Molecular alterations of the TLR4-signaling cascade in canine epilepsy

Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this...
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Autor*in:	Eva-Lotta von Rüden [verfasserIn] Fabio Gualtieri [verfasserIn] Katharina Schönhoff [verfasserIn] Maria Reiber [verfasserIn] Fabio Wolf [verfasserIn] Wolfgang Baumgärtner [verfasserIn] Florian Hansmann [verfasserIn] Andrea Tipold [verfasserIn] Heidrun Potschka [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70

Übergeordnetes Werk:	In: BMC Veterinary Research - BMC, 2005, 16(2020), 1, Seite 14
Übergeordnetes Werk:	volume:16 ; year:2020 ; number:1 ; pages:14

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s12917-020-2241-x

Katalog-ID:	DOAJ017290147

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520			\|a Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target.
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allfields	10.1186/s12917-020-2241-x doi (DE-627)DOAJ017290147 (DE-599)DOAJ1b13645435504471a5438fa249104a85 DE-627 ger DE-627 rakwb eng SF600-1100 Eva-Lotta von Rüden verfasserin aut Molecular alterations of the TLR4-signaling cascade in canine epilepsy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target. Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70 Veterinary medicine Fabio Gualtieri verfasserin aut Katharina Schönhoff verfasserin aut Maria Reiber verfasserin aut Fabio Wolf verfasserin aut Wolfgang Baumgärtner verfasserin aut Florian Hansmann verfasserin aut Andrea Tipold verfasserin aut Heidrun Potschka verfasserin aut In BMC Veterinary Research BMC, 2005 16(2020), 1, Seite 14 (DE-627)489256538 (DE-600)2191675-5 17466148 nnns volume:16 year:2020 number:1 pages:14 https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/article/1b13645435504471a5438fa249104a85 kostenfrei https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/toc/1746-6148 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 16 2020 1 14
spelling	10.1186/s12917-020-2241-x doi (DE-627)DOAJ017290147 (DE-599)DOAJ1b13645435504471a5438fa249104a85 DE-627 ger DE-627 rakwb eng SF600-1100 Eva-Lotta von Rüden verfasserin aut Molecular alterations of the TLR4-signaling cascade in canine epilepsy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target. Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70 Veterinary medicine Fabio Gualtieri verfasserin aut Katharina Schönhoff verfasserin aut Maria Reiber verfasserin aut Fabio Wolf verfasserin aut Wolfgang Baumgärtner verfasserin aut Florian Hansmann verfasserin aut Andrea Tipold verfasserin aut Heidrun Potschka verfasserin aut In BMC Veterinary Research BMC, 2005 16(2020), 1, Seite 14 (DE-627)489256538 (DE-600)2191675-5 17466148 nnns volume:16 year:2020 number:1 pages:14 https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/article/1b13645435504471a5438fa249104a85 kostenfrei https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/toc/1746-6148 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 16 2020 1 14
allfields_unstemmed	10.1186/s12917-020-2241-x doi (DE-627)DOAJ017290147 (DE-599)DOAJ1b13645435504471a5438fa249104a85 DE-627 ger DE-627 rakwb eng SF600-1100 Eva-Lotta von Rüden verfasserin aut Molecular alterations of the TLR4-signaling cascade in canine epilepsy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target. Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70 Veterinary medicine Fabio Gualtieri verfasserin aut Katharina Schönhoff verfasserin aut Maria Reiber verfasserin aut Fabio Wolf verfasserin aut Wolfgang Baumgärtner verfasserin aut Florian Hansmann verfasserin aut Andrea Tipold verfasserin aut Heidrun Potschka verfasserin aut In BMC Veterinary Research BMC, 2005 16(2020), 1, Seite 14 (DE-627)489256538 (DE-600)2191675-5 17466148 nnns volume:16 year:2020 number:1 pages:14 https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/article/1b13645435504471a5438fa249104a85 kostenfrei https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/toc/1746-6148 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 16 2020 1 14
