Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury

Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regula...
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Autor*in:	Lv, Jiawen [verfasserIn] Zeng, Junchao Guo, Fukun Li, Yiran Xu, Mengying Cheng, Yuanxiong Zhang, Lin Cai, Shaoxi Chen, Yinghua Zheng, Yi Hu, Guodong

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	ALI/ARDS Pulmonary microvascular injury and repair Cre/Loxp technique Cdc42 PAK1/AKT pathway

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: Respiratory research - London : BioMed Central, 2001, 19(2018), 1 vom: 08. Feb.
Übergeordnetes Werk:	volume:19 ; year:2018 ; number:1 ; day:08 ; month:02

Links:	Volltext

DOI / URN:	10.1186/s12931-018-0729-8

Katalog-ID:	SPR028524845

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520			\|a Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS.
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Indexfelder

author_variant	j l jl j z jz f g fg y l yl m x mx y c yc l z lz s c sc y c yc y z yz g h gh
matchkey_str	article:1465993X:2018----::nohlacc2eiinymaredteileeeainnvsuarpiatr
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publishDate	2018
allfields	10.1186/s12931-018-0729-8 doi (DE-627)SPR028524845 (SPR)s12931-018-0729-8-e DE-627 ger DE-627 rakwb eng Lv, Jiawen verfasserin aut Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. ALI/ARDS (dpeaa)DE-He213 Pulmonary microvascular injury and repair (dpeaa)DE-He213 Cre/Loxp technique (dpeaa)DE-He213 Cdc42 (dpeaa)DE-He213 PAK1/AKT pathway (dpeaa)DE-He213 Zeng, Junchao aut Guo, Fukun aut Li, Yiran aut Xu, Mengying aut Cheng, Yuanxiong aut Zhang, Lin aut Cai, Shaoxi aut Chen, Yinghua aut Zheng, Yi aut Hu, Guodong aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 08. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:08 month:02 https://dx.doi.org/10.1186/s12931-018-0729-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2153 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 19 2018 1 08 02
spelling	10.1186/s12931-018-0729-8 doi (DE-627)SPR028524845 (SPR)s12931-018-0729-8-e DE-627 ger DE-627 rakwb eng Lv, Jiawen verfasserin aut Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. ALI/ARDS (dpeaa)DE-He213 Pulmonary microvascular injury and repair (dpeaa)DE-He213 Cre/Loxp technique (dpeaa)DE-He213 Cdc42 (dpeaa)DE-He213 PAK1/AKT pathway (dpeaa)DE-He213 Zeng, Junchao aut Guo, Fukun aut Li, Yiran aut Xu, Mengying aut Cheng, Yuanxiong aut Zhang, Lin aut Cai, Shaoxi aut Chen, Yinghua aut Zheng, Yi aut Hu, Guodong aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 08. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:08 month:02 https://dx.doi.org/10.1186/s12931-018-0729-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2153 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 19 2018 1 08 02
allfields_unstemmed	10.1186/s12931-018-0729-8 doi (DE-627)SPR028524845 (SPR)s12931-018-0729-8-e DE-627 ger DE-627 rakwb eng Lv, Jiawen verfasserin aut Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. ALI/ARDS (dpeaa)DE-He213 Pulmonary microvascular injury and repair (dpeaa)DE-He213 Cre/Loxp technique (dpeaa)DE-He213 Cdc42 (dpeaa)DE-He213 PAK1/AKT pathway (dpeaa)DE-He213 Zeng, Junchao aut Guo, Fukun aut Li, Yiran aut Xu, Mengying aut Cheng, Yuanxiong aut Zhang, Lin aut Cai, Shaoxi aut Chen, Yinghua aut Zheng, Yi aut Hu, Guodong aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 08. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:08 month:02 https://dx.doi.org/10.1186/s12931-018-0729-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2153 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 19 2018 1 08 02
allfieldsGer	10.1186/s12931-018-0729-8 doi (DE-627)SPR028524845 (SPR)s12931-018-0729-8-e DE-627 ger DE-627 rakwb eng Lv, Jiawen verfasserin aut Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. ALI/ARDS (dpeaa)DE-He213 Pulmonary microvascular injury and repair (dpeaa)DE-He213 Cre/Loxp technique (dpeaa)DE-He213 Cdc42 (dpeaa)DE-He213 PAK1/AKT pathway (dpeaa)DE-He213 Zeng, Junchao aut Guo, Fukun aut Li, Yiran aut Xu, Mengying aut Cheng, Yuanxiong aut Zhang, Lin aut Cai, Shaoxi aut Chen, Yinghua aut Zheng, Yi aut Hu, Guodong aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 08. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:08 month:02 https://dx.doi.org/10.1186/s12931-018-0729-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2153 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 19 2018 1 08 02
