Regulation of Glucose Transporter (GLUT1) Gene Expression by Angiotensin II in Mesangial Cells: Involvement of HB-EGF and EGF Receptor Transactivation
In the development of diabetic nephropathy, angiotensin (Ang) II is thought to exert numerous actions on the glomerulus, and especially on the mesangium. However, the role(s) played by Ang II in the glucose metabolism per se in mesangial cells remains unclear. Ang II, at least via its type 1 recepto...
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| Veröffentlicht in: | Hypertension Research 2003, Vol.26(1), pp.67-73 |
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| creator | NOSE, Atsuko MORI, Yasukiyo UCHIYAMA-TANAKA, Yoko KISHIMOTO, Noriko MARUYAMA, Katsuya MATSUBARA, Hiroaki IWASAKA, Toshiji |
| description | In the development of diabetic nephropathy, angiotensin (Ang) II is thought to exert numerous actions on the glomerulus, and especially on the mesangium. However, the role(s) played by Ang II in the glucose metabolism per se in mesangial cells remains unclear. Ang II, at least via its type 1 receptor (AT1-R)-mediated effect, phosphorylates extracellular signal regulated kinase (ERK) by transactivation of epidermal growth factor receptors (EGF-Rs) via the Ca2+ or protein kinase C (PKC) pathways. Our objective in the present study was to assess the effect of Ang II on glucose transporter 1 (GLUT1) gene expression and to clarify the involvement of EGF-R in Ang II-mediated GLUT1 mRNA expression in glomerular mesangial cells. The results showed that Ang II upregulated GLUT1 mRNA accumulation in a time- and dose-dependent manner (peaking at 12 h; ～3.8-fold vs. control), and this upregulation was completely inhibited by the PKC inhibitor calphostin-C. The Ang II-induced GLUT1 expression was significantly inhibited by the EGF-R inhibitor AG1478 (～80% inhibition), by inactivation of ERK by PD98059, and by pretreatment with heparin and the metalloproteinase (MMP) inhibitor batimastat. On the other hand, phorbol ester markedly upregulated GLUT1 mRNA (～8.6-fold). Batimostat and AG1478 significantly reduced the phorbol ester-induced GLUT1 mRNA expression (～72 and ～69% inhibition, respectively). In conclusion, PKC-mediated heparin-binding (HB)-EGF/EGF transactivation followed by ERK activation plays a predominant role in the induction of GLUT1 expression by Ang II. (Hypertens Res 2003; 26: 67-73) |
| doi_str_mv | 10.1291/hypres.26.67 |
| format | Article |
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However, the role(s) played by Ang II in the glucose metabolism per se in mesangial cells remains unclear. Ang II, at least via its type 1 receptor (AT1-R)-mediated effect, phosphorylates extracellular signal regulated kinase (ERK) by transactivation of epidermal growth factor receptors (EGF-Rs) via the Ca2+ or protein kinase C (PKC) pathways. Our objective in the present study was to assess the effect of Ang II on glucose transporter 1 (GLUT1) gene expression and to clarify the involvement of EGF-R in Ang II-mediated GLUT1 mRNA expression in glomerular mesangial cells. The results showed that Ang II upregulated GLUT1 mRNA accumulation in a time- and dose-dependent manner (peaking at 12 h; ～3.8-fold vs. control), and this upregulation was completely inhibited by the PKC inhibitor calphostin-C. The Ang II-induced GLUT1 expression was significantly inhibited by the EGF-R inhibitor AG1478 (～80% inhibition), by inactivation of ERK by PD98059, and by pretreatment with heparin and the metalloproteinase (MMP) inhibitor batimastat. On the other hand, phorbol ester markedly upregulated GLUT1 mRNA (～8.6-fold). Batimostat and AG1478 significantly reduced the phorbol ester-induced GLUT1 mRNA expression (～72 and ～69% inhibition, respectively). In