Reversibility of established diabetic glomerulopathy by anti-TGF-β antibodies in db/db mice
Treatment with a neutralizing anti-transforming growth factor-β (TGF-β) antibody can prevent the development of diabetic nephropathy in the db/db mouse, a model of type 2 diabetes. However, it is unknown whether anti-TGF-β therapy can reverse the histological lesions of diabetic glomerulopathy once...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2003, Vol.300 (1), p.16-22 |
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| creator | Chen, Sheldon Carmen Iglesias-de la Cruz, M Jim, Belinda Hong, Soon Won Isono, Motohide Ziyadeh, Fuad N |
| description | Treatment with a neutralizing anti-transforming growth factor-β (TGF-β) antibody can prevent the development of diabetic nephropathy in the
db/db mouse, a model of type 2 diabetes. However, it is unknown whether anti-TGF-β therapy can reverse the histological lesions of diabetic glomerulopathy once they are established. Diabetic
db/db mice and their non-diabetic
db/m littermates were allowed to grow until 16 weeks of age, by which time the
db/db mice had developed glomerular basement membrane (GBM) thickening and mesangial matrix expansion. The mice were then treated with an irrelevant control IgG or a panselective, neutralizing anti-TGF-β antibody for eight more weeks. Compared with control
db/m mice, the
db/db mice treated with IgG had developed increased GBM width (16.64±0.80
nm vs. 21.55±0.78 nm,
P |
| doi_str_mv | 10.1016/S0006-291X(02)02708-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72891010</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006291X02027080</els_id><sourcerecordid>72891010</sourcerecordid><originalsourceid>FETCH-LOGICAL-c328t-12b4ffae397def13d94c9125ff807f9b5a07ffde214f97e57edc42a0362792113</originalsourceid><addsrcrecordid>eNqFkMtKJEEQRRNx0PbxCUquRBc1RmRVdVWuRBpfIAzMKLgQknxEakpVV5tZLfRvzYf4TVY_mFm6iliciMs9jB0h_ETA8fkfABhnQuLTKYgzEBXUGWyxEYKETCAU22z0D9lleym9ASAWY7nDdlEUNZRYjNjzb_qgmIIJTegXvPOcUq9NE9IrOe6CNtQHy1-arqU4b7qZ7l8X3Cy4nvYhe7i5zj7_rnbTuUCJhyl35twZ3gZLB-yH102iw83cZ4_XVw-T2-z-183d5PI-s7mo-wyFKbzXlMvKkcfcycJKFKX3NVRemlIPwzsSWHhZUVmRs4XQkI9FJQVivs9O1n9nsXufDwVUG5KlptFT6uZJVaKWgzQYwHIN2tilFMmrWQytjguFoJZa1UqrWjpTINRKq1reHW8C5qYl9_9q43EALtYADTU_AkWVbKCpJRci2V65LnwT8QUqMIiw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>72891010</pqid></control><display><type>article</type><title>Reversibility of established diabetic glomerulopathy by anti-TGF-β antibodies in db/db mice</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Chen, Sheldon ; Carmen Iglesias-de la Cruz, M ; Jim, Belinda ; Hong, Soon Won ; Isono, Motohide ; Ziyadeh, Fuad N</creator><creatorcontrib>Chen, Sheldon ; Carmen Iglesias-de la Cruz, M ; Jim, Belinda ; Hong, Soon Won ; Isono, Motohide ; Ziyadeh, Fuad N</creatorcontrib><description>Treatment with a neutralizing anti-transforming growth factor-β (TGF-β) antibody can prevent the development of diabetic nephropathy in the
db/db mouse, a model of type 2 diabetes. However, it is unknown whether anti-TGF-β therapy can reverse the histological lesions of diabetic glomerulopathy once they are established. Diabetic
db/db mice and their non-diabetic
db/m littermates were allowed to grow until 16 weeks of age, by which time the
db/db mice had developed glomerular basement membrane (GBM) thickening and mesangial matrix expansion. The mice were then treated with an irrelevant control IgG or a panselective, neutralizing anti-TGF-β antibody for eight more weeks. Compared with control
db/m mice, the
db/db mice treated with IgG had developed increased GBM width (16.64±0.80
nm vs. 21.55±0.78 nm,
P<0.05) and increased mesangial matrix fraction (4.01±0.81% of total glomerular area vs. 9.55±1.04%,
P<0.05). However, the
db/db mice treated with anti-TGF-β antibody showed amelioration of GBM thickening (18.40±0.72
nm,
P<0.05 vs.
db/db-IgG) and mesangial matrix accumulation (6.32±1.79%,
P<0.05 vs.
