High glucose-induced TGF-beta 1 regulates mesangial production of heparan sulfate proteoglycan
V. Kolm, U. Sauer, B. Olgemooller and E. D. Schleicher Institute for Diabetes Research, Department of Biochemistry, Academic Hospital, University of Munich, Germany. Previous investigations have demonstrated that growing mesangial cells in high glucose concentration stimulates extracellular matrix s...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 1996-05, Vol.270 (5), p.812-F821 |
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| container_title | American journal of physiology. Renal physiology |
| container_volume | 270 |
| creator | Kolm, V Sauer, U Olgemooller, B Schleicher, E. D |
| description | V. Kolm, U. Sauer, B. Olgemooller and E. D. Schleicher
Institute for Diabetes Research, Department of Biochemistry, Academic Hospital, University of Munich, Germany.
Previous investigations have demonstrated that growing mesangial cells in
high glucose concentration stimulates extracellular matrix synthesis and
also increases the expression of transforming growth factor-beta
(TGF-beta). We examined the effects of hyperglycemia on mesangial
proliferation and heparan sulfate proteoglycan (HSPG) and fibronectin
production. Prolonged exposure of mesangial cells to increasing glucose
concentrations resulted in dose-dependent effects on growth inhibition and
stimulation of matrix production. Treatment of mesangial cells with high
glucose-conditioned medium or with TGF-beta 1 mimicked the effects of
high-glucose incubation. Furthermore, TGF-beta 1 caused a dose-dependent
increase in HSPG mRNA levels. The high-glucose effects on mesangial cells
were preceded by an increase in total TGF-beta 1 protein. The presence of
TGF-beta 1 antisense oligonucleotide attenuated the glucose-mediated
effects on mesangial proliferation and matrix production. The data show
that even moderately elevated glucose concentrations appear to affect the
mesangial cells. The results indicate that 1) TGF-beta 1 protein production
is necessary to obtain the high glucose-induced effects and 2) TGF-beta 1
stimulates mesangial HSPG expression and production. Because these effects
may be attenuated by oligonucleotides antisense to TGF-beta 1, the results
suggest a possible way for effective intervention in TGF-beta-mediated
glomerulosclerosis. |
| doi_str_mv | 10.1152/ajprenal.1996.270.5.F812 |
| format | Article |
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Institute for Diabetes Research, Department of Biochemistry, Academic Hospital, University of Munich, Germany.
Previous investigations have demonstrated that growing mesangial cells in
high glucose concentration stimulates extracellular matrix synthesis and
also increases the expression of transforming growth factor-beta
(TGF-beta). We examined the effects of hyperglycemia on mesangial
proliferation and heparan sulfate proteoglycan (HSPG) and fibronectin
production. Prolonged exposure of mesangial cells to increasing glucose
concentrations resulted in dose-dependent effects on growth inhibition and
stimulation of matrix production. Treatment of mesangial cells with high
glucose-conditioned medium or with TGF-beta 1 mimicked the effects of
high-glucose incubation. Furthermore, TGF-beta 1 caused a dose-dependent
increase in HSPG mRNA levels. The high-glucose effects on mesangial cells
were preceded by an increase in total TGF-beta 1 protein. The presence of
TGF-beta 1 antisense oligonucleotide attenuated the glucose-mediated
effects on mesangial proliferation and matrix production. The data show
that even moderately elevated glucose concentrations appear to affect the
mesangial cells. The results indicate that 1) TGF-beta 1 protein production
is necessary to obtain the high glucose-induced effects and 2) TGF-beta 1
stimulates mesangial HSPG expression and production. Because these effects
may be attenuated by oligonucleotides antisense to TGF-beta 1, the results
suggest a possible way for effective intervention in TGF-beta-mediated
glomerulosclerosis.</description><identifier>ISSN: 0363-6127</identifier><identifier>ISSN: 0002-9513</identifier><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 2161-1157</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.1996.270.5.F812</identifier><identifier>PMID: 8928843</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Aorta - cytology ; Aorta - metabolism ; Cell Division - drug effects ; Cells, Cultured ; Culture Media, Conditioned ; Endothelium, Vascular - cytology ; Endothelium, Vascular - metabolism ; Fibronectins - biosynthesis ; Glomerular Mesangium - cytology ; Glomerular Mesangium - metabolism ; Glucose - pharmacology ; Heparan Sulfate Proteoglycans ; Heparitin Sulfate - biosynthesis ; Heparitin Sulfate - genetics ; Heparitin Sulfate - pharmacology ; Oligonucleotides, Antisense - pharmacology ; Osmolar Concentration ; Polymers - pharmacology ; Proteoglycans - biosynthesis ; Proteoglycans - genetics ; Proteoglycans - pharmacology ; RNA, Messenger - metabolism ; Swine ; Transforming Growth Factor beta - genetics ; Transforming Growth Factor beta - pharmacology ; Transforming Growth Factor beta - physiology</subject><ispartof>American journal of physiology. Renal physiology, 1996-05, Vol.270 (5), p.812-F821</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c281t-a165b06282dc3361c7ec9369121f22f0c6460c1d083658167b1a9d77c2fc4d033</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8928843$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kolm, V</creatorcontrib><creatorcontrib>Sauer, U</creatorcontrib><creatorcontrib>Olgemooller, B</creatorcontrib><creatorcontrib>Schleicher, E. D</creatorcontrib><title>High glucose-induced TGF-beta 1 regulates mesangial production of heparan sulfate proteoglycan</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol</addtitle><description>V. Kolm, U. Sauer, B. Olgemooller and E. D. Schleicher
Institute for Diabetes Research, Department of Biochemistry, Academic Hospital, University of Munich, Germany.
