Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells
Background. High levels of glucose have previously been shown to inhibit endothelial cell migration and increase secretion of the von Willebrand factor (vWF), a marker of endothelial cell damage. This study investigates whether thiamine, an important coenzyme in intracellular glucose metabolism, imp...
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| Veröffentlicht in: | Surgery 2001-11, Vol.130 (5), p.851-858 |
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| creator | Ascher, Enrico Gade, Prasad V. Hingorani, Anil Puthukkeril, Silvy Kallakuri, Sreedhar Scheinman, Marcel Jacob, Theresa |
| description | Background. High levels of glucose have previously been shown to inhibit endothelial cell migration and increase secretion of the von Willebrand factor (vWF), a marker of endothelial cell damage. This study investigates whether thiamine, an important coenzyme in intracellular glucose metabolism, improves endothelial cell migration and decreases von Willebrand factor secretion under hyperglycemic conditions. Methods. Bovine aortic endothelial cells (BAECs) were grown under physiological glucose (5.5 mmol/L) and hyperglycemic (13.8 mmol/L and 27.7 mmol/L) conditions with or without thiamine (200 μmol/L) supplementation. Endothelial cell migration was investigated in monolayers of BAECs that were wounded by scraping. The distance of migration, the number of migrating cells, and the surface area covered by the migrating cells were measured. Secretion of vWF by BAECs under physiological glucose and high glucose conditions with or without thiamine (200 μmol/L) supplementation was studied with enzyme-linked immunosorbent assay. Results. Under hyperglycemic conditions, there was a significant decrease in the number of endothelial cells and an increase in the secretion of vWF (P |
| doi_str_mv | 10.1067/msy.2001.117194 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1067_msy_2001_117194</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0039606001922470</els_id><sourcerecordid>11685195</sourcerecordid><originalsourceid>FETCH-LOGICAL-c373t-cf353a248f6a5d41751fa6a2a5673de0022101430bc4614bf92a4e865cae304a3</originalsourceid><addsrcrecordid>eNp1kE1Lw0AQhhdRbK2evUkuHtPOZDeb5CjFLyiIUM9huztrV_JRdpNC_r2RFHryNDA878vMw9g9whJBZqs6DMsEAJeIGRbigs0x5UmccYmXbA7Ai1iChBm7CeEHAAqB-TWbIco8xSKds8_t3qnaNRR5OpIPFKL9cCD_XQ2aaqdi15hek4nMEGzf6M61TeSaSPdV1_txT41puz1VTlWRpqoKt-zKqirQ3Wku2NfL83b9Fm8-Xt_XT5tY84x3sbY85SoRuZUqNQKzFK2SKlGpzLghgCRBQMFhp4VEsbNFogTlMtWKOAjFF2w19WrfhuDJlgfvauWHEqH8k1OOcso_OeUkZ0w8TIlDv6vJnPmTjRF4PAEqaFVZrxrtwpkTOBrEbOSKiaPxv6MjXwbtqBk1OU-6K03r_j3iF5vygUg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Ascher, Enrico ; Gade, Prasad V. ; Hingorani, Anil ; Puthukkeril, Silvy ; Kallakuri, Sreedhar ; Scheinman, Marcel ; Jacob, Theresa</creator><creatorcontrib>Ascher, Enrico ; Gade, Prasad V. ; Hingorani, Anil ; Puthukkeril, Silvy ; Kallakuri, Sreedhar ; Scheinman, Marcel ; Jacob, Theresa</creatorcontrib><description>Background. High levels of glucose have previously been shown to inhibit endothelial cell migration and increase secretion of the von Willebrand factor (vWF), a marker of endothelial cell damage. This study investigates whether thiamine, an important coenzyme in intracellular glucose metabolism, improves endothelial cell migration and decreases von Willebrand factor secretion under hyperglycemic conditions. Methods. Bovine aortic endothelial cells (BAECs) were grown under physiological glucose (5.5 mmol/L) and hyperglycemic (13.8 mmol/L and 27.7 mmol/L) conditions with or without thiamine (200 μmol/L) supplementation. Endothelial cell migration was investigated in monolayers of BAECs that were wounded by scraping. The distance of migration, the number of migrating cells, and the surface area covered by the migrating cells were measured. Secretion of vWF by BAECs under physiological glucose and high glucose conditions with or without thiamine (200 μmol/L) supplementation was studied with enzyme-linked immunosorbent assay. Results. Under hyperglycemic conditions, there was a significant decrease in the number of endothelial cells and an increase in the secretion of vWF (P <.001). Thiamine treatment limited this inhibitory effect of elevated glucose levels on BAECs. Glucose (27.7 mmol/L) significantly decreased the migration distance of BAECs into the wounded area to 4.0 ± 1.4 cm, as compared with 6.2 ± 0.3 cm in the control. Thiamine supplementation restored the migration distance by BAECs (6.94 ± 0.7 cm) and the wound surface area covered (47.7 ± 5.6 cm2)(P <.001). Conclusions. Hyperglycemia activates BAECs and promotes secretion of vWF, a marker of endothelial cell damage. Thiamine inhibits this endothelial cell activation and the effects of hyperglycemia on endothelial cell migration. This beneficial effect of thiamine limiting endothelial cell dysfunction is possibly through the diversion of glucose flux from anaerobic to aerobic pathways. The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes. (Surgery 2001;130:851-8.)