Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products

<p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 pro...
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Autor*in:	Greten Johannes [verfasserIn] Weichenhan Dieter [verfasserIn] Most Patrick [verfasserIn] Bierhaus Angelika [verfasserIn] Eggers Kai [verfasserIn] Ehlermann Philipp [verfasserIn] Nawroth Peter P [verfasserIn] Katus Hugo A [verfasserIn] Remppis Andrew [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2006

Übergeordnetes Werk:	In: Cardiovascular Diabetology - BMC, 2003, 5(2006), 1, p 6
Übergeordnetes Werk:	volume:5 ; year:2006 ; number:1, p 6

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1475-2840-5-6

Katalog-ID:	DOAJ063287188

Internformat


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245	1	0	\|a Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
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520			\|a <p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p<
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700	0		\|a Bierhaus Angelika \|e verfasserin \|4 aut
700	0		\|a Eggers Kai \|e verfasserin \|4 aut
700	0		\|a Ehlermann Philipp \|e verfasserin \|4 aut
700	0		\|a Nawroth Peter P \|e verfasserin \|4 aut
700	0		\|a Katus Hugo A \|e verfasserin \|4 aut
700	0		\|a Remppis Andrew \|e verfasserin \|4 aut
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912			\|a GBV_ILN_2061
912			\|a GBV_ILN_2111
912			\|a GBV_ILN_2113
912			\|a GBV_ILN_2190
912			\|a GBV_ILN_4012
912			\|a GBV_ILN_4037
912			\|a GBV_ILN_4112
912			\|a GBV_ILN_4125
912			\|a GBV_ILN_4126
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912			\|a GBV_ILN_4306
912			\|a GBV_ILN_4307
912			\|a GBV_ILN_4313
912			\|a GBV_ILN_4322
912			\|a GBV_ILN_4323
912			\|a GBV_ILN_4324
912			\|a GBV_ILN_4325
912			\|a GBV_ILN_4338
912			\|a GBV_ILN_4367
912			\|a GBV_ILN_4700
951			\|a AR
952			\|d 5 \|j 2006 \|e 1, p 6

