Müller cells under hydrostatic pressure modulate retinal cell survival via TRPV1/PLCγ1 complex-mediated calcium influx in experimental glaucoma
Glaucoma, an irreversible blinding eye disease, is currently unclear whose pathological mechanism is. This study investigated how transient receptor potential cation channel subfamily V member 1 (TRPV1), 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase gamma-1 (PLCγ1), and P2X purinoceptor...
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| Veröffentlicht in: | The FEBS journal 2024-06, Vol.291 (12), p.2703-2714 |
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| creator | Hu, Huiling Nie, Danyao Fang, Min He, Wenling Zhang, Jing Liu, Xinhua Zhang, Guoming |
| description | Glaucoma, an irreversible blinding eye disease, is currently unclear whose pathological mechanism is. This study investigated how transient receptor potential cation channel subfamily V member 1 (TRPV1), 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase gamma-1 (PLCγ1), and P2X purinoceptor 7 (P2X7) modulate the levels of intracellular calcium ions (Ca
) and adenosine triphosphate (ATP) in Müller cells and retinal ganglion cells (RGCs) under conditions of elevated intraocular pressure (IOP). Müller cells were maintained at hydrostatic pressure (HP). TRPV1- and PLCG1-silenced Müller cells and P2X7-silenced RGCs were constructed by transfection with short interfering RNA (siRNAs). RGCs were cultured with the conditioned media of Müller cells under HP. A mouse model of chronic ocular hypertension (COH) was established and used to investigate the role of TRPV1 in RGCs in vivo. Müller cells and RGCs were analyzed by ATP release assays, intracellular calcium assays, CCK-8 assays, EdU (5-ethynyl-2'-deoxyuridine) staining, TUNEL staining, flow cytometry, and transmission electron microscopy. In vivo changes in inner retinal function were evaluated by hematoxylin and eosin (H&E) staining and TUNEL staining. Western blot analyses were performed to measure the levels of related proteins. Our data showed that HP increased the levels of ATP and Ca
influx in Müller cells, and those increases were accompanied by the upregulation of TRPV1 and p-PLCγ1 expression. Suppression of TRPV1 or PLCG1 expression in Müller cells significantly decreased the ATP levels and intracellular Ca
accumulation induced by HP. Knockdown of TRPV1, PLCG1, or P2X7 significantly decreased apoptosis and autophagy in RGCs cultured in the conditioned media of HP-treated Müller cells. Moreover, TRPV1 silencing decreased RGC apoptosis and autophagy in the in vivo model of COH. Collectively, inhibition of TRPV1/PLCγ1 and P2X7 expression may be a useful therapeutic strategy for managing RGC death in glaucoma. |
| doi_str_mv | 10.1111/febs.17075 |
| format | Article |
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) and adenosine triphosphate (ATP) in Müller cells and retinal ganglion cells (RGCs) under conditions of elevated intraocular pressure (IOP). Müller cells were maintained at hydrostatic pressure (HP). TRPV1- and PLCG1-silenced Müller cells and P2X7-silenced RGCs were constructed by transfection with short interfering RNA (siRNAs). RGCs were cultured with the conditioned media of Müller cells under HP. A mouse model of chronic ocular hypertension (COH) was established and used to investigate the role of TRPV1 in RGCs in vivo. Müller cells and RGCs were analyzed by ATP release assays, intracellular calcium assays, CCK-8 assays, EdU (5-ethynyl-2'-deoxyuridine) staining, TUNEL staining, flow cytometry, and transmission electron microscopy. In vivo changes in inner retinal function were evaluated by hematoxylin and eosin (H&E) staining and TUNEL staining. Western blot analyses were performed to measure the levels of related proteins. Our data showed that HP increased the levels of ATP and Ca