Previous investigations have demonstrated that growing mesangial cells in
high glucose concentration stimulates extracellular matrix synthesis and
also increases the expression of transforming growth factor-beta
(TGF-beta). We examined the effects of hyperglycemia on mesangial
proliferation and heparan sulfate proteoglycan (HSPG) and fibronectin
production. Prolonged exposure of mesangial cells to increasing glucose
concentrations resulted in dose-dependent effects on growth inhibition and
stimulation of matrix production. Treatment of mesangial cells with high
glucose-conditioned medium or with TGF-beta 1 mimicked the effects of
high-glucose incubation. Furthermore, TGF-beta 1 caused a dose-dependent
increase in HSPG mRNA levels. The high-glucose effects on mesangial cells
were preceded by an increase in total TGF-beta 1 protein. The presence of
TGF-beta 1 antisense oligonucleotide attenuated the glucose-mediated
effects on mesangial proliferation and matrix production. The data show
that even moderately elevated glucose concentrations appear to affect the
mesangial cells. The results indicate that 1) TGF-beta 1 protein production
is necessary to obtain the high glucose-induced effects and 2) TGF-beta 1
stimulates mesangial HSPG expression and production. Because these effects
may be attenuated by oligonucleotides antisense to TGF-beta 1, the results
suggest a possible way for effective intervention in TGF-beta-mediated
glomerulosclerosis.</description><subject>Animals</subject><subject>Aorta - cytology</subject><subject>Aorta - metabolism</subject><subject>Cell Division - drug effects</subject><subject>Cells, Cultured</subject><subject>Culture Media, Conditioned</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Fibronectins - biosynthesis</subject><subject>Glomerular Mesangium - cytology</subject><subject>Glomerular Mesangium - metabolism</subject><subject>Glucose - pharmacology</subject><subject>Heparan Sulfate Proteoglycans</subject><subject>Heparitin Sulfate - biosynthesis</subject><subject>Heparitin Sulfate - genetics</subject><subject>Heparitin Sulfate - pharmacology</subject><subject>Oligonucleotides, Antisense - pharmacology</subject><subject>Osmolar Concentration</subject><subject>Polymers - pharmacology</subject><subject>Proteoglycans - biosynthesis</subject><subject>Proteoglycans - genetics</subject><subject>Proteoglycans - pharmacology</subject><subject>RNA, Messenger - metabolism</subject><subject>Swine</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Transforming Growth Factor beta - physiology</subject><issn>0363-6127</issn><issn>0002-9513</issn><issn>1931-857X</issn><issn>2161-1157</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkMFu2zAQRImgQeIm-YQAPPUmhUtaJHUsgjoOEKAX91qCplayAlpUSQmF_r407LY57WHezAKPEAqsBKj4k30fIw7Wl1DXsuSKlVW50cCvyIqDhCJD6hNZMSFFIYGrW_I5pXfGOJda3pAbXXOt12JFfm777kA7P7uQsOiHZnbY0N3LptjjZCnQiN3s7YSJHjHZoeutp2MMmZv6MNDQ0gOONtqBptm3GTylE4bOL84O9-S6tT7hw-XekR-bb7vnbfH2_eX1-etb4biGqbAgqz2TXPPGCSHBKXS1kDVwaDlvmZNryRw0TAtZaZBqD7ZulHK8deuGCXFHvpx38_NfM6bJHPvk0Hs7YJiTUZrJNa9VBvUZdDGkFLE1Y-yPNi4GmDmpNX_VmpNak9WaypzU5urj5ce8P2Lzr3hxmfPynB-y0t99RDMeltQHH7rl_-qHwT-5nYhZ</recordid><startdate>19960501</startdate><enddate>19960501</enddate><creator>Kolm, V</creator><creator>Sauer, U</creator><creator>Olgemooller, B</creator><creator>Schleicher, E. D</creator><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>19960501</creationdate><title>High glucose-induced TGF-beta 1 regulates mesangial production of heparan sulfate proteoglycan</title><author>Kolm, V ; Sauer, U ; Olgemooller, B ; Schleicher, E. D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c281t-a165b06282dc3361c7ec9369121f22f0c6460c1d083658167b1a9d77c2fc4d033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Aorta - cytology</topic><topic>Aorta - metabolism</topic><topic>Cell Division - drug effects</topic><topic>Cells, Cultured</topic><topic>Culture Media, Conditioned</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Fibronectins - biosynthesis</topic><topic>Glomerular Mesangium - cytology</topic><topic>Glomerular Mesangium - metabolism</topic><topic>Glucose - pharmacology</topic><topic>Heparan Sulfate Proteoglycans</topic><topic>Heparitin Sulfate - biosynthesis</topic><topic>Heparitin Sulfate - genetics</topic><topic>Heparitin Sulfate - pharmacology</topic><topic>Oligonucleotides, Antisense - pharmacology</topic><topic>Osmolar Concentration</topic><topic>Polymers - pharmacology</topic><topic>Proteoglycans - biosynthesis</topic><topic>Proteoglycans - genetics</topic><topic>Proteoglycans - pharmacology</topic><topic>RNA, Messenger - metabolism</topic><topic>Swine</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>Transforming Growth Factor beta - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kolm, V</creatorcontrib><creatorcontrib>Sauer, U</creatorcontrib><creatorcontrib>Olgemooller, B</creatorcontrib><creatorcontrib>Schleicher, E. D</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>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kolm, V</au><au>Sauer, U</au><au>Olgemooller, B</au><au>Schleicher, E. D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High glucose-induced TGF-beta 1 regulates mesangial production of heparan sulfate proteoglycan</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1996-05-01</date><risdate>1996</risdate><volume>270</volume><issue>5</issue><spage>812</spage><epage>F821</epage><pages>812-F821</pages><issn>0363-6127</issn><issn>0002-9513</issn><issn>1931-857X</issn><eissn>2161-1157</eissn><eissn>1522-1466</eissn><abstract>V. Kolm, U. Sauer, B. Olgemooller and E. D. Schleicher
Institute for Diabetes Research, Department of Biochemistry, Academic Hospital, University of Munich, Germany.
Previous investigations have demonstrated that growing mesangial cells in
high glucose concentration stimulates extracellular matrix synthesis and
also increases the expression of transforming growth factor-beta
(TGF-beta). We examined the effects of hyperglycemia on mesangial
proliferation and heparan sulfate proteoglycan (HSPG) and fibronectin
production. Prolonged exposure of mesangial cells to increasing glucose
concentrations resulted in dose-dependent effects on growth inhibition and
stimulation of matrix production. Treatment of mesangial cells with high
glucose-conditioned medium or with TGF-beta 1 mimicked the effects of
high-glucose incubation. Furthermore, TGF-beta 1 caused a dose-dependent
increase in HSPG mRNA levels. The high-glucose effects on mesangial cells
were preceded by an increase in total TGF-beta 1 protein. The presence of
TGF-beta 1 antisense oligonucleotide attenuated the glucose-mediated
effects on mesangial proliferation and matrix production. The data show
that even moderately elevated glucose concentrations appear to affect the
mesangial cells. The results indicate that 1) TGF-beta 1 protein production
is necessary to obtain the high glucose-induced effects and 2) TGF-beta 1
stimulates mesangial HSPG expression and production. Because these effects
may be attenuated by oligonucleotides antisense to TGF-beta 1, the results
suggest a possible way for effective intervention in TGF-beta-mediated
glomerulosclerosis.</abstract><cop>United States</cop><pmid>8928843</pmid><doi>10.1152/ajprenal.1996.270.5.F812</doi></addata></record> |
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| identifier | ISSN: 0363-6127 |
| ispartof | American journal of physiology. Renal physiology, 1996-05, Vol.270 (5), p.812-F821 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Aorta - cytology Aorta - metabolism Cell Division - drug effects Cells, Cultured Culture Media, Conditioned Endothelium, Vascular - cytology Endothelium, Vascular - metabolism Fibronectins - biosynthesis Glomerular Mesangium - cytology Glomerular Mesangium - metabolism Glucose - pharmacology Heparan Sulfate Proteoglycans Heparitin Sulfate - biosynthesis Heparitin Sulfate - genetics Heparitin Sulfate - pharmacology Oligonucleotides, Antisense - pharmacology Osmolar Concentration Polymers - pharmacology Proteoglycans - biosynthesis Proteoglycans - genetics Proteoglycans - pharmacology RNA, Messenger - metabolism Swine Transforming Growth Factor beta - genetics Transforming Growth Factor beta - pharmacology Transforming Growth Factor beta - physiology |
| title | High glucose-induced TGF-beta 1 regulates mesangial production of heparan sulfate proteoglycan |
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