Increased AGE-RAGE ratio in idiopathic pulmonary fibrosis
The abnormal epithelial-mesenchymal restorative capacity in idiopathic pulmonary fibrosis (IPF) has been recently associated with an accelerated aging process as a key point for the altered wound healing. The advanced glycation end-products (AGEs) are the consequence of non-enzymatic reactions betwe...
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| Veröffentlicht in: | Respiratory research 2016-11, Vol.17 (1), p.144-144, Article 144 |
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| creator | Machahua, Carlos Montes-Worboys, Ana Llatjos, Roger Escobar, Ignacio Dorca, Jordi Molina-Molina, Maria Vicens-Zygmunt, Vanesa |
| description | The abnormal epithelial-mesenchymal restorative capacity in idiopathic pulmonary fibrosis (IPF) has been recently associated with an accelerated aging process as a key point for the altered wound healing. The advanced glycation end-products (AGEs) are the consequence of non-enzymatic reactions between lipid and protein with several oxidants in the aging process. The receptor for AGEs (RAGEs) has been implicated in the lung fibrotic process and the alveolar homeostasis. However, this AGE-RAGE aging pathway has been under-explored in IPF.
Lung samples from 16 IPF and 9 control patients were obtained through surgical lung biopsy. Differences in AGEs and RAGE expression between both groups were evaluated by RT-PCR, Western blot and immunohistochemistry. The effect of AGEs on cell viability of primary lung fibrotic fibroblasts and alveolar epithelial cells was assessed. Cell transformation of fibrotic fibroblasts cultured into glycated matrices was evaluated in different experimental conditions.
Our study demonstrates an increase of AGEs together with a decrease of RAGEs in IPF lungs, compared with control samples. Two specific AGEs involved in aging, pentosidine and Nε-Carboxymethyl lysine, were significantly increased in IPF samples. The immunohistochemistry identified higher staining of AGEs related to extracellular matrix (ECM) proteins and the apical surface of the alveolar epithelial cells (AECs) surrounding fibroblast foci in fibrotic lungs. On the other hand, RAGE location was present at the cell membrane of AECs in control lungs, while it was almost missing in pulmonary fibrotic tissue. In addition, in vitro cultures showed that the effect of AGEs on cell viability was different for AECs and fibrotic fibroblasts. AGEs decreased cell viability in AECs, even at low concentration, while fibroblast viability was less affected. Furthermore, fibroblast to myofibroblast transformation could be enhanced by ECM glycation.
All of these findings suggest a possible role of the increased ratio AGEs-RAGEs in IPF, which could be a relevant accelerating aging tissue reaction in the abnormal wound healing of the lung fibrotic process. |
| doi_str_mv | 10.1186/s12931-016-0460-2 |
| format | Article |
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Lung samples from 16 IPF and 9 control patients were obtained through surgical lung biopsy. Differences in AGEs and RAGE expression between both groups were evaluated by RT-PCR, Western blot and immunohistochemistry. The effect of AGEs on cell viability of primary lung fibrotic fibroblasts and alveolar epithelial cells was assessed. Cell transformation of fibrotic fibroblasts cultured into glycated matrices was evaluated in different experimental conditions.
Our study demonstrates an increase of AGEs together with a decrease of RAGEs in IPF lungs, compared with control samples. Two specific AGEs involved in aging, pentosidine and Nε-Carboxymethyl lysine, were significantly increased in IPF samples. The immunohistochemistry identified higher staining of AGEs related to extracellular matrix (ECM) proteins and the apical surface of the alveolar epithelial cells (AECs) surrounding fibroblast foci in fibrotic lungs. On the other hand, RAGE location was present at the cell membrane of AECs in control lungs, while it was almost missing in pulmonary fibrotic tissue. In addition, in vitro cultures showed that the effect of AGEs on cell viability was different for AECs and fibrotic fibroblasts. AGEs decreased cell viability in AECs, even at low concentration, while fibroblast viability was less affected. Furthermore, fibroblast to myofibroblast transformation could be enhanced by ECM glycation.