influx in Müller cells, and those increases were accompanied by the upregulation of TRPV1 and p-PLCγ1 expression. Suppression of TRPV1 or PLCG1 expression in Müller cells significantly decreased the ATP levels and intracellular Ca
accumulation induced by HP. Knockdown of TRPV1, PLCG1, or P2X7 significantly decreased apoptosis and autophagy in RGCs cultured in the conditioned media of HP-treated Müller cells. Moreover, TRPV1 silencing decreased RGC apoptosis and autophagy in the in vivo model of COH. Collectively, inhibition of TRPV1/PLCγ1 and P2X7 expression may be a useful therapeutic strategy for managing RGC death in glaucoma.</description><identifier>ISSN: 1742-464X</identifier><identifier>ISSN: 1742-4658</identifier><identifier>EISSN: 1742-4658</identifier><identifier>DOI: 10.1111/febs.17075</identifier><identifier>PMID: 38390745</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adenosine triphosphate ; Adenosine Triphosphate - metabolism ; Animals ; Apoptosis ; Assaying ; ATP ; Autophagy ; Calcium ; Calcium (intracellular) ; Calcium - metabolism ; Calcium influx ; Calcium ions ; Capsaicin receptors ; Cell survival ; Cell Survival - genetics ; cell viability ; Cells, Cultured ; Cholecystokinin ; death ; Disease Models, Animal ; eosin ; Ependymoglial Cells - metabolism ; Ependymoglial Cells - pathology ; Eye diseases ; Flow cytometry ; ganglia ; Glaucoma ; Glaucoma - genetics ; Glaucoma - metabolism ; Glaucoma - pathology ; Hydrostatic Pressure ; Hypertension ; In vivo methods and tests ; Intracellular ; Intraocular Pressure ; Ion channels ; Male ; Mice ; Mice, Inbred C57BL ; Mueller cells ; Phosphatidylinositol ; Phospholipase C gamma - genetics ; Phospholipase C gamma - metabolism ; purinergic receptors ; Receptors, Purinergic P2X7 - genetics ; Receptors, Purinergic P2X7 - metabolism ; Retina ; Retinal cells ; Retinal ganglion cells ; Retinal Ganglion Cells - metabolism ; Retinal Ganglion Cells - pathology ; RNA ; siRNA ; Staining ; subfamily ; therapeutics ; Transfection ; Transient receptor potential proteins ; transient receptor potential vanilloid channels ; Transmission electron microscopy ; TRPV Cation Channels - genetics ; TRPV Cation Channels - metabolism ; Western blotting</subject><ispartof>The FEBS journal, 2024-06, Vol.291 (12), p.2703-2714</ispartof><rights>2024 Federation of European Biochemical Societies.</rights><rights>Copyright © 2024 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c307t-d698dd325842dd520205f2c785f46d003a62de40a0c3407027df8666f4d4e37f3</cites><orcidid>0000-0002-2286-4913 ; 0000-0001-5071-2792</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38390745$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Huiling</creatorcontrib><creatorcontrib>Nie, Danyao</creatorcontrib><creatorcontrib>Fang, Min</creatorcontrib><creatorcontrib>He, Wenling</creatorcontrib><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Liu, Xinhua</creatorcontrib><creatorcontrib>Zhang, Guoming</creatorcontrib><title>Müller cells under hydrostatic pressure modulate retinal cell survival via TRPV1/PLCγ1 complex-mediated calcium influx in experimental glaucoma</title><title>The FEBS journal</title><addtitle>FEBS J</addtitle><description>Glaucoma, an irreversible blinding eye disease, is currently unclear whose pathological mechanism is. This study investigated how transient receptor potential cation channel subfamily V member 1 (TRPV1), 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase gamma-1 (PLCγ1), and P2X purinoceptor 7 (P2X7) modulate the levels of intracellular calcium ions (Ca