Indexfelder

author_variant	g j gj w d wd m p mp b a ba e k ek e p ep n p p npp k h a kha r a ra
matchkey_str	article:14752840:2006----::nraeponlmaoynohlarsosts0aaatrratvtotruh
hierarchy_sort_str	2006
callnumber-subject-code	RC
publishDate	2006
allfields	10.1186/1475-2840-5-6 doi (DE-627)DOAJ063287188 (DE-599)DOAJ2d37ff0a62ad42b8a42357aacbaf6ae2 DE-627 ger DE-627 rakwb eng RC666-701 Greten Johannes verfasserin aut Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p< Diseases of the circulatory (Cardiovascular) system Weichenhan Dieter verfasserin aut Most Patrick verfasserin aut Bierhaus Angelika verfasserin aut Eggers Kai verfasserin aut Ehlermann Philipp verfasserin aut Nawroth Peter P verfasserin aut Katus Hugo A verfasserin aut Remppis Andrew verfasserin aut In Cardiovascular Diabetology BMC, 2003 5(2006), 1, p 6 (DE-627)356593665 (DE-600)2093769-6 14752840 nnns volume:5 year:2006 number:1, p 6 https://doi.org/10.1186/1475-2840-5-6 kostenfrei https://doaj.org/article/2d37ff0a62ad42b8a42357aacbaf6ae2 kostenfrei http://www.cardiab.com/content/5/1/6 kostenfrei https://doaj.org/toc/1475-2840 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 6
spelling	10.1186/1475-2840-5-6 doi (DE-627)DOAJ063287188 (DE-599)DOAJ2d37ff0a62ad42b8a42357aacbaf6ae2 DE-627 ger DE-627 rakwb eng RC666-701 Greten Johannes verfasserin aut Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p< Diseases of the circulatory (Cardiovascular) system Weichenhan Dieter verfasserin aut Most Patrick verfasserin aut Bierhaus Angelika verfasserin aut Eggers Kai verfasserin aut Ehlermann Philipp verfasserin aut Nawroth Peter P verfasserin aut Katus Hugo A verfasserin aut Remppis Andrew verfasserin aut In Cardiovascular Diabetology BMC, 2003 5(2006), 1, p 6 (DE-627)356593665 (DE-600)2093769-6 14752840 nnns volume:5 year:2006 number:1, p 6 https://doi.org/10.1186/1475-2840-5-6 kostenfrei https://doaj.org/article/2d37ff0a62ad42b8a42357aacbaf6ae2 kostenfrei http://www.cardiab.com/content/5/1/6 kostenfrei https://doaj.org/toc/1475-2840 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 6
allfields_unstemmed	10.1186/1475-2840-5-6 doi (DE-627)DOAJ063287188 (DE-599)DOAJ2d37ff0a62ad42b8a42357aacbaf6ae2 DE-627 ger DE-627 rakwb eng RC666-701 Greten Johannes verfasserin aut Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p< Diseases of the circulatory (Cardiovascular) system Weichenhan Dieter verfasserin aut Most Patrick verfasserin aut Bierhaus Angelika verfasserin aut Eggers Kai verfasserin aut Ehlermann Philipp verfasserin aut Nawroth Peter P verfasserin aut Katus Hugo A verfasserin aut Remppis Andrew verfasserin aut In Cardiovascular Diabetology BMC, 2003 5(2006), 1, p 6 (DE-627)356593665 (DE-600)2093769-6 14752840 nnns volume:5 year:2006 number:1, p 6 https://doi.org/10.1186/1475-2840-5-6 kostenfrei https://doaj.org/article/2d37ff0a62ad42b8a42357aacbaf6ae2 kostenfrei http://www.cardiab.com/content/5/1/6 kostenfrei https://doaj.org/toc/1475-2840 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 6
allfieldsGer	10.1186/1475-2840-5-6 doi (DE-627)DOAJ063287188 (DE-599)DOAJ2d37ff0a62ad42b8a42357aacbaf6ae2 DE-627 ger DE-627 rakwb eng RC666-701 Greten Johannes verfasserin aut Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p< Diseases of the circulatory (Cardiovascular) system Weichenhan Dieter verfasserin aut Most Patrick verfasserin aut Bierhaus Angelika verfasserin aut Eggers Kai verfasserin aut Ehlermann Philipp verfasserin aut Nawroth Peter P verfasserin aut Katus Hugo A verfasserin aut Remppis Andrew verfasserin aut In Cardiovascular Diabetology BMC, 2003 5(2006), 1, p 6 (DE-627)356593665 (DE-600)2093769-6 14752840 nnns volume:5 year:2006 number:1, p 6 https://doi.org/10.1186/1475-2840-5-6 kostenfrei https://doaj.org/article/2d37ff0a62ad42b8a42357aacbaf6ae2 kostenfrei http://www.cardiab.com/content/5/1/6 kostenfrei https://doaj.org/toc/1475-2840 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 6
allfieldsSound	10.1186/1475-2840-5-6 doi (DE-627)DOAJ063287188 (DE-599)DOAJ2d37ff0a62ad42b8a42357aacbaf6ae2 DE-627 ger DE-627 rakwb eng RC666-701 Greten Johannes verfasserin aut Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products 2006 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p< Diseases of the circulatory (Cardiovascular) system Weichenhan Dieter verfasserin aut Most Patrick verfasserin aut Bierhaus Angelika verfasserin aut Eggers Kai verfasserin aut Ehlermann Philipp verfasserin aut Nawroth Peter P verfasserin aut Katus Hugo A verfasserin aut Remppis Andrew verfasserin aut In Cardiovascular Diabetology BMC, 2003 5(2006), 1, p 6 (DE-627)356593665 (DE-600)2093769-6 14752840 nnns volume:5 year:2006 number:1, p 6 https://doi.org/10.1186/1475-2840-5-6 kostenfrei https://doaj.org/article/2d37ff0a62ad42b8a42357aacbaf6ae2 kostenfrei http://www.cardiab.com/content/5/1/6 kostenfrei https://doaj.org/toc/1475-2840 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 5 2006 1, p 6