</description><identifier>ISSN: 0039-6060</identifier><identifier>EISSN: 1532-7361</identifier><identifier>DOI: 10.1067/msy.2001.117194</identifier><identifier>PMID: 11685195</identifier><identifier>CODEN: SURGAZ</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiopathies: etiologic forms (general aspects and miscellaneous) ; Cattle ; Cell Count ; Cell Division - drug effects ; Cell Movement - drug effects ; Cells, Cultured ; Diabetic Retinopathy - etiology ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Glucose - toxicity ; Heart ; Medical sciences ; Thiamine - pharmacology ; von Willebrand Factor - secretion</subject><ispartof>Surgery, 2001-11, Vol.130 (5), p.851-858</ispartof><rights>2001 Mosby, Inc.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-cf353a248f6a5d41751fa6a2a5673de0022101430bc4614bf92a4e865cae304a3</citedby><cites>FETCH-LOGICAL-c373t-cf353a248f6a5d41751fa6a2a5673de0022101430bc4614bf92a4e865cae304a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0039606001922470$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14100917$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11685195$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ascher, Enrico</creatorcontrib><creatorcontrib>Gade, Prasad V.</creatorcontrib><creatorcontrib>Hingorani, Anil</creatorcontrib><creatorcontrib>Puthukkeril, Silvy</creatorcontrib><creatorcontrib>Kallakuri, Sreedhar</creatorcontrib><creatorcontrib>Scheinman, Marcel</creatorcontrib><creatorcontrib>Jacob, Theresa</creatorcontrib><title>Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells</title><title>Surgery</title><addtitle>Surgery</addtitle><description>Background. High levels of glucose have previously been shown to inhibit endothelial cell migration and increase secretion of the von Willebrand factor (vWF), a marker of endothelial cell damage. This study investigates whether thiamine, an important coenzyme in intracellular glucose metabolism, improves endothelial cell migration and decreases von Willebrand factor secretion under hyperglycemic conditions. Methods. Bovine aortic endothelial cells (BAECs) were grown under physiological glucose (5.5 mmol/L) and hyperglycemic (13.8 mmol/L and 27.7 mmol/L) conditions with or without thiamine (200 μmol/L) supplementation. Endothelial cell migration was investigated in monolayers of BAECs that were wounded by scraping. The distance of migration, the number of migrating cells, and the surface area covered by the migrating cells were measured. Secretion of vWF by BAECs under physiological glucose and high glucose conditions with or without thiamine (200 μmol/L) supplementation was studied with enzyme-linked immunosorbent assay. Results. Under hyperglycemic conditions, there was a significant decrease in the number of endothelial cells and an increase in the secretion of vWF (P <.001). Thiamine treatment limited this inhibitory effect of elevated glucose levels on BAECs. Glucose (27.7 mmol/L) significantly decreased the migration distance of BAECs into the wounded area to 4.0 ± 1.4 cm, as compared with 6.2 ± 0.3 cm in the control. Thiamine supplementation restored the migration distance by BAECs (6.94 ± 0.7 cm) and the wound surface area covered (47.7 ± 5.6 cm2)(P <.001). Conclusions. Hyperglycemia activates BAECs and promotes secretion of vWF, a marker of endothelial cell damage. Thiamine inhibits this endothelial cell activation and the effects of hyperglycemia on endothelial cell migration. This beneficial effect of thiamine limiting endothelial cell dysfunction is possibly through the diversion of glucose flux from anaerobic to aerobic pathways. The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes. (Surgery 2001;130:851-8.)</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cardiopathies: etiologic forms (general aspects and miscellaneous)</subject><subject>Cattle</subject><subject>Cell Count</subject><subject>Cell Division - drug effects</subject><subject>Cell Movement - drug effects</subject><subject>Cells, Cultured</subject><subject>Diabetic Retinopathy - etiology</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Glucose - toxicity</subject><subject>Heart</subject><subject>Medical sciences</subject><subject>Thiamine - pharmacology</subject><subject>von Willebrand Factor - secretion</subject><issn>0039-6060</issn><issn>1532-7361</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1Lw0AQhhdRbK2evUkuHtPOZDeb5CjFLyiIUM9huztrV_JRdpNC_r2RFHryNDA878vMw9g9whJBZqs6DMsEAJeIGRbigs0x5UmccYmXbA7Ai1iChBm7CeEHAAqB-TWbIco8xSKds8_t3qnaNRR5OpIPFKL9cCD_XQ2aaqdi15hek4nMEGzf6M61TeSaSPdV1_txT41puz1VTlWRpqoKt-zKqirQ3Wku2NfL83b9Fm8-Xt_XT5tY84x3sbY85SoRuZUqNQKzFK2SKlGpzLghgCRBQMFhp4VEsbNFogTlMtWKOAjFF2w19WrfhuDJlgfvauWHEqH8k1OOcso_OeUkZ0w8TIlDv6vJnPmTjRF4PAEqaFVZrxrtwpkTOBrEbOSKiaPxv6MjXwbtqBk1OU-6K03r_j3iF5vygUg</recordid><startdate>20011101</startdate><enddate>20011101</enddate><creator>Ascher, Enrico</creator><creator>Gade, Prasad V.