) and adenosine triphosphate (ATP) in Müller cells and retinal ganglion cells (RGCs) under conditions of elevated intraocular pressure (IOP). Müller cells were maintained at hydrostatic pressure (HP). TRPV1- and PLCG1-silenced Müller cells and P2X7-silenced RGCs were constructed by transfection with short interfering RNA (siRNAs). RGCs were cultured with the conditioned media of Müller cells under HP. A mouse model of chronic ocular hypertension (COH) was established and used to investigate the role of TRPV1 in RGCs in vivo. Müller cells and RGCs were analyzed by ATP release assays, intracellular calcium assays, CCK-8 assays, EdU (5-ethynyl-2'-deoxyuridine) staining, TUNEL staining, flow cytometry, and transmission electron microscopy. In vivo changes in inner retinal function were evaluated by hematoxylin and eosin (H&E) staining and TUNEL staining. Western blot analyses were performed to measure the levels of related proteins. Our data showed that HP increased the levels of ATP and Ca
influx in Müller cells, and those increases were accompanied by the upregulation of TRPV1 and p-PLCγ1 expression. Suppression of TRPV1 or PLCG1 expression in Müller cells significantly decreased the ATP levels and intracellular Ca
accumulation induced by HP. Knockdown of TRPV1, PLCG1, or P2X7 significantly decreased apoptosis and autophagy in RGCs cultured in the conditioned media of HP-treated Müller cells. Moreover, TRPV1 silencing decreased RGC apoptosis and autophagy in the in vivo model of COH. Collectively, inhibition of TRPV1/PLCγ1 and P2X7 expression may be a useful therapeutic strategy for managing RGC death in glaucoma.</description><subject>Adenosine triphosphate</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Assaying</subject><subject>ATP</subject><subject>Autophagy</subject><subject>Calcium</subject><subject>Calcium (intracellular)</subject><subject>Calcium - metabolism</subject><subject>Calcium influx</subject><subject>Calcium ions</subject><subject>Capsaicin receptors</subject><subject>Cell survival</subject><subject>Cell Survival - genetics</subject><subject>cell viability</subject><subject>Cells, Cultured</subject><subject>Cholecystokinin</subject><subject>death</subject><subject>Disease Models, Animal</subject><subject>eosin</subject><subject>Ependymoglial Cells - metabolism</subject><subject>Ependymoglial Cells - pathology</subject><subject>Eye diseases</subject><subject>Flow cytometry</subject><subject>ganglia</subject><subject>Glaucoma</subject><subject>Glaucoma - genetics</subject><subject>Glaucoma - metabolism</subject><subject>Glaucoma - pathology</subject><subject>Hydrostatic Pressure</subject><subject>Hypertension</subject><subject>In vivo methods and tests</subject><subject>Intracellular</subject><subject>Intraocular Pressure</subject><subject>Ion channels</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mueller cells</subject><subject>Phosphatidylinositol</subject><subject>Phospholipase C gamma - genetics</subject><subject>Phospholipase C gamma - metabolism</subject><subject>purinergic receptors</subject><subject>Receptors, Purinergic P2X7 - genetics</subject><subject>Receptors, Purinergic P2X7 - metabolism</subject><subject>Retina</subject><subject>Retinal cells</subject><subject>Retinal ganglion cells</subject><subject>Retinal Ganglion Cells - metabolism</subject><subject>Retinal Ganglion Cells - pathology</subject><subject>RNA</subject><subject>siRNA</subject><subject>Staining</subject><subject>subfamily</subject><subject>therapeutics</subject><subject>Transfection</subject><subject>Transient receptor potential proteins</subject><subject>transient receptor potential vanilloid channels</subject><subject>Transmission electron microscopy</subject><subject>TRPV Cation Channels - genetics</subject><subject>TRPV Cation Channels - metabolism</subject><subject>Western blotting</subject><issn>1742-464X</issn><issn>1742-4658</issn><issn>1742-4658</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctqVTEUhoNYbK1OfAAJOBFht8nOdQ_l4A1OaZEqzjZpsqIp2ReTncPpY_gsTp0595nM6W3gxEzWWuRbP6z_R-gZJUe0vmMPF_mIKqLEA3RAFW8bLoV-eN_zL_vocc6XhDDBu-4R2meadURxcYB-nPz-FSMkbCHGjMvoav_tyqUpL2YJFs8Jci4J8DC5Es0COMESRhOvN3D92oRNnTbB4POPZ5_p8dl69ecnxXYa5gjbZgAX6prD1kQbyoDD6GPZ1oJhO0MKA4xLFfgaTak75gna8yZmeHpbD9Gnt2_OV--b9em7D6vX68YyopbGyU47x1qheeucaElLhG-t0sJz6eqpRrYOODHEMk4UaZXzWkrpuePAlGeH6OWN7pym7wXy0g8h724yI0wl94wKJrSWrPs_WvU1laqjFX3xD3o5lVTt2lGyU5Qzwiv16oay1eecwPdz9cGkq56Sfpdpv8u0v860ws9vJctFNfMevQuR_QU7Cp8c</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Hu, Huiling</creator><creator>Nie, Danyao</creator><creator>Fang, Min</creator><creator>He, Wenling</creator><creator>Zhang, Jing</creator><creator>Liu, Xinhua</creator><creator>Zhang, Guoming</creator><general>Blackwell