The Neuropilin-1 Inhibitor, ATWLPPR Peptide, Prevents Experimental Diabetes-Induced Retinal Injury by Preserving Vascular Integrity and Decreasing Oxidative Stress
Neuropilin-1 (NRP-1) is a transmembrane glycoprotein. As a VEGF co-receptor, NRP1 significantly enhances VEGFR2 signaling and promotes vascular permeability and migration. The purpose of this study was to evaluate the effects of an NRP-1 inhibitor, ATWLPPR peptide, on the early stages of diabetic re...
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| description | Neuropilin-1 (NRP-1) is a transmembrane glycoprotein. As a VEGF co-receptor, NRP1 significantly enhances VEGFR2 signaling and promotes vascular permeability and migration. The purpose of this study was to evaluate the effects of an NRP-1 inhibitor, ATWLPPR peptide, on the early stages of diabetic retinopathy. Eight-week-old male C57BL/6 mice were divided into three groups: a Normal group, a Diabetes (DB) ATWLPPR treatment group and a DB saline group. Electroretinography (ERG), fundus fluorescence angiography (FFA) and leukostasis were examined to evaluate the retinal injury induced by diabetes at the end of the fifth week after STZ injection. Occludin expression and extravasation of albumin were measured to determine the extent of vascular injury. The oxidative stress level and the levels of inflammation-associated proteins were also assayed. The results indicated that treatment with ATWLPPR prevents the abnormal condition of ERG (amplitudes of b-wave decreased and implicit time increased) and vascular injury (occludin degradation and increase in extravasated albumin). These effects were associated with a reduction in the oxidase stress level and the expression of VEGF, GFAP, and ICAM-1. We conclude that ATWLPPR, an NRP-1 inhibitor, may reduce the early retinal damage induced by diabetes by preserving vascular integrity and decreasing the oxidative stress level. Blockade of NRP-1 may be a new therapeutic strategy for the early stages of DR. |
| doi_str_mv | 10.1371/journal.pone.0142571 |
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As a VEGF co-receptor, NRP1 significantly enhances VEGFR2 signaling and promotes vascular permeability and migration. The purpose of this study was to evaluate the effects of an NRP-1 inhibitor, ATWLPPR peptide, on the early stages of diabetic retinopathy. Eight-week-old male C57BL/6 mice were divided into three groups: a Normal group, a Diabetes (DB) ATWLPPR treatment group and a DB saline group. Electroretinography (ERG), fundus fluorescence angiography (FFA) and leukostasis were examined to evaluate the retinal injury induced by diabetes at the end of the fifth week after STZ injection. Occludin expression and extravasation of albumin were measured to determine the extent of vascular injury. The oxidative stress level and the levels of inflammation-associated proteins were also assayed. The results indicated that treatment with ATWLPPR prevents the abnormal condition of ERG (amplitudes of b-wave decreased and implicit time increased) and vascular injury (occludin degradation and increase in extravasated albumin). These effects were associated with a reduction in the oxidase stress level and the expression of VEGF, GFAP, and ICAM-1. We conclude that ATWLPPR, an NRP-1 inhibitor, may reduce the early retinal damage induced by diabetes by preserving vascular integrity and decreasing the oxidative stress level. Blockade of NRP-1 may be a new therapeutic strategy for the early stages of DR.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0142571</identifier><identifier>PMID: 26554379</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Albumin ; Angiogenesis ; Angiography ; Animals ; Blood-brain barrier ; Brain research ; Cell adhesion & migration ; Development and progression ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Diabetic retinopathy ; Diabetic Retinopathy - metabolism ; Diabetic Retinopathy - prevention & control ; Electroretinograms ; Electroretinography ; Extravasation ; Fluorescence ; Genetic aspects ; Glial fibrillary acidic protein ; Glycoproteins ; Health aspects ; Inflammation ; Inhibitors ; Injury prevention ; Integrity ; Intercellular adhesion molecule 1 ; Male ; Membrane proteins ; Mice ; Mice, Inbred C57BL ; Neuropilin ; Neuropilin-1 - antagonists & inhibitors ; Neuropilin-1 - metabolism ; Oligopeptides - pharmacology ; Oligopeptides - therapeutic use ; Oxidative stress ; Oxidative Stress - drug effects ; Pathogenesis ; Peptides ; Permeability ; Properties ; Proteins ; Receptors, Vascular Endothelial Growth Factor - metabolism ; Retina ; Retinal Vessels - drug effects ; Retinal Vessels - metabolism ; Retinopathy ; Signal transduction ; Signaling ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>PloS one, 2015-11, Vol.10 (11), p.e0142571-e0142571</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Wang et al 2015 Wang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-9f3b3d6d990f137ed2c5c37dcb278453cebf33a839e93fa912d91494eaca7ea63</citedby><cites>FETCH-LOGICAL-c692t-9f3b3d6d990f137ed2c5c37dcb278453cebf33a839e93fa912d91494eaca7ea63</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/PMC4640834/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640834/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53769,53771,79346,79347</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26554379$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Lewin, Alfred S</contributor><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Wang, Shuaiwei</creatorcontrib><creatorcontrib>Li, Mengling</creatorcontrib><creatorcontrib>Wu, Dongdong</creatorcontrib><creatorcontrib>Liu, Fang</creatorcontrib><creatorcontrib>Yang, Ruisheng</creatorcontrib><creatorcontrib>Ji, Shaoping</creatorcontrib><creatorcontrib>Ji, Ailing</creatorcontrib><creatorcontrib>Li, Yanzhang</creatorcontrib><title>The Neuropilin-1 Inhibitor, ATWLPPR Peptide, Prevents Experimental Diabetes-Induced Retinal Injury by Preserving Vascular Integrity and Decreasing Oxidative Stress</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Neuropilin-1 (NRP-1) is a transmembrane glycoprotein. As a VEGF co-receptor, NRP1 significantly enhances VEGFR2 signaling and promotes vascular permeability and migration. The purpose of this study was to evaluate the effects of an NRP-1 inhibitor, ATWLPPR peptide, on the early stages of diabetic retinopathy. Eight-week-old male C57BL/6 mice were divided into three groups: a Normal group, a Diabetes (DB) ATWLPPR treatment group and a DB saline group. Electroretinography (ERG), fundus fluorescence angiography (FFA) and leukostasis were examined to evaluate the retinal injury induced by diabetes at the end of the fifth week after STZ injection. Occludin expression and extravasation of albumin were measured to determine the extent of vascular injury. The oxidative stress level and the levels of inflammation-associated proteins were also assayed. The results indicated that treatment with ATWLPPR prevents the abnormal condition of ERG (amplitudes of b-wave decreased and implicit time increased) and vascular injury (occludin degradation and increase in extravasated albumin). These effects were associated with a reduction in the oxidase stress level and the expression of VEGF, GFAP, and ICAM-1. We conclude that ATWLPPR, an NRP-1 inhibitor, may reduce the early retinal damage induced by diabetes by preserving vascular integrity and decreasing the oxidative stress level. Blockade of NRP-1 may be a new therapeutic strategy for the early stages of DR.</description><subject>Albumin</subject><subject>Angiogenesis</subject><subject>Angiography</subject><subject>Animals</subject><subject>Blood-brain barrier</subject><subject>Brain research</subject><subject>Cell adhesion & migration</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetic retinopathy</subject><subject>Diabetic Retinopathy - metabolism</subject><subject>Diabetic Retinopathy - prevention & control</subject><subject>Electroretinograms</subject><subject>Electroretinography</subject><subject>Extravasation</subject><subject>Fluorescence</subject><subject>Genetic aspects</subject><subject>Glial fibrillary acidic protein</subject><subject>Glycoproteins</subject><subject>Health aspects</subject><subject>Inflammation</subject><subject>Inhibitors</subject><subject>Injury prevention</subject><subject>Integrity</subject><subject>Intercellular adhesion molecule 1</subject><subject>Male</subject><subject>Membrane