</creator><creator>Hingorani, Anil</creator><creator>Puthukkeril, Silvy</creator><creator>Kallakuri, Sreedhar</creator><creator>Scheinman, Marcel</creator><creator>Jacob, Theresa</creator><general>Elsevier Inc</general><general>Elsevier</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></search><sort><creationdate>20011101</creationdate><title>Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells</title><author>Ascher, Enrico ; Gade, Prasad V. ; Hingorani, Anil ; Puthukkeril, Silvy ; Kallakuri, Sreedhar ; Scheinman, Marcel ; Jacob, Theresa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c373t-cf353a248f6a5d41751fa6a2a5673de0022101430bc4614bf92a4e865cae304a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cardiopathies: etiologic forms (general aspects and miscellaneous)</topic><topic>Cattle</topic><topic>Cell Count</topic><topic>Cell Division - drug effects</topic><topic>Cell Movement - drug effects</topic><topic>Cells, Cultured</topic><topic>Diabetic Retinopathy - etiology</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Glucose - toxicity</topic><topic>Heart</topic><topic>Medical sciences</topic><topic>Thiamine - pharmacology</topic><topic>von Willebrand Factor - secretion</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ascher, Enrico</creatorcontrib><creatorcontrib>Gade, Prasad V.</creatorcontrib><creatorcontrib>Hingorani, Anil</creatorcontrib><creatorcontrib>Puthukkeril, Silvy</creatorcontrib><creatorcontrib>Kallakuri, Sreedhar</creatorcontrib><creatorcontrib>Scheinman, Marcel</creatorcontrib><creatorcontrib>Jacob, Theresa</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><jtitle>Surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ascher, Enrico</au><au>Gade, Prasad V.</au><au>Hingorani, Anil</au><au>Puthukkeril, Silvy</au><au>Kallakuri, Sreedhar</au><au>Scheinman, Marcel</au><au>Jacob, Theresa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells</atitle><jtitle>Surgery</jtitle><addtitle>Surgery</addtitle><date>2001-11-01</date><risdate>2001</risdate><volume>130</volume><issue>5</issue><spage>851</spage><epage>858</epage><pages>851-858</pages><issn>0039-6060</issn><eissn>1532-7361</eissn><coden>SURGAZ</coden><abstract>Background. High levels of glucose have previously been shown to inhibit endothelial cell migration and increase secretion of the von Willebrand factor (vWF), a marker of endothelial cell damage. This study investigates whether thiamine, an important coenzyme in intracellular glucose metabolism, improves endothelial cell migration and decreases von Willebrand factor secretion under hyperglycemic conditions. Methods. Bovine aortic endothelial cells (BAECs) were grown under physiological glucose (5.5 mmol/L) and hyperglycemic (13.8 mmol/L and 27.7 mmol/L) conditions with or without thiamine (200 μmol/L) supplementation. Endothelial cell migration was investigated in monolayers of BAECs that were wounded by scraping. The distance of migration, the number of migrating cells, and the surface area covered by the migrating cells were measured. Secretion of vWF by BAECs under physiological glucose and high glucose conditions with or without thiamine (200 μmol/L) supplementation was studied with enzyme-linked immunosorbent assay. Results. Under hyperglycemic conditions, there was a significant decrease in the number of endothelial cells and an increase in the secretion of vWF (P <.001). Thiamine treatment limited this inhibitory effect of elevated glucose levels on BAECs. Glucose (27.7 mmol/L) significantly decreased the migration distance of BAECs into the wounded area to 4.0 ± 1.4 cm, as compared with 6.2 ± 0.3 cm in the control. Thiamine supplementation restored the migration distance by BAECs (6.94 ± 0.7 cm) and the wound surface area covered (47.7 ± 5.6 cm2)(P <.001). Conclusions. Hyperglycemia activates BAECs and promotes secretion of vWF, a marker of endothelial cell damage. Thiamine inhibits this endothelial cell activation and the effects of hyperglycemia on endothelial cell migration. This beneficial effect of thiamine limiting endothelial cell dysfunction is possibly through the diversion of glucose flux from anaerobic to aerobic pathways. The data from this study lead to the speculation that thiamine intake may mitigate or delay vascular complications of diabetes. (Surgery 2001;130:851-8.)</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>11685195</pmid><doi>10.1067/msy.2001.117194</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Cardiology. Vascular system Cardiopathies: etiologic forms (general aspects and miscellaneous) Cattle Cell Count Cell Division - drug effects Cell Movement - drug effects Cells, Cultured Diabetic Retinopathy - etiology Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Glucose - toxicity Heart Medical sciences Thiamine - pharmacology von Willebrand Factor - secretion |
| title | Thiamine reverses hyperglycemia-induced dysfunction in cultured endothelial cells |
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