language	English
source	In Cardiovascular Diabetology 5(2006), 1, p 6 volume:5 year:2006 number:1, p 6
sourceStr	In Cardiovascular Diabetology 5(2006), 1, p 6 volume:5 year:2006 number:1, p 6
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Diseases of the circulatory (Cardiovascular) system
isfreeaccess_bool	true
container_title	Cardiovascular Diabetology
authorswithroles_txt_mv	Greten Johannes @@aut@@ Weichenhan Dieter @@aut@@ Most Patrick @@aut@@ Bierhaus Angelika @@aut@@ Eggers Kai @@aut@@ Ehlermann Philipp @@aut@@ Nawroth Peter P @@aut@@ Katus Hugo A @@aut@@ Remppis Andrew @@aut@@
publishDateDaySort_date	2006-01-01T00:00:00Z
hierarchy_top_id	356593665
id	DOAJ063287188
language_de	englisch
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As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. 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callnumber-first	R - Medicine
author	Greten Johannes
spellingShingle	Greten Johannes misc RC666-701 misc Diseases of the circulatory (Cardiovascular) system Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
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topic_title	RC666-701 Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
topic	misc RC666-701 misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc Diseases of the circulatory (Cardiovascular) system
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title	Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
ctrlnum	(DE-627)DOAJ063287188 (DE-599)DOAJ2d37ff0a62ad42b8a42357aacbaf6ae2
title_full	Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
author_sort	Greten Johannes
journal	Cardiovascular Diabetology
journalStr	Cardiovascular Diabetology
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lang_code	eng
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author_browse	Greten Johannes Weichenhan Dieter Most Patrick Bierhaus Angelika Eggers Kai Ehlermann Philipp Nawroth Peter P Katus Hugo A Remppis Andrew
container_volume	5
class	RC666-701
format_se	Elektronische Aufsätze
author-letter	Greten Johannes
doi_str_mv	10.1186/1475-2840-5-6
author2-role	verfasserin
title_sort	increased proinflammatory endothelial response to s100a8/a9 after preactivation through advanced glycation end products
callnumber	RC666-701
title_auth	Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
abstract	<p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p<
abstractGer	<p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p<
abstract_unstemmed	<p<Summary</p< <p<Background</p< <p<Atherosclerosis is an inflammatory disease in which a perpetuated activation of NFkappaB via the RAGE (receptor for advanced glycation end products)-MAPK signalling pathway may play an important pathogenetic role. As recently S100 proteins have been identified as ligands of RAGE, we sought to determine the effects of the proinflammatory heterodimer of S100A8/S100A9 on the RAGE-NFkappaB mediated induction of proinflammatory gene expression.</p< <p<Methods</p< <p<Human umbilical vein endothelial cells (HUVEC) were preincubated for 72 h with AGE-albumin or unmodified albumin for control, whereas AGE-albumin induction resulted in an upregulation of RAGE. Following this preactivation, cells were stimulated for 48 h with heterodimeric human recombinant S100A8/S100A9.</p< <p<Results</p< <p<Heterodimeric S100A8/S100A9 enhanced secretion of IL-6, ICAM-1, VCAM-1 and MCP1 in AGE-albumin pretreated HUVEC in a dose dependent manner. These effects could not be detected after stimulation with the homodimeric proteins S100A8, S100A9, S100A1 and S100B. The effects of heterodimeric S100A8/S100A9 were reduced by inhibition of the MAP-kinase pathways ERK1/2 and p38 by PD 98059 and SB 203580, respectively.</p< <p<Conclusion</p< <p<The heterodimeric S100A8/S100A9 might therefore play a hitherto unknown role in triggering atherosclerosis in diabetes and renal failure, pathophysiological entities associated with a high AGE burden. Thus, blocking heterodimeric S100A8/S100A9 might represent a novel therapeutic modality in treating atherosclerosis.</p<
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title_short	Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products
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Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products

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