Lisofylline, a Novel Antiinflammatory Compound, Protects Mesangial Cells from Hyperglycemia- and Angiotensin II-Mediated Extracellular Matrix Deposition
Chronic elevated glucose levels and activation of the renal renin-angiotensin system have been implicated in the pathogenesis of diabetic nephropathy. We tested the ability of lisofylline (LSF), a novel antiinflammatory compound, to prevent extracellular matrix (ECM) accumulation and growth factor p...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2003-12, Vol.144 (12), p.5227-5231 |
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| creator | Bolick, David T Hatley, Melissa E Srinivasan, Suseela Hedrick, Catherine C Nadler, Jerry L |
| description | Chronic elevated glucose levels and activation of the renal renin-angiotensin system have been implicated in the pathogenesis of diabetic nephropathy. We tested the ability of lisofylline (LSF), a novel antiinflammatory compound, to prevent extracellular matrix (ECM) accumulation and growth factor production by human mesangial cells (HMCs) cultured in chronic elevated glucose (HG) or angiotensin II (AngII). HMCs were cultured in normal glucose (NG) (5.5 mm) and in HG (25 mm) for 7 d or with 10–7 m AngII for 4 h with or without LSF. Levels of the ECM protein fibronectin and TGF-β in media were shown to increase in HG compared with NG. LSF decreased HG-induced fibronectin and TGF-β production to control levels. Increased expression of collagen type IV and laminin was observed in AngII-cultured HMCs. LSF protected HMCs from the AngII induction of these key matrix proteins. cAMP-responsive binding element phosphorylation was significantly higher in both HG and AngII-cultured HMCs. LSF reduced phosphorylation of both cAMP-responsive binding element and p38 MAPK compared with control. These data demonstrate that LSF protects HMCs from HG- and AngII-mediated ECM deposition by the reduction of matrix protein secretion possibly through regulation of TGF-β production and modulation of the p38 MAPK pathway. These results suggest that LSF may provide therapeutic benefit for prevention or treatment of diabetic nephropathy. |
| doi_str_mv | 10.1210/en.2003-0739 |
| format | Article |
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We tested the ability of lisofylline (LSF), a novel antiinflammatory compound, to prevent extracellular matrix (ECM) accumulation and growth factor production by human mesangial cells (HMCs) cultured in chronic elevated glucose (HG) or angiotensin II (AngII). HMCs were cultured in normal glucose (NG) (5.5 mm) and in HG (25 mm) for 7 d or with 10–7 m AngII for 4 h with or without LSF. Levels of the ECM protein fibronectin and TGF-β in media were shown to increase in HG compared with NG. LSF decreased HG-induced fibronectin and TGF-β production to control levels. Increased expression of collagen type IV and laminin was observed in AngII-cultured HMCs. LSF protected HMCs from the AngII induction of these key matrix proteins. cAMP-responsive binding element phosphorylation was significantly higher in both HG and AngII-cultured HMCs. LSF reduced phosphorylation of both cAMP-responsive binding element and p38 MAPK compared with control. These data demonstrate that LSF protects HMCs from HG- and AngII-mediated ECM deposition by the reduction of matrix protein secretion possibly through regulation of TGF-β production and modulation of the p38 MAPK pathway. These results suggest that LSF may provide therapeutic benefit for prevention or treatment of diabetic nephropathy.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2003-0739</identifier><identifier>PMID: 12960000</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Angiotensin ; Angiotensin II ; Angiotensin II - pharmacology ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; Binding ; Bioaccumulation ; Biological and medical sciences ; Cell activation ; Cells, Cultured ; Collagen (type IV) ; Connective Tissue Growth Factor ; Cyclic AMP ; Cyclic AMP Response Element-Binding Protein - metabolism ; Deposition ; Diabetes ; Diabetes mellitus ; Diabetic nephropathy ; Extracellular matrix ; Extracellular Matrix - drug effects ; Extracellular Matrix - metabolism ; Extracellular Matrix Proteins - genetics ; Fibronectin ; Fibronectins - secretion ; Fundamental and applied biological sciences. Psychology ; Gene Expression - drug effects ; Glomerular Mesangium - cytology ; Glomerular Mesangium - drug effects ; Glomerular Mesangium - metabolism ; Glucose ; Glucose - pharmacology ; Growth factors ; Humans ; Hyperglycemia ; Hyperglycemia - drug therapy ; Immediate-Early Proteins - genetics ; Intercellular Signaling Peptides and Proteins - genetics ; Laminin ; MAP kinase ; MAP Kinase Signaling System - drug effects ; Matrix protein ; Mesangial cells ; Mitogen-Activated Protein Kinases - metabolism ; Nephropathy ; p38 Mitogen-Activated Protein Kinases ; Pathogenesis ; Pentoxifylline - analogs & derivatives ; Pentoxifylline - pharmacology ; Phosphorylation ; Phosphorylation - drug effects ; Proteins ; Regulatory sequences ; Renin ; Transforming Growth Factor beta - metabolism ; Transforming Growth Factor beta - secretion ; Transforming growth factor-b ; Vasoconstrictor Agents - pharmacology ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2003-12, Vol.144 (12), p.5227-5231</ispartof><rights>Copyright © 2003 by The Endocrine Society 2003</rights><rights>2004 INIST-CNRS</rights><rights>Copyright © 2003 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-70a5acb577917b62791f4f98521af00c7a5130d1c588064e6f85f59197fa955b3</citedby><cites>FETCH-LOGICAL-c459t-70a5acb577917b62791f4f98521af00c7a5130d1c588064e6f85f59197fa955b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15311654$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12960000$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bolick, David T</creatorcontrib><creatorcontrib>Hatley, Melissa E</creatorcontrib><creatorcontrib>Srinivasan, Suseela</creatorcontrib><creatorcontrib>Hedrick, Catherine C</creatorcontrib><creatorcontrib>Nadler, Jerry L</creatorcontrib><title>Lisofylline, a Novel Antiinflammatory Compound, Protects Mesangial Cells from Hyperglycemia- and Angiotensin II-Mediated Extracellular Matrix Deposition</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Chronic elevated glucose levels and activation of the renal renin-angiotensin system have been implicated in the pathogenesis of diabetic nephropathy. We tested the ability of lisofylline (LSF), a novel antiinflammatory compound, to prevent extracellular matrix (ECM) accumulation and growth factor production by human mesangial cells (HMCs) cultured in chronic elevated glucose (HG) or angiotensin II (AngII). HMCs were cultured in normal glucose (NG) (5.5 mm) and in HG (25 mm) for 7 d or with 10–7 m AngII for 4 h with or without LSF. Levels of the ECM protein fibronectin and TGF-β in media were shown to increase in HG compared with NG. LSF decreased HG-induced fibronectin and TGF-β production to control levels. Increased expression of collagen type IV and laminin was observed in AngII-cultured HMCs. LSF protected HMCs from the AngII induction of these key matrix proteins. cAMP-responsive binding element phosphorylation was significantly higher in both HG and AngII-cultured HMCs. LSF reduced phosphorylation of both cAMP-responsive binding element and p38 MAPK compared with control. These data demonstrate that LSF protects HMCs from HG- and AngII-mediated ECM deposition by the reduction of matrix protein secretion possibly through regulation of TGF-β production and modulation of the p38 MAPK pathway. These results suggest that LSF may provide therapeutic benefit for prevention or treatment of diabetic nephropathy.</description><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>Binding</subject><subject>Bioaccumulation</subject><subject>Biological and medical sciences</subject><subject>Cell activation</subject><subject>Cells, Cultured</subject><subject>Collagen (type IV)</subject><subject>Connective Tissue Growth Factor</subject><subject>Cyclic AMP</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>Deposition</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic nephropathy</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix - drug effects</subject><subject>Extracellular Matrix - metabolism</subject><subject>Extracellular Matrix Proteins - genetics</subject><subject>Fibronectin</subject><subject>Fibronectins - secretion</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression - drug effects</subject><subject>Glomerular Mesangium - cytology</subject><subject>Glomerular Mesangium - drug effects</subject><subject>Glomerular Mesangium - metabolism</subject><subject>Glucose</subject><subject>Glucose - pharmacology</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - drug therapy</subject><subject>Immediate-Early Proteins - genetics</subject><subject>Intercellular Signaling Peptides and Proteins - genetics</subject><subject>Laminin</subject><subject>MAP kinase</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Matrix protein</subject><subject>Mesangial cells</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Nephropathy</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Pathogenesis</subject><subject>Pentoxifylline - analogs & derivatives</subject><subject>Pentoxifylline - pharmacology</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Proteins</subject><subject>Regulatory sequences</subject><subject>Renin</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming Growth Factor beta - secretion</subject><subject>Transforming growth factor-b</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kVGL1DAUhYMo7rj65rMEZPVluiZt0zSPy7jrDsyoD_pc7qTJkCVNatLK9p_4czdlCgOiIXAJfPecEw5Cbym5pjkln5S7zgkpMsIL8QytqChZxiknz9GKEFpkPM_5BXoV40N6lmVZvEQXNBcVSWeF_uxM9Hqy1ji1xoC_-t_K4hs3GOO0ha6DwYcJb3zX-9G1a_w9-EHJIeK9iuCOBizeKGsj1sF3-H7qVTjaSarOQIbBtUnraNKKi8bh7Tbbq9bAoFp8-zgEkGl1tBDwHoZgHvFn1ftoBuPda_RCg43qzTIv0c-72x-b-2z37ct2c7PLZMnEkHECDOSBcS4oP1R5GrrUomY5BU2I5MBoQVoqWV2TqlSVrplmggquQTB2KC7Rh5NuH_yvUcWh6UycY4FTfowNpyVlQpQJfP8X-ODH4FK2pkgWLN28TtT6RMngYwxKN30wHYSpoaSZ-2qUa-a-mrmvhL9bRMdDp9ozvBSUgKsFgCjB6gBOmnjmWEFpxeZ0H0-cH_v_WWaLZXEilWu9DKn3PqgYz7_5Z9AnQD27Lw</recordid><startdate>20031201</startdate><enddate>20031201</enddate><creator>Bolick, David T</creator><creator>Hatley, Melissa E</creator><creator>Srinivasan, Suseela</creator><creator>Hedrick, Catherine C</creator><creator>Nadler, Jerry L</creator><general>Endocrine Society</general><general>Oxford University Press</general><scope>IQODW</scope><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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20031201</creationdate><title>Lisofylline, a Novel Antiinflammatory Compound, Protects Mesangial Cells from Hyperglycemia- and Angiotensin II-Mediated Extracellular Matrix Deposition</title><author>Bolick, David T ; Hatley, Melissa E ; Srinivasan, Suseela ; Hedrick, Catherine C ; Nadler, Jerry L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-70a5acb577917b62791f4f98521af00c7a5130d1c588064e6f85f59197fa955b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>Binding</topic><topic>Bioaccumulation</topic><topic>Biological and medical sciences</topic><topic>Cell activation</topic><topic>Cells, Cultured</topic><topic>Collagen (type IV)</topic><topic>Connective Tissue Growth Factor</topic><topic>Cyclic AMP</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>Deposition</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic nephropathy</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix - drug effects</topic><topic>Extracellular Matrix - metabolism</topic><topic>Extracellular Matrix Proteins - genetics</topic><topic>Fibronectin</topic><topic>Fibronectins - secretion</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression - drug effects</topic><topic>Glomerular Mesangium - cytology</topic><topic>Glomerular Mesangium - drug effects</topic><topic>Glomerular Mesangium - metabolism</topic><topic>Glucose</topic><topic>Glucose - pharmacology</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - drug therapy</topic><topic>Immediate-Early Proteins - genetics</topic><topic>Intercellular Signaling Peptides and Proteins - genetics</topic><topic>Laminin</topic><topic>MAP kinase</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Matrix protein</topic><topic>Mesangial cells</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Nephropathy</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Pathogenesis</topic><topic>Pentoxifylline - analogs & derivatives</topic><topic>Pentoxifylline - pharmacology</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Proteins</topic><topic>Regulatory sequences</topic><topic>Renin</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming Growth