Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo
Glaucoma is a common cause of vision loss or blindness and reduction of intraocular pressure (IOP) has been proven beneficial in a large fraction of glaucoma patients. The IOP is maintained by the trabecular meshwork (TM) and the elevation of IOP in open-angle glaucoma is associated with dysfunction...
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Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2016-06, Vol.113 (25), p.E3492-E3500 |
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description | Glaucoma is a common cause of vision loss or blindness and reduction of intraocular pressure (IOP) has been proven beneficial in a large fraction of glaucoma patients. The IOP is maintained by the trabecular meshwork (TM) and the elevation of IOP in open-angle glaucoma is associated with dysfunction and loss of the postmitotic cells residing within this tissue. To determine if IOP control can be maintained by replacing lost TM cells, we transplanted TM-like cells derived from induced pluripotent stem cells into the anterior chamber of a transgenic mouse model of glaucoma. Transplantation led to significantly reduced IOP and improved aqueous humor outflow facility, which was sustained for at least 9 wk. The ability to maintain normal IOP engendered survival of retinal ganglion cells, whose loss is ultimately the cause for reduced vision in glaucoma. In vivo and in vitro analyses demonstrated higher TM cellularity in treated mice compared with littermate controls and indicated that this increase is primarily because of a proliferative response of endogenous TM cells. Thus, our study provides in vivo demonstration that regeneration of the glaucomatous TM is possible and points toward novel approaches in the treatment of this disease. |
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The IOP is maintained by the trabecular meshwork (TM) and the elevation of IOP in open-angle glaucoma is associated with dysfunction and loss of the postmitotic cells residing within this tissue. To determine if IOP control can be maintained by replacing lost TM cells, we transplanted TM-like cells derived from induced pluripotent stem cells into the anterior chamber of a transgenic mouse model of glaucoma. Transplantation led to significantly reduced IOP and improved aqueous humor outflow facility, which was sustained for at least 9 wk. The ability to maintain normal IOP engendered survival of retinal ganglion cells, whose loss is ultimately the cause for reduced vision in glaucoma. In vivo and in vitro analyses demonstrated higher TM cellularity in treated mice compared with littermate controls and indicated that this increase is primarily because of a proliferative response of endogenous TM cells. Thus, our study provides in vivo demonstration that regeneration of the glaucomatous TM is possible and points toward novel approaches in the treatment of this disease.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1604153113</identifier><identifier>PMID: 27274060</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Biological Sciences ; Blindness ; Cytoskeletal Proteins - genetics ; Disease Models, Animal ; Eye Proteins - genetics ; Genotype & phenotype ; Glaucoma ; Glaucoma - pathology ; Glaucoma - physiopathology ; Glaucoma - therapy ; Glycoproteins - genetics ; Humans ; Intraocular Pressure ; Mice ; Mice, Transgenic ; Mutation ; PNAS Plus ; Rodents ; Stem Cell Transplantation ; Stem cells ; Trabecular Meshwork - pathology</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2016-06, Vol.113 (25), p.E3492-E3500</ispartof><rights>Volumes 1–89 and 106–113, copyright as a collective work only; author(s) retains copyright to individual articles</rights><rights>Copyright National Academy of Sciences Jun 21, 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c509t-be3e2b685108c5744efcc38b9d449887644f16fa2d7e700b2e0d8457c141947b3</citedby><cites>FETCH-LOGICAL-c509t-be3e2b685108c5744efcc38b9d449887644f16fa2d7e700b2e0d8457c141947b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/26470362$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/26470362$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27903,27904,53769,53771,57995,58228</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27274060$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Wei</creatorcontrib><creatorcontrib>Gramlich, Oliver W.</creatorcontrib><creatorcontrib>Laboissonniere, Lauren</creatorcontrib><creatorcontrib>Jain, Ankur</creatorcontrib><creatorcontrib>Sheffield, Val C.</creatorcontrib><creatorcontrib>Trimarchi, Jeffrey M.</creatorcontrib><creatorcontrib>Tucker, Budd A.</creatorcontrib><creatorcontrib>Kuehn, Markus H.