Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<

Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hy...
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Autor*in:	Sönke Maximilian Braß [verfasserIn] Agnesa Mazrekaj [verfasserIn] Joscha Mulorz [verfasserIn] Wiebke Ibing [verfasserIn] Kim-Jürgen Krott [verfasserIn] Kiku Takeuchi [verfasserIn] Melanie Cappallo [verfasserIn] Hsiang-Han Liu [verfasserIn] Margitta Elvers [verfasserIn] Hubert Schelzig [verfasserIn] Markus Udo Wagenhäuser [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	galectin nicotine endothelial cells aortic pathologies

Übergeordnetes Werk:	In: Journal of Cardiovascular Development and Disease - MDPI AG, 2014, 11(2023), 1, p 6
Übergeordnetes Werk:	volume:11 ; year:2023 ; number:1, p 6

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/jcdd11010006

Katalog-ID:	DOAJ096335394

Internformat


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245	1	0	\|a Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<
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520			\|a Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies.
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700	0		\|a Agnesa Mazrekaj \|e verfasserin \|4 aut
700	0		\|a Joscha Mulorz \|e verfasserin \|4 aut
700	0		\|a Wiebke Ibing \|e verfasserin \|4 aut
700	0		\|a Kim-Jürgen Krott \|e verfasserin \|4 aut
700	0		\|a Kiku Takeuchi \|e verfasserin \|4 aut
700	0		\|a Melanie Cappallo \|e verfasserin \|4 aut
700	0		\|a Hsiang-Han Liu \|e verfasserin \|4 aut
700	0		\|a Margitta Elvers \|e verfasserin \|4 aut
700	0		\|a Hubert Schelzig \|e verfasserin \|4 aut
700	0		\|a Markus Udo Wagenhäuser \|e verfasserin \|4 aut
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allfields	10.3390/jcdd11010006 doi (DE-627)DOAJ096335394 (DE-599)DOAJ7ddd34f6b7c04b5eaf872ec8e1d12db5 DE-627 ger DE-627 rakwb eng RC666-701 Sönke Maximilian Braß verfasserin aut Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i< 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies. galectin nicotine endothelial cells aortic pathologies Diseases of the circulatory (Cardiovascular) system Agnesa Mazrekaj verfasserin aut Joscha Mulorz verfasserin aut Wiebke Ibing verfasserin aut Kim-Jürgen Krott verfasserin aut Kiku Takeuchi verfasserin aut Melanie Cappallo verfasserin aut Hsiang-Han Liu verfasserin aut Margitta Elvers verfasserin aut Hubert Schelzig verfasserin aut Markus Udo Wagenhäuser verfasserin aut In Journal of Cardiovascular Development and Disease MDPI AG, 2014 11(2023), 1, p 6 (DE-627)790616017 (DE-600)2777082-5 23083425 nnns volume:11 year:2023 number:1, p 6 https://doi.org/10.3390/jcdd11010006 kostenfrei https://doaj.org/article/7ddd34f6b7c04b5eaf872ec8e1d12db5 kostenfrei https://www.mdpi.com/2308-3425/11/1/6 kostenfrei https://doaj.org/toc/2308-3425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_2014 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 11 2023 1, p 6
spelling	10.3390/jcdd11010006 doi (DE-627)DOAJ096335394 (DE-599)DOAJ7ddd34f6b7c04b5eaf872ec8e1d12db5 DE-627 ger DE-627 rakwb eng RC666-701 Sönke Maximilian Braß verfasserin aut Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i< 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies. galectin nicotine endothelial cells aortic pathologies Diseases of the circulatory (Cardiovascular) system Agnesa Mazrekaj verfasserin aut Joscha Mulorz verfasserin aut Wiebke Ibing verfasserin aut Kim-Jürgen Krott verfasserin aut Kiku Takeuchi verfasserin aut Melanie Cappallo verfasserin aut Hsiang-Han Liu verfasserin aut Margitta Elvers verfasserin aut Hubert Schelzig verfasserin aut Markus Udo Wagenhäuser verfasserin aut In Journal of Cardiovascular Development and Disease MDPI AG, 2014 11(2023), 1, p 6 (DE-627)790616017 (DE-600)2777082-5 23083425 nnns volume:11 year:2023 number:1, p 6 https://doi.org/10.3390/jcdd11010006 kostenfrei https://doaj.org/article/7ddd34f6b7c04b5eaf872ec8e1d12db5 kostenfrei https://www.mdpi.com/2308-3425/11/1/6 kostenfrei https://doaj.org/toc/2308-3425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_2014 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 11 2023 1, p 6