Publishing Ltd</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-2286-4913</orcidid><orcidid>https://orcid.org/0000-0001-5071-2792</orcidid></search><sort><creationdate>20240601</creationdate><title>Müller cells under hydrostatic pressure modulate retinal cell survival via TRPV1/PLCγ1 complex-mediated calcium influx in experimental glaucoma</title><author>Hu, Huiling ; Nie, Danyao ; Fang, Min ; He, Wenling ; Zhang, Jing ; Liu, Xinhua ; Zhang, Guoming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c307t-d698dd325842dd520205f2c785f46d003a62de40a0c3407027df8666f4d4e37f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adenosine triphosphate</topic><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Assaying</topic><topic>ATP</topic><topic>Autophagy</topic><topic>Calcium</topic><topic>Calcium (intracellular)</topic><topic>Calcium - metabolism</topic><topic>Calcium influx</topic><topic>Calcium ions</topic><topic>Capsaicin receptors</topic><topic>Cell survival</topic><topic>Cell Survival - genetics</topic><topic>cell viability</topic><topic>Cells, Cultured</topic><topic>Cholecystokinin</topic><topic>death</topic><topic>Disease Models, Animal</topic><topic>eosin</topic><topic>Ependymoglial Cells - metabolism</topic><topic>Ependymoglial Cells - pathology</topic><topic>Eye diseases</topic><topic>Flow cytometry</topic><topic>ganglia</topic><topic>Glaucoma</topic><topic>Glaucoma - genetics</topic><topic>Glaucoma - metabolism</topic><topic>Glaucoma - pathology</topic><topic>Hydrostatic Pressure</topic><topic>Hypertension</topic><topic>In vivo methods and tests</topic><topic>Intracellular</topic><topic>Intraocular Pressure</topic><topic>Ion channels</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mueller cells</topic><topic>Phosphatidylinositol</topic><topic>Phospholipase C gamma - genetics</topic><topic>Phospholipase C gamma - metabolism</topic><topic>purinergic receptors</topic><topic>Receptors, Purinergic P2X7 - genetics</topic><topic>Receptors, Purinergic P2X7 - metabolism</topic><topic>Retina</topic><topic>Retinal cells</topic><topic>Retinal ganglion cells</topic><topic>Retinal Ganglion Cells - metabolism</topic><topic>Retinal Ganglion Cells - pathology</topic><topic>RNA</topic><topic>siRNA</topic><topic>Staining</topic><topic>subfamily</topic><topic>therapeutics</topic><topic>Transfection</topic><topic>Transient receptor potential proteins</topic><topic>transient receptor potential vanilloid channels</topic><topic>Transmission electron microscopy</topic><topic>TRPV Cation Channels - genetics</topic><topic>TRPV Cation Channels - metabolism</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Huiling</creatorcontrib><creatorcontrib>Nie, Danyao</creatorcontrib><creatorcontrib>Fang, Min</creatorcontrib><creatorcontrib>He, Wenling</creatorcontrib><creatorcontrib>Zhang, Jing</creatorcontrib><creatorcontrib>Liu, Xinhua</creatorcontrib><creatorcontrib>Zhang, Guoming</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>The FEBS journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Huiling</au><au>Nie, Danyao</au><au>Fang, Min</au><au>He, Wenling</au><au>Zhang, Jing</au><au>Liu, Xinhua</au><au>Zhang, Guoming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Müller cells under hydrostatic pressure modulate retinal cell survival via TRPV1/PLCγ1 complex-mediated calcium influx in experimental glaucoma</atitle><jtitle>The FEBS journal</jtitle><addtitle>FEBS J</addtitle><date>2024-06-01</date><risdate>2024</risdate><volume>291</volume><issue>12</issue><spage>2703</spage><epage>2714</epage><pages>2703-2714</pages><issn>1742-464X</issn><issn>1742-4658</issn><eissn>1742-4658</eissn><abstract>Glaucoma, an irreversible blinding eye disease, is currently unclear whose pathological mechanism is. This study investigated how transient receptor potential cation channel subfamily V member 1 (TRPV1), 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase gamma-1 (PLCγ1), and P2X purinoceptor 7 (P2X7) modulate the levels of intracellular calcium ions (Ca