db/db-IgG). Our results demonstrate that inhibiting renal TGF-β activity can partially reverse the GBM thickening and mesangial matrix expansion in this mouse model of type 2 diabetes. Anti-TGF-β regimens would be useful in the treatment of diabetic nephropathy.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/S0006-291X(02)02708-0</identifier><identifier>PMID: 12480514</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Basement Membrane - pathology ; Blood Glucose - metabolism ; Diabetic Nephropathies - genetics ; Diabetic Nephropathies - pathology ; Diabetic Nephropathies - prevention & control ; Diabetic Nephropathies - therapy ; Female ; Glomerular basement membrane thickening ; Glomerular Mesangium - pathology ; Humans ; Immunoglobulin G - administration & dosage ; Mesangial matrix expansion ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Neutralization Tests ; Reversal ; Transforming Growth Factor beta - antagonists & inhibitors ; Transforming Growth Factor beta - physiology ; Type 2 diabetes</subject><ispartof>Biochemical and biophysical research communications, 2003, Vol.300 (1), p.16-22</ispartof><rights>2003 Elsevier Science (USA)</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c328t-12b4ffae397def13d94c9125ff807f9b5a07ffde214f97e57edc42a0362792113</citedby><cites>FETCH-LOGICAL-c328t-12b4ffae397def13d94c9125ff807f9b5a07ffde214f97e57edc42a0362792113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-291X(02)02708-0$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12480514$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Sheldon</creatorcontrib><creatorcontrib>Carmen Iglesias-de la Cruz, M</creatorcontrib><creatorcontrib>Jim, Belinda</creatorcontrib><creatorcontrib>Hong, Soon Won</creatorcontrib><creatorcontrib>Isono, Motohide</creatorcontrib><creatorcontrib>Ziyadeh, Fuad N</creatorcontrib><title>Reversibility of established diabetic glomerulopathy by anti-TGF-β antibodies in db/db mice</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Treatment with a neutralizing anti-transforming growth factor-β (TGF-β) antibody can prevent the development of diabetic nephropathy in the
db/db mouse, a model of type 2 diabetes. However, it is unknown whether anti-TGF-β therapy can reverse the histological lesions of diabetic glomerulopathy once they are established. Diabetic
db/db mice and their non-diabetic
db/m littermates were allowed to grow until 16 weeks of age, by which time the
db/db mice had developed glomerular basement membrane (GBM) thickening and mesangial matrix expansion. The mice were then treated with an irrelevant control IgG or a panselective, neutralizing anti-TGF-β antibody for eight more weeks. Compared with control
db/m mice, the
db/db mice treated with IgG had developed increased GBM width (16.64±0.80
nm vs. 21.55±0.78 nm,
P<0.05) and increased mesangial matrix fraction (4.01±0.81% of total glomerular area vs. 9.55±1.04%,
P<0.05). However, the
db/db mice treated with anti-TGF-β antibody showed amelioration of GBM thickening (18.40±0.72
nm,
P<0.05 vs.
db/db-IgG) and mesangial matrix accumulation (6.32±1.79%,
P<0.05 vs.
db/db-IgG). Our results demonstrate that inhibiting renal TGF-β activity can partially reverse the GBM thickening and mesangial matrix expansion in this mouse model of type 2 diabetes. Anti-TGF-β regimens would be useful in the treatment of diabetic nephropathy.</description><subject>Animals</subject><subject>Basement Membrane - pathology</subject><subject>Blood Glucose - metabolism</subject><subject>Diabetic Nephropathies - genetics</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic Nephropathies - prevention & control</subject><subject>Diabetic Nephropathies - therapy</subject><subject>Female</subject><subject>Glomerular basement membrane thickening</subject><subject>Glomerular Mesangium - pathology</subject><subject>Humans</subject><subject>Immunoglobulin G - administration & dosage</subject><subject>Mesangial matrix expansion</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Mutant Strains</subject><subject>Neutralization Tests</subject><subject>Reversal</subject><subject>Transforming Growth Factor beta - antagonists & inhibitors</subject><subject>Transforming Growth Factor beta - physiology</subject><subject>Type 2 diabetes</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtKJEEQRRNx0PbxCUquRBc1RmRVdVWuRBpfIAzMKLgQknxEakpVV5tZLfRvzYf4TVY_mFm6iliciMs9jB0h_ETA8fkfABhnQuLTKYgzEBXUGWyxEYKETCAU22z0D9lleym9ASAWY7nDdlEUNZRYjNjzb_qgmIIJTegXvPOcUq9NE9IrOe6CNtQHy1-arqU4b7qZ7l8X3Cy4nvYhe7i5zj7_rnbTuUCJhyl35twZ3gZLB-yH102iw83cZ4_XVw-T2-z-183d5PI-s7mo-wyFKbzXlMvKkcfcycJKFKX3NVRemlIPwzsSWHhZUVmRs4XQkI9FJQVivs9O1n9nsXufDwVUG5KlptFT6uZJVaKWgzQYwHIN2tilFMmrWQytjguFoJZa1UqrWjpTINRKq1reHW8C5qYl9_9q43EALtYADTU_AkWVbKCpJRci2V65LnwT8QUqMIiw</recordid><startdate>2003</startdate><enddate>2003</enddate><creator>Chen, Sheldon</creator><creator>Carmen