All of these findings suggest a possible role of the increased ratio AGEs-RAGEs in IPF, which could be a relevant accelerating aging tissue reaction in the abnormal wound healing of the lung fibrotic process.</description><identifier>ISSN: 1465-993X</identifier><identifier>ISSN: 1465-9921</identifier><identifier>EISSN: 1465-993X</identifier><identifier>EISSN: 1465-9921</identifier><identifier>DOI: 10.1186/s12931-016-0460-2</identifier><identifier>PMID: 27816054</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Aged ; Aging ; Alveolar Epithelial Cells - metabolism ; Antigens, Neoplasm - metabolism ; Arginine - analogs & derivatives ; Arginine - metabolism ; Envelliment ; Epithelial Cells ; Extracellular matrix ; Extracellular Matrix Proteins - metabolism ; Female ; Fibroblasts - metabolism ; Fibrosi pulmonar ; Glycation End Products, Advanced - metabolism ; Humans ; Idiopathic Pulmonary Fibrosis - metabolism ; Immunohistochemistry ; Immunohistoquímica ; Lung - metabolism ; Lysine - analogs & derivatives ; Lysine - metabolism ; Male ; Matriu extracel·lular ; Middle Aged ; Mitogen-Activated Protein Kinases - metabolism ; Oxidizing agents ; Pulmonary fibrosis ; Signal Transduction</subject><ispartof>Respiratory research, 2016-11, Vol.17 (1), p.144-144, Article 144</ispartof><rights>Copyright BioMed Central 2016</rights><rights>cc-by (c) Machahua-Huamani, Carlos et al., 2016 info:eu-repo/semantics/openAccess <a href="http://creativecommons.org/licenses/by/3.0/es">http://creativecommons.org/licenses/by/3.0/es</a></rights><rights>The Author(s). 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c535t-cd05fa0406b129366e3513c6d35c5cb976fed74dbdfa4c276b9f4415d47bbcec3</citedby><cites>FETCH-LOGICAL-c535t-cd05fa0406b129366e3513c6d35c5cb976fed74dbdfa4c276b9f4415d47bbcec3</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/PMC5097848/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5097848/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,26953,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27816054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Machahua, Carlos</creatorcontrib><creatorcontrib>Montes-Worboys, Ana</creatorcontrib><creatorcontrib>Llatjos, Roger</creatorcontrib><creatorcontrib>Escobar, Ignacio</creatorcontrib><creatorcontrib>Dorca, Jordi</creatorcontrib><creatorcontrib>Molina-Molina, Maria</creatorcontrib><creatorcontrib>Vicens-Zygmunt, Vanesa</creatorcontrib><title>Increased AGE-RAGE ratio in idiopathic pulmonary fibrosis</title><title>Respiratory research</title><addtitle>Respir Res</addtitle><description>The abnormal epithelial-mesenchymal restorative capacity in idiopathic pulmonary fibrosis (IPF) has been recently associated with an accelerated aging process as a key point for the altered wound healing. The advanced glycation end-products (AGEs) are the consequence of non-enzymatic reactions between lipid and protein with several oxidants in the aging process. The receptor for AGEs (RAGEs) has been implicated in the lung fibrotic process and the alveolar homeostasis. However, this AGE-RAGE aging pathway has been under-explored in IPF.
Lung samples from 16 IPF and 9 control patients were obtained through surgical lung biopsy. Differences in AGEs and RAGE expression between both groups were evaluated by RT-PCR, Western blot and immunohistochemistry. The effect of AGEs on cell viability of primary lung fibrotic fibroblasts and alveolar epithelial cells was assessed. Cell transformation of fibrotic fibroblasts cultured into glycated matrices was evaluated in different experimental conditions.
Our study demonstrates an increase of AGEs together with a decrease of RAGEs in IPF lungs, compared with control samples. Two specific AGEs involved in aging, pentosidine and Nε-Carboxymethyl lysine, were significantly increased in IPF samples. The immunohistochemistry identified higher staining of AGEs related to extracellular matrix (ECM) proteins and the apical surface of the alveolar epithelial cells (AECs) surrounding fibroblast foci in fibrotic lungs. On the other hand, RAGE location was present at the cell membrane of AECs in control lungs, while it was almost missing in pulmonary fibrotic tissue. In addition, in vitro cultures showed that the effect of AGEs on cell viability was different for AECs and fibrotic fibroblasts. AGEs decreased cell viability in AECs, even at low concentration, while fibroblast viability was less affected. Furthermore, fibroblast to myofibroblast transformation could be enhanced by ECM glycation.
