Erythropoietin protects retinal pigment epithelial cells against the increase of permeability induced by diabetic conditions: Essential role of JAK2/ PI3K signaling
The outer blood-retinal barrier is formed by retinal pigment epithelial (RPE) cells and its disruption significantly contributes to the development of diabetic macular edema (DME). The aim of the study was to explore whether erythropoietin (Epo) has beneficial effects on the barrier function of huma...
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| description | The outer blood-retinal barrier is formed by retinal pigment epithelial (RPE) cells and its disruption significantly contributes to the development of diabetic macular edema (DME). The aim of the study was to explore whether erythropoietin (Epo) has beneficial effects on the barrier function of human RPE cells and the main downstream pathways involved. ARPE-19 cells were cultured in standard conditions and under conditions leading to the disruption of the monolayer [25
mmol/L
d-glucose plus IL-1β (10
ng/mL)]. Epo (200
mU/mL/day) was added during the last 2
days of the experiment. The experiments were repeated in the presence of an Epo neutralizing antibody and specific inhibitors of JAK2 and PI3K (AG490 and LY294002, respectively). Permeability was evaluated by fluorescein isothiocyanate dextran (70
kDa) movements. Distribution of tight junction proteins was examined by immunofluorescence. Changes in cytosolic Ca
2+ induced by Epo were also measured. Epo treatment was able to prevent but not to restore the increase of permeability induced by high glucose plus IL-1β. The protective effect of Epo on RPE barrier function was completely blocked by AG490 and almost completely abolished by LY294002. In addition, Epo was able to increase cytosolic Ca
2+ with dependence on extracellular calcium influx and this effect was blocked by either JAK2 or PI3K inhibition. We conclude that RPE disruption induced by high glucose plus IL-1β is prevented by Epo through the downstream signaling of JAK2 and PI3K/AKT pathways. |
| doi_str_mv | 10.1016/j.cellsig.2011.05.011 |
| format | Article |
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mmol/L
d-glucose plus IL-1β (10
ng/mL)]. Epo (200
mU/mL/day) was added during the last 2
days of the experiment. The experiments were repeated in the presence of an Epo neutralizing antibody and specific inhibitors of JAK2 and PI3K (AG490 and LY294002, respectively). Permeability was evaluated by fluorescein isothiocyanate dextran (70
kDa) movements. Distribution of tight junction proteins was examined by immunofluorescence. Changes in cytosolic Ca
2+ induced by Epo were also measured. Epo treatment was able to prevent but not to restore the increase of permeability induced by high glucose plus IL-1β. The protective effect of Epo on RPE barrier function was completely blocked by AG490 and almost completely abolished by LY294002. In addition, Epo was able to increase cytosolic Ca
2+ with dependence on extracellular calcium influx and this effect was blocked by either JAK2 or PI3K inhibition. We conclude that RPE disruption induced by high glucose plus IL-1β is prevented by Epo through the downstream signaling of JAK2 and PI3K/AKT pathways.</description><identifier>ISSN: 0898-6568</identifier><identifier>EISSN: 1873-3913</identifier><identifier>DOI: 10.1016/j.cellsig.2011.05.011</identifier><identifier>PMID: 21620963</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Antibodies ; Calcium (extracellular) ; Calcium - metabolism ; Cell Count - methods ; Cell Line, Tumor ; Chromones - pharmacology ; Dextran ; Dextrans - metabolism ; Diabetes mellitus ; Diabetic macular edema ; Diabetic Retinopathy - drug therapy ; Edema ; Erythropoietin ; Erythropoietin - pharmacology ; Erythropoietin - therapeutic use ; Fluorescein isothiocyanate ; Fluorescein-5-isothiocyanate - analogs & derivatives ; Fluorescein-5-isothiocyanate - metabolism ; Glucose ; Glucose - pharmacology ; Humans ; Immunoblotting ; Immunofluorescence ; Immunohistochemistry ; Interleukin 1 ; Interleukin-1beta - pharmacology ; JAK2 ; Janus kinase 2 ; Janus Kinase 2 - antagonists & inhibitors ; Janus Kinase 2 - metabolism ; Membrane Proteins - metabolism ; Morpholines - pharmacology ; Permeability ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; PI3K/AKT ; Pigments ; Protective Agents - pharmacology ; Retina ; Retinal pigment epithelial cells ; retinal pigment epithelium ; Retinal Pigment Epithelium - cytology ; Retinal Pigment Epithelium - drug effects ; Retinal Pigment Epithelium - metabolism ; Signal Transduction ; Tight junctions ; Tyrphostins - pharmacology</subject><ispartof>Cellular signalling, 2011-10, Vol.23 (10), p.1596-1602</ispartof><rights>2011 Elsevier Inc.