allfieldsSound	10.1186/s12931-018-0729-8 doi (DE-627)SPR028524845 (SPR)s12931-018-0729-8-e DE-627 ger DE-627 rakwb eng Lv, Jiawen verfasserin aut Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. ALI/ARDS (dpeaa)DE-He213 Pulmonary microvascular injury and repair (dpeaa)DE-He213 Cre/Loxp technique (dpeaa)DE-He213 Cdc42 (dpeaa)DE-He213 PAK1/AKT pathway (dpeaa)DE-He213 Zeng, Junchao aut Guo, Fukun aut Li, Yiran aut Xu, Mengying aut Cheng, Yuanxiong aut Zhang, Lin aut Cai, Shaoxi aut Chen, Yinghua aut Zheng, Yi aut Hu, Guodong aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 08. Feb. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:08 month:02 https://dx.doi.org/10.1186/s12931-018-0729-8 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2153 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 19 2018 1 08 02
language	English
source	Enthalten in Respiratory research 19(2018), 1 vom: 08. Feb. volume:19 year:2018 number:1 day:08 month:02
sourceStr	Enthalten in Respiratory research 19(2018), 1 vom: 08. Feb. volume:19 year:2018 number:1 day:08 month:02
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	ALI/ARDS Pulmonary microvascular injury and repair Cre/Loxp technique Cdc42 PAK1/AKT pathway
isfreeaccess_bool	true
container_title	Respiratory research
authorswithroles_txt_mv	Lv, Jiawen @@aut@@ Zeng, Junchao @@aut@@ Guo, Fukun @@aut@@ Li, Yiran @@aut@@ Xu, Mengying @@aut@@ Cheng, Yuanxiong @@aut@@ Zhang, Lin @@aut@@ Cai, Shaoxi @@aut@@ Chen, Yinghua @@aut@@ Zheng, Yi @@aut@@ Hu, Guodong @@aut@@
publishDateDaySort_date	2018-02-08T00:00:00Z
hierarchy_top_id	326646485
id	SPR028524845
language_de	englisch
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author	Lv, Jiawen
spellingShingle	Lv, Jiawen misc ALI/ARDS misc Pulmonary microvascular injury and repair misc Cre/Loxp technique misc Cdc42 misc PAK1/AKT pathway Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury
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topic_title	Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury ALI/ARDS (dpeaa)DE-He213 Pulmonary microvascular injury and repair (dpeaa)DE-He213 Cre/Loxp technique (dpeaa)DE-He213 Cdc42 (dpeaa)DE-He213 PAK1/AKT pathway (dpeaa)DE-He213
topic	misc ALI/ARDS misc Pulmonary microvascular injury and repair misc Cre/Loxp technique misc Cdc42 misc PAK1/AKT pathway
topic_unstemmed	misc ALI/ARDS misc Pulmonary microvascular injury and repair misc Cre/Loxp technique misc Cdc42 misc PAK1/AKT pathway
topic_browse	misc ALI/ARDS misc Pulmonary microvascular injury and repair misc Cre/Loxp technique misc Cdc42 misc PAK1/AKT pathway
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title	Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury
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title_full	Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury
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author_browse	Lv, Jiawen Zeng, Junchao Guo, Fukun Li, Yiran Xu, Mengying Cheng, Yuanxiong Zhang, Lin Cai, Shaoxi Chen, Yinghua Zheng, Yi Hu, Guodong
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title_sort	endothelial cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury
title_auth	Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury
abstract	Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. © The Author(s). 2018
abstractGer	Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. © The Author(s). 2018
abstract_unstemmed	Background Endothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury. Methods and results The role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects. Conclusion We found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS. © The Author(s). 2018
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title_short	Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury
url	https://dx.doi.org/10.1186/s12931-018-0729-8
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author2	Zeng, Junchao Guo, Fukun Li, Yiran Xu, Mengying Cheng, Yuanxiong Zhang, Lin Cai, Shaoxi Chen, Yinghua Zheng, Yi Hu, Guodong
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up_date	2024-07-03T19:59:24.043Z
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Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury

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