Iglesias-de la Cruz, M</creator><creator>Jim, Belinda</creator><creator>Hong, Soon Won</creator><creator>Isono, Motohide</creator><creator>Ziyadeh, Fuad N</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>7X8</scope></search><sort><creationdate>2003</creationdate><title>Reversibility of established diabetic glomerulopathy by anti-TGF-β antibodies in db/db mice</title><author>Chen, Sheldon ; Carmen Iglesias-de la Cruz, M ; Jim, Belinda ; Hong, Soon Won ; Isono, Motohide ; Ziyadeh, Fuad N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c328t-12b4ffae397def13d94c9125ff807f9b5a07ffde214f97e57edc42a0362792113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Basement Membrane - pathology</topic><topic>Blood Glucose - metabolism</topic><topic>Diabetic Nephropathies - genetics</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Diabetic Nephropathies - prevention & control</topic><topic>Diabetic Nephropathies - therapy</topic><topic>Female</topic><topic>Glomerular basement membrane thickening</topic><topic>Glomerular Mesangium - pathology</topic><topic>Humans</topic><topic>Immunoglobulin G - administration & dosage</topic><topic>Mesangial matrix expansion</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Mutant Strains</topic><topic>Neutralization Tests</topic><topic>Reversal</topic><topic>Transforming Growth Factor beta - antagonists & inhibitors</topic><topic>Transforming Growth Factor beta - physiology</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Sheldon</creatorcontrib><creatorcontrib>Carmen Iglesias-de la Cruz, M</creatorcontrib><creatorcontrib>Jim, Belinda</creatorcontrib><creatorcontrib>Hong, Soon Won</creatorcontrib><creatorcontrib>Isono, Motohide</creatorcontrib><creatorcontrib>Ziyadeh, Fuad N</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Sheldon</au><au>Carmen Iglesias-de la Cruz, M</au><au>Jim, Belinda</au><au>Hong, Soon Won</au><au>Isono, Motohide</au><au>Ziyadeh, Fuad N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reversibility of established diabetic glomerulopathy by anti-TGF-β antibodies in db/db mice</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2003</date><risdate>2003</risdate><volume>300</volume><issue>1</issue><spage>16</spage><epage>22</epage><pages>16-22</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Treatment with a neutralizing anti-transforming growth factor-β (TGF-β) antibody can prevent the development of diabetic nephropathy in the
db/db mouse, a model of type 2 diabetes. However, it is unknown whether anti-TGF-β therapy can reverse the histological lesions of diabetic glomerulopathy once they are established. Diabetic
db/db mice and their non-diabetic
db/m littermates were allowed to grow until 16 weeks of age, by which time the
db/db mice had developed glomerular basement membrane (GBM) thickening and mesangial matrix expansion. The mice were then treated with an irrelevant control IgG or a panselective, neutralizing anti-TGF-β antibody for eight more weeks. Compared with control
db/m mice, the
db/db mice treated with IgG had developed increased GBM width (16.64±0.80
nm vs. 21.55±0.78 nm,
P<0.05) and increased mesangial matrix fraction (4.01±0.81% of total glomerular area vs. 9.55±1.04%,
P<0.05). However, the
db/db mice treated with anti-TGF-β antibody showed amelioration of GBM thickening (18.40±0.72
nm,
P<0.05 vs.
db/db-IgG) and mesangial matrix accumulation (6.32±1.79%,
P<0.05 vs.
db/db-IgG). Our results demonstrate that inhibiting renal TGF-β activity can partially reverse the GBM thickening and mesangial matrix expansion in this mouse model of type 2 diabetes. Anti-TGF-β regimens would be useful in the treatment of diabetic nephropathy.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12480514</pmid><doi>10.1016/S0006-291X(02)02708-0</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Basement Membrane - pathology Blood Glucose - metabolism Diabetic Nephropathies - genetics Diabetic Nephropathies - pathology Diabetic Nephropathies - prevention & control Diabetic Nephropathies - therapy Female Glomerular basement membrane thickening Glomerular Mesangium - pathology Humans Immunoglobulin G - administration & dosage Mesangial matrix expansion Mice Mice, Inbred C57BL Mice, Mutant Strains Neutralization Tests Reversal Transforming Growth Factor beta - antagonists & inhibitors Transforming Growth Factor beta - physiology Type 2 diabetes |
| title | Reversibility of established diabetic glomerulopathy by anti-TGF-β antibodies in db/db mice |
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