</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-cbd65c82e3018ddfc9111cdd8d4f7dbf70561b2f475d7e7aa8cb1676d5f6e653</citedby><cites>FETCH-LOGICAL-c397t-cbd65c82e3018ddfc9111cdd8d4f7dbf70561b2f475d7e7aa8cb1676d5f6e653</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.cellsig.2011.05.011$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21620963$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Garcia-Ramírez, Marta</creatorcontrib><creatorcontrib>Hernández, Cristina</creatorcontrib><creatorcontrib>Ruiz-Meana, Marisol</creatorcontrib><creatorcontrib>Villarroel, Marta</creatorcontrib><creatorcontrib>Corraliza, Lidia</creatorcontrib><creatorcontrib>García-Dorado, David</creatorcontrib><creatorcontrib>Simó, Rafael</creatorcontrib><title>Erythropoietin protects retinal pigment epithelial cells against the increase of permeability induced by diabetic conditions: Essential role of JAK2/ PI3K signaling</title><title>Cellular signalling</title><addtitle>Cell Signal</addtitle><description>The outer blood-retinal barrier is formed by retinal pigment epithelial (RPE) cells and its disruption significantly contributes to the development of diabetic macular edema (DME). The aim of the study was to explore whether erythropoietin (Epo) has beneficial effects on the barrier function of human RPE cells and the main downstream pathways involved. ARPE-19 cells were cultured in standard conditions and under conditions leading to the disruption of the monolayer [25
mmol/L
d-glucose plus IL-1β (10
ng/mL)]. Epo (200
mU/mL/day) was added during the last 2
days of the experiment. The experiments were repeated in the presence of an Epo neutralizing antibody and specific inhibitors of JAK2 and PI3K (AG490 and LY294002, respectively). Permeability was evaluated by fluorescein isothiocyanate dextran (70
kDa) movements. Distribution of tight junction proteins was examined by immunofluorescence. Changes in cytosolic Ca
2+ induced by Epo were also measured. Epo treatment was able to prevent but not to restore the increase of permeability induced by high glucose plus IL-1β. The protective effect of Epo on RPE barrier function was completely blocked by AG490 and almost completely abolished by LY294002. In addition, Epo was able to increase cytosolic Ca
2+ with dependence on extracellular calcium influx and this effect was blocked by either JAK2 or PI3K inhibition. We conclude that RPE disruption induced by high glucose plus IL-1β is prevented by Epo through the downstream signaling of JAK2 and PI3K/AKT pathways.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Antibodies</subject><subject>Calcium (extracellular)</subject><subject>Calcium - metabolism</subject><subject>Cell Count - methods</subject><subject>Cell Line, Tumor</subject><subject>Chromones - pharmacology</subject><subject>Dextran</subject><subject>Dextrans - metabolism</subject><subject>Diabetes mellitus</subject><subject>Diabetic macular edema</subject><subject>Diabetic Retinopathy - drug therapy</subject><subject>Edema</subject><subject>Erythropoietin</subject><subject>Erythropoietin - pharmacology</subject><subject>Erythropoietin - therapeutic use</subject><subject>Fluorescein isothiocyanate</subject><subject>Fluorescein-5-isothiocyanate - analogs & derivatives</subject><subject>Fluorescein-5-isothiocyanate - metabolism</subject><subject>Glucose</subject><subject>Glucose - pharmacology</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunofluorescence</subject><subject>Immunohistochemistry</subject><subject>Interleukin 1</subject><subject>Interleukin-1beta - pharmacology</subject><subject>JAK2</subject><subject>Janus kinase 2</subject><subject>Janus Kinase 2 - antagonists & inhibitors</subject><subject>Janus Kinase 2 - metabolism</subject><subject>Membrane Proteins - metabolism</subject><subject>Morpholines - pharmacology</subject><subject>Permeability</subject><subject>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>PI3K/AKT</subject><subject>Pigments</subject><subject>Protective Agents - pharmacology</subject><subject>Retina</subject><subject>Retinal pigment epithelial cells</subject><subject>retinal pigment epithelium</subject><subject>Retinal Pigment Epithelium - cytology</subject><subject>Retinal Pigment Epithelium - drug effects</subject><subject>Retinal Pigment Epithelium - metabolism</subject><subject>Signal Transduction</subject><subject>Tight junctions</subject><subject>Tyrphostins - pharmacology</subject><issn>0898-6568</issn><issn>1873-3913</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctu1DAUhi0EokPhEUDewSZTO44vYYOqagqllWDRveXYJ1OPkjjYnkrzPjxonc7AElZHPv7Ofy4_Qu8pWVNCxcVubWEYkt-ua0LpmvB1CS_QiirJKtZS9hKtiGpVJbhQZ-hNSjtCKCeifo3Oaipq0gq2Qr838ZAfYpiDh-wnPMeQweaE4_I0A579doQpY5h9foDBl9RzY2y2xk8p45LFfrIRTAIcejxDHMF0fvD5UD7c3oLD3QE7b7qiabENk_PZhyl9xpuUivgiGsPwXP798ra-wD9v2C0uy5UJ_LR9i171Zkjw7hTP0f315v7qW3X34-vN1eVdZVkrc2U7J7hVNTBClXO9bSml1jnlml66rpeEC9rVfSO5kyCNUbajQgrHewGCs3P08ShbjvBrDynr0adlWTNB2CetFJG0kawp5Kd_kpS0rOGNbEhB-RG1MaQUoddz9KOJhwLpxUm90ycn9eKkJlyXUOo-nFrsuxHc36o_1hXgyxGAcpFHD1En62Eq1_axOKhd8P9p8QTpfrWm</recordid><startdate>20111001</startdate><enddate>20111001</enddate><creator>Garcia-Ramírez, Marta</creator><creator>Hernández, Cristina</creator><creator>Ruiz-Meana, Marisol</creator><creator>Villarroel, Marta</creator><creator>Corraliza, Lidia</creator><creator>García-Dorado, David</creator><creator>Simó, Rafael</creator><general>Elsevier Inc</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20111001</creationdate><title>Erythropoietin protects retinal pigment epithelial cells against the increase of permeability induced by diabetic conditions: Essential role of JAK2/ PI3K signaling</title><author>Garcia-Ramírez, Marta ; Hernández, Cristina ; Ruiz-Meana, Marisol ; Villarroel, Marta ; Corraliza, Lidia ; García-Dorado, David ; Simó, Rafael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-cbd65c82e3018ddfc9111cdd8d4f7dbf70561b2f475d7e7aa8cb1676d5f6e653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Antibodies</topic><topic>Calcium (extracellular)</topic><topic>Calcium - metabolism</topic><topic>Cell Count - methods</topic><topic>Cell Line, Tumor</topic><topic>Chromones - pharmacology</topic><topic>Dextran</topic><topic>Dextrans - metabolism</topic><topic>Diabetes mellitus</topic><topic>Diabetic macular edema</topic><topic>Diabetic Retinopathy - drug therapy</topic><topic>Edema</topic><topic>Erythropoietin</topic><topic>Erythropoietin - pharmacology</topic><topic>Erythropoietin - therapeutic use</topic><topic>Fluorescein isothiocyanate</topic><topic>Fluorescein-5-isothiocyanate - analogs & derivatives</topic><topic>Fluorescein-5-isothiocyanate - metabolism</topic><topic>Glucose</topic><topic>Glucose - pharmacology</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunofluorescence</topic><topic>Immunohistochemistry</topic><topic>Interleukin 1</topic><topic>Interleukin-1beta - pharmacology</topic><topic>JAK2</topic><topic>Janus kinase 2</topic><topic>Janus Kinase 2 - antagonists & inhibitors</topic><topic>Janus Kinase 2 - metabolism</topic><topic>Membrane Proteins - metabolism</topic><topic>Morpholines - pharmacology</topic><topic>Permeability</topic><topic>Phosphatidylinositol 3-Kinases - antagonists & inhibitors</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>PI3K/AKT</topic><topic>Pigments</topic><topic>Protective Agents - pharmacology</topic><topic>Retina</topic><topic>Retinal pigment epithelial cells</topic><topic>retinal pigment epithelium</topic><topic>Retinal Pigment Epithelium - cytology</topic><topic>Retinal Pigment Epithelium - drug effects</topic><topic>Retinal Pigment Epithelium - metabolism</topic><topic>Signal Transduction</topic><topic>Tight junctions</topic><topic>Tyrphostins - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Garcia-Ramírez, Marta</creatorcontrib><creatorcontrib>Hernández, Cristina</creatorcontrib><creatorcontrib>Ruiz-Meana, Marisol</creatorcontrib><creatorcontrib>Villarroel, Marta</creatorcontrib><creatorcontrib>Corraliza, Lidia</creatorcontrib><creatorcontrib>García-Dorado, David</creatorcontrib><creatorcontrib>Simó, Rafael</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cellular signalling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Garcia-Ramírez, Marta</au><au>Hernández, Cristina</au><au>Ruiz-Meana, Marisol</au><au>Villarroel, Marta</au><au>Corraliza, Lidia</au><au>García-Dorado, David</au><au>Simó, Rafael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Erythropoietin protects retinal pigment epithelial cells against the increase of permeability induced by diabetic conditions: Essential role of JAK2/ PI3K signaling</atitle><jtitle>Cellular signalling</jtitle><addtitle>Cell Signal</addtitle><date>2011-10-01</date><risdate>2011</risdate><volume>23</volume><issue>10</issue><spage>1596</spage><epage>1602</epage><pages>1596-1602</pages><issn>0898-6568</issn><eissn>1873-3913</eissn><abstract>The outer blood-retinal barrier is formed by retinal pigment epithelial (RPE) cells and its disruption significantly contributes to the development of diabetic macular edema (DME). The aim of the study was to explore whether erythropoietin (Epo) has beneficial effects on the barrier function of human RPE cells and the main downstream pathways involved. ARPE-19 cells were cultured in standard conditions and under conditions leading to the disruption of the monolayer [25
mmol/L
d-glucose plus IL-1β (10
ng/mL)]. Epo (200
mU/mL/day) was added during the last 2
days of the experiment. The experiments were repeated in the presence of an Epo neutralizing antibody and specific inhibitors of JAK2 and PI3K (AG490 and LY294002, respectively). Permeability was evaluated by fluorescein isothiocyanate dextran (70
kDa) movements. Distribution of tight junction proteins was examined by immunofluorescence. Changes in cytosolic Ca
2+ induced by Epo were also measured. Epo treatment was able to prevent but not to restore the increase of permeability induced by high glucose plus IL-1β. The protective effect of Epo on RPE barrier function was completely blocked by AG490 and almost completely abolished by LY294002. In addition, Epo was able to increase cytosolic Ca
2+ with dependence on extracellular calcium influx and this effect was blocked by either JAK2 or PI3K inhibition. We conclude that RPE disruption induced by high glucose plus IL-1β is prevented by Epo through the downstream signaling of JAK2 and PI3K/AKT pathways.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>21620963</pmid><doi>10.1016/j.cellsig.2011.05.011</doi><tpages>7</tpages></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Antibodies Calcium (extracellular) Calcium - metabolism Cell Count - methods Cell Line, Tumor Chromones - pharmacology Dextran Dextrans - metabolism Diabetes mellitus Diabetic macular edema Diabetic Retinopathy - drug therapy Edema Erythropoietin Erythropoietin - pharmacology Erythropoietin - therapeutic use Fluorescein isothiocyanate Fluorescein-5-isothiocyanate - analogs & derivatives Fluorescein-5-isothiocyanate - metabolism Glucose Glucose - pharmacology Humans Immunoblotting Immunofluorescence Immunohistochemistry Interleukin 1 Interleukin-1beta - pharmacology JAK2 Janus kinase 2 Janus Kinase 2 - antagonists & inhibitors Janus Kinase 2 - metabolism Membrane Proteins - metabolism Morpholines - pharmacology Permeability Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - metabolism Phosphorylation PI3K/AKT Pigments Protective Agents - pharmacology Retina Retinal pigment epithelial cells retinal pigment epithelium Retinal Pigment Epithelium - cytology Retinal Pigment Epithelium - drug effects Retinal Pigment Epithelium - metabolism Signal Transduction Tight junctions Tyrphostins - pharmacology |
| title | Erythropoietin protects retinal pigment epithelial cells against the increase of permeability induced by diabetic conditions: Essential role of JAK2/ PI3K signaling |
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