conclusion, PKC-mediated heparin-binding (HB)-EGF/EGF transactivation followed by ERK activation plays a predominant role in the induction of GLUT1 expression by Ang II. (Hypertens Res 2003; 26: 67-73)</description><identifier>ISSN: 0916-9636</identifier><identifier>EISSN: 1348-4214</identifier><identifier>DOI: 10.1291/hypres.26.67</identifier><identifier>PMID: 12661915</identifier><language>eng</language><publisher>England: The Japanese Society of Hypertension</publisher><subject>angiotensin II ; Angiotensin II - pharmacology ; Animals ; Calcium - metabolism ; Carcinogens - pharmacology ; Cells, Cultured ; epidermal growth factor ; Epidermal Growth Factor - metabolism ; Glomerular Mesangium - cytology ; Glomerular Mesangium - metabolism ; glucose transporter ; Glucose Transporter Type 1 ; Heparin-binding EGF-like Growth Factor ; heparin-binding epidermal growth factor-like growth factor ; Intercellular Signaling Peptides and Proteins ; Male ; MAP Kinase Signaling System - drug effects ; MAP Kinase Signaling System - physiology ; mesangial cell ; Mice ; Mice, Inbred C57BL ; Monosaccharide Transport Proteins - genetics ; Phorbol Esters - pharmacology ; Protein Kinase C - metabolism ; Receptor, Epidermal Growth Factor - metabolism ; RNA, Messenger - metabolism ; Up-Regulation ; Vasoconstrictor Agents - pharmacology</subject><ispartof>Hypertension Research, 2003, Vol.26(1), pp.67-73</ispartof><rights>2003 by the Japanese Society of Hypertension</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c574t-b120a020e307132c8e605ba32c17638e6a63a8d0c873a935db8fa1edd0eda57e3</citedby><cites>FETCH-LOGICAL-c574t-b120a020e307132c8e605ba32c17638e6a63a8d0c873a935db8fa1edd0eda57e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1883,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12661915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NOSE, Atsuko</creatorcontrib><creatorcontrib>MORI, Yasukiyo</creatorcontrib><creatorcontrib>UCHIYAMA-TANAKA, Yoko</creatorcontrib><creatorcontrib>KISHIMOTO, Noriko</creatorcontrib><creatorcontrib>MARUYAMA, Katsuya</creatorcontrib><creatorcontrib>MATSUBARA, Hiroaki</creatorcontrib><creatorcontrib>IWASAKA, Toshiji</creatorcontrib><title>Regulation of Glucose Transporter (GLUT1) Gene Expression by Angiotensin II in Mesangial Cells: Involvement of HB-EGF and EGF Receptor Transactivation</title><title>Hypertension Research</title><addtitle>Hypertension Research</addtitle><description>In the development of diabetic nephropathy, angiotensin (Ang) II is thought to exert numerous actions on the glomerulus, and especially on the mesangium. However, the role(s) played by Ang II in the glucose metabolism per se in mesangial cells remains unclear. Ang II, at least via its type 1 receptor (AT1-R)-mediated effect, phosphorylates extracellular signal regulated kinase (ERK) by transactivation of epidermal growth factor receptors (EGF-Rs) via the Ca2+ or protein kinase C (PKC) pathways. Our objective in the present study was to assess the effect of Ang II on glucose transporter 1 (GLUT1) gene expression and to clarify the involvement of EGF-R in Ang II-mediated GLUT1 mRNA expression in glomerular mesangial cells. The results showed that Ang II upregulated GLUT1 mRNA accumulation in a time- and dose-dependent manner (peaking at 12 h; ～3.8-fold vs. control), and this upregulation was completely inhibited by the PKC inhibitor calphostin-C. The Ang II-induced GLUT1 expression was significantly inhibited by the EGF-R inhibitor AG1478 (～80% inhibition), by inactivation of ERK by PD98059, and by pretreatment with heparin and the metalloproteinase (MMP) inhibitor batimastat. On the other hand, phorbol ester markedly upregulated GLUT1 mRNA (～8.6-fold). Batimostat and AG1478 significantly reduced the phorbol