) and adenosine triphosphate (ATP) in Müller cells and retinal ganglion cells (RGCs) under conditions of elevated intraocular pressure (IOP). Müller cells were maintained at hydrostatic pressure (HP). TRPV1- and PLCG1-silenced Müller cells and P2X7-silenced RGCs were constructed by transfection with short interfering RNA (siRNAs). RGCs were cultured with the conditioned media of Müller cells under HP. A mouse model of chronic ocular hypertension (COH) was established and used to investigate the role of TRPV1 in RGCs in vivo. Müller cells and RGCs were analyzed by ATP release assays, intracellular calcium assays, CCK-8 assays, EdU (5-ethynyl-2'-deoxyuridine) staining, TUNEL staining, flow cytometry, and transmission electron microscopy. In vivo changes in inner retinal function were evaluated by hematoxylin and eosin (H&E) staining and TUNEL staining. Western blot analyses were performed to measure the levels of related proteins. Our data showed that HP increased the levels of ATP and Ca
influx in Müller cells, and those increases were accompanied by the upregulation of TRPV1 and p-PLCγ1 expression. Suppression of TRPV1 or PLCG1 expression in Müller cells significantly decreased the ATP levels and intracellular Ca
accumulation induced by HP. Knockdown of TRPV1, PLCG1, or P2X7 significantly decreased apoptosis and autophagy in RGCs cultured in the conditioned media of HP-treated Müller cells. Moreover, TRPV1 silencing decreased RGC apoptosis and autophagy in the in vivo model of COH. Collectively, inhibition of TRPV1/PLCγ1 and P2X7 expression may be a useful therapeutic strategy for managing RGC death in glaucoma.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>38390745</pmid><doi>10.1111/febs.17075</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-2286-4913</orcidid><orcidid>https://orcid.org/0000-0001-5071-2792</orcidid></addata></record> |
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| subjects | Adenosine triphosphate Adenosine Triphosphate - metabolism Animals Apoptosis Assaying ATP Autophagy Calcium Calcium (intracellular) Calcium - metabolism Calcium influx Calcium ions Capsaicin receptors Cell survival Cell Survival - genetics cell viability Cells, Cultured Cholecystokinin death Disease Models, Animal eosin Ependymoglial Cells - metabolism Ependymoglial Cells - pathology Eye diseases Flow cytometry ganglia Glaucoma Glaucoma - genetics Glaucoma - metabolism Glaucoma - pathology Hydrostatic Pressure Hypertension In vivo methods and tests Intracellular Intraocular Pressure Ion channels Male Mice Mice, Inbred C57BL Mueller cells Phosphatidylinositol Phospholipase C gamma - genetics Phospholipase C gamma - metabolism purinergic receptors Receptors, Purinergic P2X7 - genetics Receptors, Purinergic P2X7 - metabolism Retina Retinal cells Retinal ganglion cells Retinal Ganglion Cells - metabolism Retinal Ganglion Cells - pathology RNA siRNA Staining subfamily therapeutics Transfection Transient receptor potential proteins transient receptor potential vanilloid channels Transmission electron microscopy TRPV Cation Channels - genetics TRPV Cation Channels - metabolism Western blotting |
| title | Müller cells under hydrostatic pressure modulate retinal cell survival via TRPV1/PLCγ1 complex-mediated calcium influx in experimental glaucoma |
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