoplasmic reticulum stress-related apoptosis |
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