ester-induced GLUT1 mRNA expression (～72 and ～69% inhibition, respectively). In conclusion, PKC-mediated heparin-binding (HB)-EGF/EGF transactivation followed by ERK activation plays a predominant role in the induction of GLUT1 expression by Ang II. (Hypertens Res 2003; 26: 67-73)</description><subject>angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Carcinogens - pharmacology</subject><subject>Cells, Cultured</subject><subject>epidermal growth factor</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Glomerular Mesangium - cytology</subject><subject>Glomerular Mesangium - metabolism</subject><subject>glucose transporter</subject><subject>Glucose Transporter Type 1</subject><subject>Heparin-binding EGF-like Growth Factor</subject><subject>heparin-binding epidermal growth factor-like growth factor</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Male</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MAP Kinase Signaling System - physiology</subject><subject>mesangial cell</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monosaccharide Transport Proteins - genetics</subject><subject>Phorbol Esters - pharmacology</subject><subject>Protein Kinase C - metabolism</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Up-Regulation</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>0916-9636</issn><issn>1348-4214</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkE1r20AQhpfS0Dhpbz2HPbYQuTu71krKzTW2YnApBOcsRquxoyCvxO7axH-kv7dSFdJc5vNh3uFl7CuIKcgMfjydO0d-KvVUJx_YBNQsjWYSZh_ZRGSgo0wrfcmuvH8WQqZxBp_YJUitIYN4wv480P7YYKhby9sdz5ujaT3xrUPru9YFcvxbvnncwneekyW-fBnU_ICXZz63-7oNZH1t-XrN-_iLPPZDbPiCmsbf8bU9tc2JDmTDIHD_M1rmK4624kN-IENdaN0oiCbUp3-_fGYXO2w8fXnN1-xxtdwu7qPN73y9mG8iEyezEJUgBQopSIkElDQpaRGX2FeQaNV3qBWmlTBpojBTcVWmOwSqKkEVxgmpa3Y73jWu9d7RruhcfUB3LkAUg73FaG8hdaGTHr8Z8e5YHqj6D7_62QPzEXj2Aff0BqALtWno3TUYg07eduYJXUFW_QXhPJBb</recordid><startdate>2003</startdate><enddate>2003</enddate><creator>NOSE, Atsuko</creator><creator>MORI, Yasukiyo</creator><creator>UCHIYAMA-TANAKA, Yoko</creator><creator>KISHIMOTO, Noriko</creator><creator>MARUYAMA, Katsuya</creator><creator>MATSUBARA, Hiroaki</creator><creator>IWASAKA, Toshiji</creator><general>The Japanese Society of Hypertension</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></search><sort><creationdate>2003</creationdate><title>Regulation of Glucose Transporter (GLUT1) Gene Expression by Angiotensin II in Mesangial Cells: Involvement of HB-EGF and EGF Receptor Transactivation</title><author>NOSE, Atsuko ; MORI, Yasukiyo ; UCHIYAMA-TANAKA, Yoko ; KISHIMOTO, Noriko ; MARUYAMA, Katsuya ; MATSUBARA, Hiroaki ; IWASAKA, Toshiji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c574t-b120a020e307132c8e605ba32c17638e6a63a8d0c873a935db8fa1edd0eda57e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Carcinogens - pharmacology</topic><topic>Cells, Cultured</topic><topic>epidermal growth factor</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Glomerular Mesangium - cytology</topic><topic>Glomerular Mesangium - metabolism</topic><topic>glucose transporter</topic><topic>Glucose Transporter Type 1</topic><topic>Heparin-binding EGF-like Growth Factor</topic><topic>heparin-binding epidermal growth factor-like growth factor</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Male</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>mesangial cell</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monosaccharide Transport Proteins - genetics</topic><topic>Phorbol Esters - pharmacology</topic><topic>Protein Kinase C - metabolism</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Up-Regulation</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NOSE, Atsuko</creatorcontrib><creatorcontrib>MORI, Yasukiyo</creatorcontrib><creatorcontrib>UCHIYAMA-TANAKA, Yoko</creatorcontrib><creatorcontrib>KISHIMOTO, Noriko</creatorcontrib><creatorcontrib>MARUYAMA, Katsuya</creatorcontrib><creatorcontrib>MATSUBARA, Hiroaki</creatorcontrib><creatorcontrib>IWASAKA, Toshiji</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Hypertension Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NOSE, Atsuko</au><au>MORI, Yasukiyo</au><au>UCHIYAMA-TANAKA, Yoko</au><au>KISHIMOTO, Noriko</au><au>MARUYAMA, Katsuya</au><au>MATSUBARA, Hiroaki</au><au>IWASAKA, Toshiji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of Glucose Transporter (GLUT1) Gene Expression by Angiotensin II in Mesangial Cells: Involvement of HB-EGF and EGF Receptor Transactivation</atitle><jtitle>Hypertension Research</jtitle><addtitle>Hypertension Research</addtitle><date>2003</date><risdate>2003</risdate><volume>26</volume><issue>1</issue><spage>67</spage><epage>73</epage><pages>67-73</pages><issn>0916-9636</issn><eissn>1348-4214</eissn><abstract>In the development of diabetic nephropathy, angiotensin (Ang) II is thought to exert numerous actions on the glomerulus, and especially on the mesangium. However, the role(s) played by Ang II in the glucose metabolism per se in mesangial cells remains unclear. Ang II, at least via its type 1 receptor (AT1-R)-mediated effect, phosphorylates extracellular signal regulated kinase (ERK) by transactivation of epidermal growth factor receptors (EGF-Rs) via the Ca2+ or protein kinase C (PKC) pathways. Our objective in the present study was to assess the effect of Ang II on glucose transporter 1 (GLUT1) gene expression and to clarify the involvement of EGF-R in Ang II-mediated GLUT1 mRNA expression in glomerular mesangial cells. The results showed that Ang II upregulated GLUT1 mRNA accumulation in a time- and dose-dependent manner (peaking at 12 h; ～3.8-fold vs. control), and this upregulation was completely inhibited by the PKC inhibitor calphostin-C. The Ang II-induced GLUT1 expression was significantly inhibited by the EGF-R inhibitor AG1478 (～80% inhibition), by inactivation of ERK by PD98059, and by pretreatment with heparin and the metalloproteinase (MMP) inhibitor batimastat. On the other hand, phorbol ester markedly upregulated GLUT1 mRNA (～8.6-fold). Batimostat and AG1478 significantly reduced the phorbol ester-induced GLUT1 mRNA expression (～72 and ～69% inhibition, respectively). In conclusion, PKC-mediated heparin-binding (HB)-EGF/EGF transactivation followed by ERK activation plays a predominant role in the induction of GLUT1 expression by Ang II. (Hypertens Res 2003; 26: 67-73)</abstract><cop>England</cop><pub>The Japanese Society of Hypertension</pub><pmid>12661915</pmid><doi>10.1291/hypres.26.67</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | angiotensin II Angiotensin II - pharmacology Animals Calcium - metabolism Carcinogens - pharmacology Cells, Cultured epidermal growth factor Epidermal Growth Factor - metabolism Glomerular Mesangium - cytology Glomerular Mesangium - metabolism glucose transporter Glucose Transporter Type 1 Heparin-binding EGF-like Growth Factor heparin-binding epidermal growth factor-like growth factor Intercellular Signaling Peptides and Proteins Male MAP Kinase Signaling System - drug effects MAP Kinase Signaling System - physiology mesangial cell Mice Mice, Inbred C57BL Monosaccharide Transport Proteins - genetics Phorbol Esters - pharmacology Protein Kinase C - metabolism Receptor, Epidermal Growth Factor - metabolism RNA, Messenger - metabolism Up-Regulation Vasoconstrictor Agents - pharmacology |
| title | Regulation of Glucose Transporter (GLUT1) Gene Expression by Angiotensin II in Mesangial Cells: Involvement of HB-EGF and EGF Receptor Transactivation |
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