All of these findings suggest a possible role of the increased ratio AGEs-RAGEs in IPF, which could be a relevant accelerating aging tissue reaction in the abnormal wound healing of the lung fibrotic process.</description><subject>Aged</subject><subject>Aging</subject><subject>Alveolar Epithelial Cells - metabolism</subject><subject>Antigens, Neoplasm - metabolism</subject><subject>Arginine - analogs & derivatives</subject><subject>Arginine - metabolism</subject><subject>Envelliment</subject><subject>Epithelial Cells</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix Proteins - metabolism</subject><subject>Female</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosi pulmonar</subject><subject>Glycation End Products, Advanced - metabolism</subject><subject>Humans</subject><subject>Idiopathic Pulmonary Fibrosis - metabolism</subject><subject>Immunohistochemistry</subject><subject>Immunohistoquímica</subject><subject>Lung - metabolism</subject><subject>Lysine - analogs & derivatives</subject><subject>Lysine - metabolism</subject><subject>Male</subject><subject>Matriu extracel·lular</subject><subject>Middle Aged</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Oxidizing agents</subject><subject>Pulmonary fibrosis</subject><subject>Signal Transduction</subject><issn>1465-993X</issn><issn>1465-9921</issn><issn>1465-993X</issn><issn>1465-9921</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>XX2</sourceid><recordid>eNpdUU1LAzEUDKL4Uf0BXmTBi5fVZPO1uQhFtBYKgih4C9kka1O2m5rsCv57s7aW6iHJC3kzmTcDwDmC1wiV7CaiQmCUQ8RySBjMiz1wjAijuRD4bX-nPgInMS4gRLzk9BAcFbxEDFJyDMS01cGqaE02ntznz2nLguqcz1ybOeP8SnVzp7NV3yx9q8JXVrsq-OjiKTioVRPt2eYcgdeH-5e7x3z2NJnejWe5pph2uTaQ1goSyKpBLWMWU4Q1M5hqqivBWW0NJ6YytSK64KwSNSGIGsKrSluNR-B2zbvqq6U12rZdUI1cBbdMcqRXTv59ad1cvvtPSaHgJSkTAVoT6NhrGay2QavuB7i9DKuAvJCYUkxEwlxtPg3-o7exk0sXtW0a1VrfR4lKzCGGnJDUevmvdeH70CZLhi5Gk8-F2BGRzIvB1tsBEJRDmHIdpkxhyiFMWSTMxe7kW8RvevgbpN-aAw</recordid><startdate>20161105</startdate><enddate>20161105</enddate><creator>Machahua, Carlos</creator><creator>Montes-Worboys, Ana</creator><creator>Llatjos, Roger</creator><creator>Escobar, Ignacio</creator><creator>Dorca, Jordi</creator><creator>Molina-Molina, Maria</creator><creator>Vicens-Zygmunt, Vanesa</creator><general>BioMed Central</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>7QL</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>XX2</scope><scope>5PM</scope></search><sort><creationdate>20161105</creationdate><title>Increased AGE-RAGE ratio in idiopathic pulmonary fibrosis</title><author>Machahua, Carlos ; Montes-Worboys, Ana ; Llatjos, Roger ; Escobar, Ignacio ; Dorca, Jordi ; Molina-Molina, Maria ; Vicens-Zygmunt, Vanesa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c535t-cd05fa0406b129366e3513c6d35c5cb976fed74dbdfa4c276b9f4415d47bbcec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aged</topic><topic>Aging</topic><topic>Alveolar Epithelial Cells - metabolism</topic><topic>Antigens, Neoplasm - metabolism</topic><topic>Arginine - analogs & derivatives</topic><topic>Arginine - metabolism</topic><topic>Envelliment</topic><topic>Epithelial Cells</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix Proteins - metabolism</topic><topic>Female</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrosi pulmonar</topic><topic>Glycation End Products, Advanced - metabolism</topic><topic>Humans</topic><topic>Idiopathic Pulmonary Fibrosis - metabolism</topic><topic>Immunohistochemistry</topic><topic>Immunohistoquímica</topic><topic>Lung - metabolism</topic><topic>Lysine - analogs & derivatives</topic><topic>Lysine - metabolism</topic><topic>Male</topic><topic>Matriu extracel·lular</topic><topic>Middle Aged</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Oxidizing agents</topic><topic>Pulmonary fibrosis</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Machahua, Carlos</creatorcontrib><creatorcontrib>Montes-Worboys, Ana</creatorcontrib><creatorcontrib>Llatjos, Roger</creatorcontrib><creatorcontrib>Escobar, Ignacio</creatorcontrib><creatorcontrib>Dorca, Jordi</creatorcontrib><creatorcontrib>Molina-Molina, Maria</creatorcontrib><creatorcontrib>Vicens-Zygmunt, Vanesa</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS 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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</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>MEDLINE - Academic</collection><collection>Recercat</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Respiratory research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Machahua, Carlos</au><au>Montes-Worboys, Ana</au><au>Llatjos, Roger</au><au>Escobar, Ignacio</au><au>Dorca, Jordi</au><au>Molina-Molina, Maria</au><au>Vicens-Zygmunt, Vanesa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased AGE-RAGE ratio in idiopathic pulmonary fibrosis</atitle><jtitle>Respiratory research</jtitle><addtitle>Respir Res</addtitle><date>2016-11-05</date><risdate>2016</risdate><volume>17</volume><issue>1</issue><spage>144</spage><epage>144</epage><pages>144-144</pages><artnum>144</artnum><issn>1465-993X</issn><issn>1465-9921</issn><eissn>1465-993X</eissn><eissn>1465-9921</eissn><abstract>The abnormal epithelial-mesenchymal restorative capacity in idiopathic pulmonary fibrosis (IPF) has been recently associated with an accelerated aging process as a key point for the altered wound healing. The advanced glycation end-products (AGEs) are the consequence of non-enzymatic reactions between lipid and protein with several oxidants in the aging process. The receptor for AGEs (RAGEs) has been implicated in the lung fibrotic process and the alveolar homeostasis. However, this AGE-RAGE aging pathway has been under-explored in IPF.
Lung samples from 16 IPF and 9 control patients were obtained through surgical lung biopsy. Differences in AGEs and RAGE expression between both groups were evaluated by RT-PCR, Western blot and immunohistochemistry. The effect of AGEs on cell viability of primary lung fibrotic fibroblasts and alveolar epithelial cells was assessed. Cell transformation of fibrotic fibroblasts cultured into glycated matrices was evaluated in different experimental conditions.
Our study demonstrates an increase of AGEs together with a decrease of RAGEs in IPF lungs, compared with control samples. Two specific AGEs involved in aging, pentosidine and Nε-Carboxymethyl lysine, were significantly increased in IPF samples. The immunohistochemistry identified higher staining of AGEs related to extracellular matrix (ECM) proteins and the apical surface of the alveolar epithelial cells (AECs) surrounding fibroblast foci in fibrotic lungs. On the other hand, RAGE location was present at the cell membrane of AECs in control lungs, while it was almost missing in pulmonary fibrotic tissue. In addition, in vitro cultures showed that the effect of AGEs on cell viability was different for AECs and fibrotic fibroblasts. AGEs decreased cell viability in AECs, even at low concentration, while fibroblast viability was less affected. Furthermore, fibroblast to myofibroblast transformation could be enhanced by ECM glycation.
All of these findings suggest a possible role of the increased ratio AGEs-RAGEs in IPF, which could be a relevant accelerating aging tissue reaction in the abnormal wound healing of the lung fibrotic process.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>27816054</pmid><doi>10.1186/s12931-016-0460-2</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aging Alveolar Epithelial Cells - metabolism Antigens, Neoplasm - metabolism Arginine - analogs & derivatives Arginine - metabolism Envelliment Epithelial Cells Extracellular matrix Extracellular Matrix Proteins - metabolism Female Fibroblasts - metabolism Fibrosi pulmonar Glycation End Products, Advanced - metabolism Humans Idiopathic Pulmonary Fibrosis - metabolism Immunohistochemistry Immunohistoquímica Lung - metabolism Lysine - analogs & derivatives Lysine - metabolism Male Matriu extracel·lular Middle Aged Mitogen-Activated Protein Kinases - metabolism Oxidizing agents Pulmonary fibrosis Signal Transduction |
| title | Increased AGE-RAGE ratio in idiopathic pulmonary fibrosis |
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