allfields_unstemmed	10.3390/jcdd11010006 doi (DE-627)DOAJ096335394 (DE-599)DOAJ7ddd34f6b7c04b5eaf872ec8e1d12db5 DE-627 ger DE-627 rakwb eng RC666-701 Sönke Maximilian Braß verfasserin aut Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i< 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies. galectin nicotine endothelial cells aortic pathologies Diseases of the circulatory (Cardiovascular) system Agnesa Mazrekaj verfasserin aut Joscha Mulorz verfasserin aut Wiebke Ibing verfasserin aut Kim-Jürgen Krott verfasserin aut Kiku Takeuchi verfasserin aut Melanie Cappallo verfasserin aut Hsiang-Han Liu verfasserin aut Margitta Elvers verfasserin aut Hubert Schelzig verfasserin aut Markus Udo Wagenhäuser verfasserin aut In Journal of Cardiovascular Development and Disease MDPI AG, 2014 11(2023), 1, p 6 (DE-627)790616017 (DE-600)2777082-5 23083425 nnns volume:11 year:2023 number:1, p 6 https://doi.org/10.3390/jcdd11010006 kostenfrei https://doaj.org/article/7ddd34f6b7c04b5eaf872ec8e1d12db5 kostenfrei https://www.mdpi.com/2308-3425/11/1/6 kostenfrei https://doaj.org/toc/2308-3425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_2014 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 11 2023 1, p 6
allfieldsGer	10.3390/jcdd11010006 doi (DE-627)DOAJ096335394 (DE-599)DOAJ7ddd34f6b7c04b5eaf872ec8e1d12db5 DE-627 ger DE-627 rakwb eng RC666-701 Sönke Maximilian Braß verfasserin aut Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i< 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies. galectin nicotine endothelial cells aortic pathologies Diseases of the circulatory (Cardiovascular) system Agnesa Mazrekaj verfasserin aut Joscha Mulorz verfasserin aut Wiebke Ibing verfasserin aut Kim-Jürgen Krott verfasserin aut Kiku Takeuchi verfasserin aut Melanie Cappallo verfasserin aut Hsiang-Han Liu verfasserin aut Margitta Elvers verfasserin aut Hubert Schelzig verfasserin aut Markus Udo Wagenhäuser verfasserin aut In Journal of Cardiovascular Development and Disease MDPI AG, 2014 11(2023), 1, p 6 (DE-627)790616017 (DE-600)2777082-5 23083425 nnns volume:11 year:2023 number:1, p 6 https://doi.org/10.3390/jcdd11010006 kostenfrei https://doaj.org/article/7ddd34f6b7c04b5eaf872ec8e1d12db5 kostenfrei https://www.mdpi.com/2308-3425/11/1/6 kostenfrei https://doaj.org/toc/2308-3425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_2014 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 11 2023 1, p 6
allfieldsSound	10.3390/jcdd11010006 doi (DE-627)DOAJ096335394 (DE-599)DOAJ7ddd34f6b7c04b5eaf872ec8e1d12db5 DE-627 ger DE-627 rakwb eng RC666-701 Sönke Maximilian Braß verfasserin aut Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i< 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies. galectin nicotine endothelial cells aortic pathologies Diseases of the circulatory (Cardiovascular) system Agnesa Mazrekaj verfasserin aut Joscha Mulorz verfasserin aut Wiebke Ibing verfasserin aut Kim-Jürgen Krott verfasserin aut Kiku Takeuchi verfasserin aut Melanie Cappallo verfasserin aut Hsiang-Han Liu verfasserin aut Margitta Elvers verfasserin aut Hubert Schelzig verfasserin aut Markus Udo Wagenhäuser verfasserin aut In Journal of Cardiovascular Development and Disease MDPI AG, 2014 11(2023), 1, p 6 (DE-627)790616017 (DE-600)2777082-5 23083425 nnns volume:11 year:2023 number:1, p 6 https://doi.org/10.3390/jcdd11010006 kostenfrei https://doaj.org/article/7ddd34f6b7c04b5eaf872ec8e1d12db5 kostenfrei https://www.mdpi.com/2308-3425/11/1/6 kostenfrei https://doaj.org/toc/2308-3425 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_2014 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 11 2023 1, p 6
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callnumber-first	R - Medicine
author	Sönke Maximilian Braß
spellingShingle	Sönke Maximilian Braß misc RC666-701 misc galectin misc nicotine misc endothelial cells misc aortic pathologies misc Diseases of the circulatory (Cardiovascular) system Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<