proteins</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neuropilin</subject><subject>Neuropilin-1 - antagonists & inhibitors</subject><subject>Neuropilin-1 - metabolism</subject><subject>Oligopeptides - pharmacology</subject><subject>Oligopeptides - therapeutic use</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pathogenesis</subject><subject>Peptides</subject><subject>Permeability</subject><subject>Properties</subject><subject>Proteins</subject><subject>Receptors, Vascular Endothelial Growth Factor - metabolism</subject><subject>Retina</subject><subject>Retinal Vessels - drug effects</subject><subject>Retinal Vessels - metabolism</subject><subject>Retinopathy</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk99u0zAUxiMEYmPwBggsTUIgLSXOyZ_6BqnaBlSaWNWVcWk59knrKo2L7VTr8_CiOFs3rWgXyBex7N_3HfuLTxS9pcmAQkk_L01nW9EM1qbFQUKzNC_ps-iQMkjjIk3g-aP5QfTKuWWS5DAsipfRQVrkeQYlO4z-zBZIfmBnzVo3uo0pGbcLXWlv7AkZzX5dTCZTMsG11wpPyMTiBlvvyPnNGq1ehbloyJkWFXp08bhVnURFpuh1OFqwWnZ2S6ptL3RoN7qdk2vhZNcIG3Y9zq32WyJaRc5QWhSuJy5vtBJeb5Bc-aBzr6MXtWgcvtl9j6KfX89np9_ji8tv49PRRSwLlvqY1VCBKhRjSR0SQpXKXEKpZJWWwywHiVUNIIbAkEEtGE0VoxnLUEhRoijgKHp_57tujOO7fB2nJaRAaQ4sEOM7Qhmx5OuQgLBbboTmtwvGzrmwXssGeV2AqmUmgak0FM-ZVIiQqITWlUKaBa8vu2pdtUIlQ5ZWNHum-zutXvC52fCsyJIh9AYfdwbW_O7Qeb7STmLTiBZNd3tuoCxhQxrQ43_Qp2-3o-YiXEC3tQl1ZW_KRxlklBUl9F6DJ6gwFK60DI-x1mF9T_BpTxAYjzd-Ljrn-Phq-v_s5fU---ERu0DR-IUzTee1ad0-mN2B0hrnLNYPIdOE9710nwbve4nveinI3j3-QQ-i--aBv0feHCM</recordid><startdate>20151110</startdate><enddate>20151110</enddate><creator>Wang, Jun</creator><creator>Wang, Shuaiwei</creator><creator>Li, Mengling</creator><creator>Wu, Dongdong</creator><creator>Liu, Fang</creator><creator>Yang, Ruisheng</creator><creator>Ji, Shaoping</creator><creator>Ji, Ailing</creator><creator>Li, Yanzhang</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20151110</creationdate><title>The Neuropilin-1 Inhibitor, ATWLPPR Peptide, Prevents Experimental Diabetes-Induced Retinal Injury by Preserving Vascular Integrity and Decreasing Oxidative Stress</title><author>Wang, Jun ; Wang, Shuaiwei ; Li, Mengling ; Wu, Dongdong ; Liu, Fang ; Yang, Ruisheng ; Ji, Shaoping ; Ji, Ailing ; Li, Yanzhang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-9f3b3d6d990f137ed2c5c37dcb278453cebf33a839e93fa912d91494eaca7ea63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Albumin</topic><topic>Angiogenesis</topic><topic>Angiography</topic><topic>Animals</topic><topic>Blood-brain barrier</topic><topic>Brain research</topic><topic>Cell adhesion & migration</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetic retinopathy</topic><topic>Diabetic Retinopathy - metabolism</topic><topic>Diabetic Retinopathy - prevention & control</topic><topic>Electroretinograms</topic><topic>Electroretinography</topic><topic>Extravasation</topic><topic>Fluorescence</topic><topic>Genetic aspects</topic><topic>Glial fibrillary acidic protein</topic><topic>Glycoproteins</topic><topic>Health aspects</topic><topic>Inflammation</topic><topic>Inhibitors</topic><topic>Injury prevention</topic><topic>Integrity</topic><topic>Intercellular adhesion molecule 1</topic><topic>Male</topic><topic>Membrane proteins</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Neuropilin</topic><topic>Neuropilin-1 - antagonists & inhibitors</topic><topic>Neuropilin-1 - metabolism</topic><topic>Oligopeptides - pharmacology</topic><topic>Oligopeptides - therapeutic use</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pathogenesis</topic><topic>Peptides</topic><topic>Permeability</topic><topic>Properties</topic><topic>Proteins</topic><topic>Receptors, Vascular Endothelial Growth Factor - metabolism</topic><topic>Retina</topic><topic>Retinal Vessels - drug effects</topic><topic>Retinal Vessels - metabolism</topic><topic>Retinopathy</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Jun</creatorcontrib><creatorcontrib>Wang, Shuaiwei</creatorcontrib><creatorcontrib>Li, Mengling</creatorcontrib><creatorcontrib>Wu, Dongdong</creatorcontrib><creatorcontrib>Liu, Fang</creatorcontrib><creatorcontrib>Yang, Ruisheng</creatorcontrib><creatorcontrib>Ji, Shaoping</creatorcontrib><creatorcontrib>Ji, Ailing</creatorcontrib><creatorcontrib>Li, Yanzhang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Jun</au><au>Wang, Shuaiwei</au><au>Li, Mengling</au><au>Wu, Dongdong</au><au>Liu, Fang</au><au>Yang, Ruisheng</au><au>Ji, Shaoping</au><au>Ji, Ailing</au><au>Li, Yanzhang</au><au>Lewin, Alfred