Factor beta - secretion</topic><topic>Transforming growth factor-b</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bolick, David T</creatorcontrib><creatorcontrib>Hatley, Melissa E</creatorcontrib><creatorcontrib>Srinivasan, Suseela</creatorcontrib><creatorcontrib>Hedrick, Catherine C</creatorcontrib><creatorcontrib>Nadler, Jerry L</creatorcontrib><collection>Pascal-Francis</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bolick, David T</au><au>Hatley, Melissa E</au><au>Srinivasan, Suseela</au><au>Hedrick, Catherine C</au><au>Nadler, Jerry L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lisofylline, a Novel Antiinflammatory Compound, Protects Mesangial Cells from Hyperglycemia- and Angiotensin II-Mediated Extracellular Matrix Deposition</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2003-12-01</date><risdate>2003</risdate><volume>144</volume><issue>12</issue><spage>5227</spage><epage>5231</epage><pages>5227-5231</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Chronic elevated glucose levels and activation of the renal renin-angiotensin system have been implicated in the pathogenesis of diabetic nephropathy. We tested the ability of lisofylline (LSF), a novel antiinflammatory compound, to prevent extracellular matrix (ECM) accumulation and growth factor production by human mesangial cells (HMCs) cultured in chronic elevated glucose (HG) or angiotensin II (AngII). HMCs were cultured in normal glucose (NG) (5.5 mm) and in HG (25 mm) for 7 d or with 10–7 m AngII for 4 h with or without LSF. Levels of the ECM protein fibronectin and TGF-β in media were shown to increase in HG compared with NG. LSF decreased HG-induced fibronectin and TGF-β production to control levels. Increased expression of collagen type IV and laminin was observed in AngII-cultured HMCs. LSF protected HMCs from the AngII induction of these key matrix proteins. cAMP-responsive binding element phosphorylation was significantly higher in both HG and AngII-cultured HMCs. LSF reduced phosphorylation of both cAMP-responsive binding element and p38 MAPK compared with control. These data demonstrate that LSF protects HMCs from HG- and AngII-mediated ECM deposition by the reduction of matrix protein secretion possibly through regulation of TGF-β production and modulation of the p38 MAPK pathway. These results suggest that LSF may provide therapeutic benefit for prevention or treatment of diabetic nephropathy.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>12960000</pmid><doi>10.1210/en.2003-0739</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Angiotensin Angiotensin II Angiotensin II - pharmacology Anti-Inflammatory Agents, Non-Steroidal - pharmacology Binding Bioaccumulation Biological and medical sciences Cell activation Cells, Cultured Collagen (type IV) Connective Tissue Growth Factor Cyclic AMP Cyclic AMP Response Element-Binding Protein - metabolism Deposition Diabetes Diabetes mellitus Diabetic nephropathy Extracellular matrix Extracellular Matrix - drug effects Extracellular Matrix - metabolism Extracellular Matrix Proteins - genetics Fibronectin Fibronectins - secretion Fundamental and applied biological sciences. Psychology Gene Expression - drug effects Glomerular Mesangium - cytology Glomerular Mesangium - drug effects Glomerular Mesangium - metabolism Glucose Glucose - pharmacology Growth factors Humans Hyperglycemia Hyperglycemia - drug therapy Immediate-Early Proteins - genetics Intercellular Signaling Peptides and Proteins - genetics Laminin MAP kinase MAP Kinase Signaling System - drug effects Matrix protein Mesangial cells Mitogen-Activated Protein Kinases - metabolism Nephropathy p38 Mitogen-Activated Protein Kinases Pathogenesis Pentoxifylline - analogs & derivatives Pentoxifylline - pharmacology Phosphorylation Phosphorylation - drug effects Proteins Regulatory sequences Renin Transforming Growth Factor beta - metabolism Transforming Growth Factor beta - secretion Transforming growth factor-b Vasoconstrictor Agents - pharmacology Vertebrates: endocrinology |
| title | Lisofylline, a Novel Antiinflammatory Compound, Protects Mesangial Cells from Hyperglycemia- and Angiotensin II-Mediated Extracellular Matrix Deposition |
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