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topic_title	RC666-701 Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i< galectin nicotine endothelial cells aortic pathologies
topic	misc RC666-701 misc galectin misc nicotine misc endothelial cells misc aortic pathologies misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc galectin misc nicotine misc endothelial cells misc aortic pathologies misc Diseases of the circulatory (Cardiovascular) system
topic_browse	misc RC666-701 misc galectin misc nicotine misc endothelial cells misc aortic pathologies misc Diseases of the circulatory (Cardiovascular) system
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title	Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<
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title_full	Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<
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author_browse	Sönke Maximilian Braß Agnesa Mazrekaj Joscha Mulorz Wiebke Ibing Kim-Jürgen Krott Kiku Takeuchi Melanie Cappallo Hsiang-Han Liu Margitta Elvers Hubert Schelzig Markus Udo Wagenhäuser
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author-letter	Sönke Maximilian Braß
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title_sort	nicotine potentially alters endothelial inflammation and cell adhesion via <i<lgals9</i<
callnumber	RC666-701
title_auth	Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<
abstract	Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies.
abstractGer	Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies.
abstract_unstemmed	Background: The endothelial cell layer is essential for the maintenance of various blood vessel functions. Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. Conclusion: Nic exposure of HAoECs causes a significant increase in <i<LGALS9</i< at a transcriptional level. <i<LGALS9</i< itself may serve as key regulator for essential endothelial cell processes via interfering with various signaling pathways and may thus represent a potentially novel target in the pathogenesis of aortic pathologies.
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container_issue	1, p 6
title_short	Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<
url	https://doi.org/10.3390/jcdd11010006 https://doaj.org/article/7ddd34f6b7c04b5eaf872ec8e1d12db5 https://www.mdpi.com/2308-3425/11/1/6 https://doaj.org/toc/2308-3425
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Major risk factors for endothelial dysfunction that contribute to aortic pathologies such as abdominal aortic aneurysm (AAA) and aortic dissection (AD) include smoking tobacco cigarettes and hypertension. This study explores the effects of nicotine (Nic) and angiotensin II (Ang II) on human aortic endothelial cells (HAoECs) at a transcriptional level. Methods: HAoECs were exposed to 100 nM Nic and/or 100 nM Ang II. RNA sequencing (RNA-Seq) was performed to identify regulated genes following exposure. Results were validated applying RT-qPCR. GeneMANIA was used to perform in silico analysis aiming to identify potential downstream interacting genes in inflammatory, cell-adhesion, endothelial cell proliferation, and coagulation pathways. Results: RNA-Seq identified <i<LGALS9</i< (Galectin-9) as being potentially regulated following Nic exposure, while subsequent RT-qPCR experiments confirmed the transcriptional regulation (<i<p</i< < 0.05). Subsequent in silico analysis identified potential candidate genes for interacting with <i<LGALS9</i< in different gene sets. Of the top 100 genes potentially interacting with <i<LGALS9</i<, 18 were inflammatory response genes, 28 were involved in cell adhesion, 2 in cell proliferation, and 6 in coagulation. 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Nicotine Potentially Alters Endothelial Inflammation and Cell Adhesion via <i<LGALS9</i<

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