S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Neuropilin-1 Inhibitor, ATWLPPR Peptide, Prevents Experimental Diabetes-Induced Retinal Injury by Preserving Vascular Integrity and Decreasing Oxidative Stress</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-11-10</date><risdate>2015</risdate><volume>10</volume><issue>11</issue><spage>e0142571</spage><epage>e0142571</epage><pages>e0142571-e0142571</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Neuropilin-1 (NRP-1) is a transmembrane glycoprotein. As a VEGF co-receptor, NRP1 significantly enhances VEGFR2 signaling and promotes vascular permeability and migration. The purpose of this study was to evaluate the effects of an NRP-1 inhibitor, ATWLPPR peptide, on the early stages of diabetic retinopathy. Eight-week-old male C57BL/6 mice were divided into three groups: a Normal group, a Diabetes (DB) ATWLPPR treatment group and a DB saline group. Electroretinography (ERG), fundus fluorescence angiography (FFA) and leukostasis were examined to evaluate the retinal injury induced by diabetes at the end of the fifth week after STZ injection. Occludin expression and extravasation of albumin were measured to determine the extent of vascular injury. The oxidative stress level and the levels of inflammation-associated proteins were also assayed. The results indicated that treatment with ATWLPPR prevents the abnormal condition of ERG (amplitudes of b-wave decreased and implicit time increased) and vascular injury (occludin degradation and increase in extravasated albumin). These effects were associated with a reduction in the oxidase stress level and the expression of VEGF, GFAP, and ICAM-1. We conclude that ATWLPPR, an NRP-1 inhibitor, may reduce the early retinal damage induced by diabetes by preserving vascular integrity and decreasing the oxidative stress level. Blockade of NRP-1 may be a new therapeutic strategy for the early stages of DR.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26554379</pmid><doi>10.1371/journal.pone.0142571</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1732311539 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Albumin Angiogenesis Angiography Animals Blood-brain barrier Brain research Cell adhesion & migration Development and progression Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Diabetic retinopathy Diabetic Retinopathy - metabolism Diabetic Retinopathy - prevention & control Electroretinograms Electroretinography Extravasation Fluorescence Genetic aspects Glial fibrillary acidic protein Glycoproteins Health aspects Inflammation Inhibitors Injury prevention Integrity Intercellular adhesion molecule 1 Male Membrane proteins Mice Mice, Inbred C57BL Neuropilin Neuropilin-1 - antagonists & inhibitors Neuropilin-1 - metabolism Oligopeptides - pharmacology Oligopeptides - therapeutic use Oxidative stress Oxidative Stress - drug effects Pathogenesis Peptides Permeability Properties Proteins Receptors, Vascular Endothelial Growth Factor - metabolism Retina Retinal Vessels - drug effects Retinal Vessels - metabolism Retinopathy Signal transduction Signaling Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism |
| title | The Neuropilin-1 Inhibitor, ATWLPPR Peptide, Prevents Experimental Diabetes-Induced Retinal Injury by Preserving Vascular Integrity and Decreasing Oxidative Stress |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-25T13%3A42%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20Neuropilin-1%20Inhibitor,%20ATWLPPR%20Peptide,%20Prevents%20Experimental%20Diabetes-Induced%20Retinal%20Injury%20by%20Preserving%20Vascular%20Integrity%20and%20Decreasing%20Oxidative%20Stress&rft.jtitle=PloS%20one&rft.au=Wang,%20Jun&rft.date=2015-11-10&rft.volume=10&rft.issue=11&rft.spage=e0142571&rft.epage=e0142571&rft.pages=e0142571-e0142571&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0142571&rft_dat=%3Cgale_plos_%3EA434196731%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1732311539&rft_id=info:pmid/26554379&rft_galeid=A434196731&rft_doaj_id=oai_doaj_org_article_f63dfc4c39d245359cdee30d01fbde14&rfr_iscdi=true |