</creatorcontrib><title>Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Glaucoma is a common cause of vision loss or blindness and reduction of intraocular pressure (IOP) has been proven beneficial in a large fraction of glaucoma patients. The IOP is maintained by the trabecular meshwork (TM) and the elevation of IOP in open-angle glaucoma is associated with dysfunction and loss of the postmitotic cells residing within this tissue. To determine if IOP control can be maintained by replacing lost TM cells, we transplanted TM-like cells derived from induced pluripotent stem cells into the anterior chamber of a transgenic mouse model of glaucoma. Transplantation led to significantly reduced IOP and improved aqueous humor outflow facility, which was sustained for at least 9 wk. The ability to maintain normal IOP engendered survival of retinal ganglion cells, whose loss is ultimately the cause for reduced vision in glaucoma. In vivo and in vitro analyses demonstrated higher TM cellularity in treated mice compared with littermate controls and indicated that this increase is primarily because of a proliferative response of endogenous TM cells. Thus, our study provides in vivo demonstration that regeneration of the glaucomatous TM is possible and points toward novel approaches in the treatment of this disease.</description><subject>Animals</subject><subject>Biological Sciences</subject><subject>Blindness</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Disease Models, Animal</subject><subject>Eye Proteins - genetics</subject><subject>Genotype & phenotype</subject><subject>Glaucoma</subject><subject>Glaucoma - pathology</subject><subject>Glaucoma - physiopathology</subject><subject>Glaucoma - therapy</subject><subject>Glycoproteins - genetics</subject><subject>Humans</subject><subject>Intraocular Pressure</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mutation</subject><subject>PNAS Plus</subject><subject>Rodents</subject><subject>Stem Cell Transplantation</subject><subject>Stem cells</subject><subject>Trabecular Meshwork - pathology</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc2LFDEQxYMo7rh69qQ0ePHSu5V05esiLINfMKLgeA7pdHo3Q0_SJt0D-9_b46y76qmg3q8e9XiEvKRwQUE2l2O05YIKQMobSptHZEVB01qghsdkBcBkrZDhGXlWyg4ANFfwlJwxySSCgBXZbLONZRxsnOwUUqxSX4Vv39d153M4-K7afqmcH4ZSZV_c7Et1PdjZpb2txhsf03Q7LrsQq0M4pOfkSW-H4l_czXPy48P77fpTvfn68fP6alM7DnqqW9941grFKSjHJaLvnWtUqztErZQUiD0VvWWd9BKgZR46hVw6ilSjbJtz8u7kO87t3nfOxynbwYw57G2-NckG868Sw425TgeDmjEqcDF4e2eQ088l1GT2oRxj2ujTXAyVWjOKjB_RN_-huzTnuMT7TXElONULdXmiXE6lZN_fP0PBHJsyx6bMQ1PLxeu_M9zzf6pZgFcnYFemlB90gRIawZpfo0yY2g</recordid><startdate>20160621</startdate><enddate>20160621</enddate><creator>Zhu, Wei</creator><creator>Gramlich, Oliver W.</creator><creator>Laboissonniere, Lauren</creator><creator>Jain, Ankur</creator><creator>Sheffield, Val C.</creator><creator>Trimarchi, Jeffrey M.</creator><creator>Tucker, Budd A.</creator><creator>Kuehn, Markus H.</creator><general>National Academy of Sciences</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</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>5PM</scope></search><sort><creationdate>20160621</creationdate><title>Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo</title><author>Zhu, Wei ; Gramlich, Oliver W. ; Laboissonniere, Lauren ; Jain, Ankur ; Sheffield, Val C. ; Trimarchi, Jeffrey M. ; Tucker, Budd A. ; Kuehn, Markus H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c509t-be3e2b685108c5744efcc38b9d449887644f16fa2d7e700b2e0d8457c141947b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Biological Sciences</topic><topic>Blindness</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Disease Models, Animal</topic><topic>Eye Proteins - genetics</topic><topic>Genotype & phenotype</topic><topic>Glaucoma</topic><topic>Glaucoma - pathology</topic><topic>Glaucoma - physiopathology</topic><topic>Glaucoma - therapy</topic><topic>Glycoproteins - genetics</topic><topic>Humans</topic><topic>Intraocular Pressure</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mutation</topic><topic>PNAS Plus</topic><topic>Rodents</topic><topic>Stem Cell Transplantation</topic><topic>Stem cells</topic><topic>Trabecular Meshwork - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Wei</creatorcontrib><creatorcontrib>Gramlich, Oliver W.</creatorcontrib><creatorcontrib>Laboissonniere, Lauren</creatorcontrib><creatorcontrib>Jain, Ankur</creatorcontrib><creatorcontrib>Sheffield, Val C.</creatorcontrib><creatorcontrib>Trimarchi, Jeffrey M.</creatorcontrib><creatorcontrib>Tucker, Budd A.</creatorcontrib><creatorcontrib>Kuehn, Markus H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors 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>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Wei</au><au>Gramlich, Oliver W.</au><au>Laboissonniere, Lauren</au><au>Jain, Ankur</au><au>Sheffield, Val C.</au><au>Trimarchi, Jeffrey M.</au><au>Tucker, Budd A.</au><au>Kuehn, Markus H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2016-06-21</date><risdate>2016</risdate><volume>113</volume><issue>25</issue><spage>E3492</spage><epage>E3500</epage><pages>E3492-E3500</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Glaucoma is a common cause of vision loss or blindness and reduction of intraocular pressure (IOP) has been proven beneficial in a large fraction of glaucoma patients. 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subjects | Animals Biological Sciences Blindness Cytoskeletal Proteins - genetics Disease Models, Animal Eye Proteins - genetics Genotype & phenotype Glaucoma Glaucoma - pathology Glaucoma - physiopathology Glaucoma - therapy Glycoproteins - genetics Humans Intraocular Pressure Mice Mice, Transgenic Mutation PNAS Plus Rodents Stem Cell Transplantation Stem cells Trabecular Meshwork - pathology |
title | Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo |
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