allfieldsGer	10.1186/s12917-020-2241-x doi (DE-627)DOAJ017290147 (DE-599)DOAJ1b13645435504471a5438fa249104a85 DE-627 ger DE-627 rakwb eng SF600-1100 Eva-Lotta von Rüden verfasserin aut Molecular alterations of the TLR4-signaling cascade in canine epilepsy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target. Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70 Veterinary medicine Fabio Gualtieri verfasserin aut Katharina Schönhoff verfasserin aut Maria Reiber verfasserin aut Fabio Wolf verfasserin aut Wolfgang Baumgärtner verfasserin aut Florian Hansmann verfasserin aut Andrea Tipold verfasserin aut Heidrun Potschka verfasserin aut In BMC Veterinary Research BMC, 2005 16(2020), 1, Seite 14 (DE-627)489256538 (DE-600)2191675-5 17466148 nnns volume:16 year:2020 number:1 pages:14 https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/article/1b13645435504471a5438fa249104a85 kostenfrei https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/toc/1746-6148 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 16 2020 1 14
allfieldsSound	10.1186/s12917-020-2241-x doi (DE-627)DOAJ017290147 (DE-599)DOAJ1b13645435504471a5438fa249104a85 DE-627 ger DE-627 rakwb eng SF600-1100 Eva-Lotta von Rüden verfasserin aut Molecular alterations of the TLR4-signaling cascade in canine epilepsy 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target. Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70 Veterinary medicine Fabio Gualtieri verfasserin aut Katharina Schönhoff verfasserin aut Maria Reiber verfasserin aut Fabio Wolf verfasserin aut Wolfgang Baumgärtner verfasserin aut Florian Hansmann verfasserin aut Andrea Tipold verfasserin aut Heidrun Potschka verfasserin aut In BMC Veterinary Research BMC, 2005 16(2020), 1, Seite 14 (DE-627)489256538 (DE-600)2191675-5 17466148 nnns volume:16 year:2020 number:1 pages:14 https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/article/1b13645435504471a5438fa249104a85 kostenfrei https://doi.org/10.1186/s12917-020-2241-x kostenfrei https://doaj.org/toc/1746-6148 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 16 2020 1 14
language	English
source	In BMC Veterinary Research 16(2020), 1, Seite 14 volume:16 year:2020 number:1 pages:14
sourceStr	In BMC Veterinary Research 16(2020), 1, Seite 14 volume:16 year:2020 number:1 pages:14
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70 Veterinary medicine
isfreeaccess_bool	true
container_title	BMC Veterinary Research
authorswithroles_txt_mv	Eva-Lotta von Rüden @@aut@@ Fabio Gualtieri @@aut@@ Katharina Schönhoff @@aut@@ Maria Reiber @@aut@@ Fabio Wolf @@aut@@ Wolfgang Baumgärtner @@aut@@ Florian Hansmann @@aut@@ Andrea Tipold @@aut@@ Heidrun Potschka @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	489256538
id	DOAJ017290147
language_de	englisch
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callnumber-first	S - Agriculture
author	Eva-Lotta von Rüden
spellingShingle	Eva-Lotta von Rüden misc SF600-1100 misc Brain misc Seizure misc Inflammation misc Toll-like receptor 4 misc HMGB1 misc HSP70 misc Veterinary medicine Molecular alterations of the TLR4-signaling cascade in canine epilepsy
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topic_title	SF600-1100 Molecular alterations of the TLR4-signaling cascade in canine epilepsy Brain Seizure Inflammation Toll-like receptor 4 HMGB1 HSP70
topic	misc SF600-1100 misc Brain misc Seizure misc Inflammation misc Toll-like receptor 4 misc HMGB1 misc HSP70 misc Veterinary medicine
topic_unstemmed	misc SF600-1100 misc Brain misc Seizure misc Inflammation misc Toll-like receptor 4 misc HMGB1 misc HSP70 misc Veterinary medicine
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title	Molecular alterations of the TLR4-signaling cascade in canine epilepsy
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title_full	Molecular alterations of the TLR4-signaling cascade in canine epilepsy
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author_browse	Eva-Lotta von Rüden Fabio Gualtieri Katharina Schönhoff Maria Reiber Fabio Wolf Wolfgang Baumgärtner Florian Hansmann Andrea Tipold Heidrun Potschka
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title_sort	molecular alterations of the tlr4-signaling cascade in canine epilepsy
callnumber	SF600-1100
title_auth	Molecular alterations of the TLR4-signaling cascade in canine epilepsy
abstract	Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target.
abstractGer	Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target.
abstract_unstemmed	Abstract Background Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multi-targeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target.
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title_short	Molecular alterations of the TLR4-signaling cascade in canine epilepsy
url	https://doi.org/10.1186/s12917-020-2241-x https://doaj.org/article/1b13645435504471a5438fa249104a85 https://doaj.org/toc/1746-6148
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Molecular alterations of the TLR4-signaling cascade in canine epilepsy

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