Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms

AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced i...
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Autor*in:	Weilai Fu [verfasserIn] Haole Liu [verfasserIn] Panpan Wei [verfasserIn] Congcong Xia [verfasserIn] Qingqing Yu [verfasserIn] Kangli Tian [verfasserIn] Yankui Li [verfasserIn] Enqi Liu [verfasserIn] Baohui Xu [verfasserIn] Masaaki Miyata [verfasserIn] Rong Wang [verfasserIn] Sihai Zhao [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	abdominal aortic aneurysm protein inhibitor of activated STAT3 inflammation macrophage animal model

Übergeordnetes Werk:	In: Frontiers in Cardiovascular Medicine - Frontiers Media S.A., 2015, 10(2023)
Übergeordnetes Werk:	volume:10 ; year:2023

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fcvm.2023.1092555

Katalog-ID:	DOAJ08858917X

Internformat


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520			\|a AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis.
650		4	\|a abdominal aortic aneurysm
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700	0		\|a Panpan Wei \|e verfasserin \|4 aut
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700	0		\|a Congcong Xia \|e verfasserin \|4 aut
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allfields	10.3389/fcvm.2023.1092555 doi (DE-627)DOAJ08858917X (DE-599)DOAJ962ac1dea1284d8ebe20808f17cf4d72 DE-627 ger DE-627 rakwb eng RC666-701 Weilai Fu verfasserin aut Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis. abdominal aortic aneurysm protein inhibitor of activated STAT3 inflammation macrophage animal model Diseases of the circulatory (Cardiovascular) system Weilai Fu verfasserin aut Haole Liu verfasserin aut Panpan Wei verfasserin aut Panpan Wei verfasserin aut Congcong Xia verfasserin aut Congcong Xia verfasserin aut Qingqing Yu verfasserin aut Kangli Tian verfasserin aut Yankui Li verfasserin aut Enqi Liu verfasserin aut Baohui Xu verfasserin aut Masaaki Miyata verfasserin aut Rong Wang verfasserin aut Sihai Zhao verfasserin aut Sihai Zhao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 10(2023) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:10 year:2023 https://doi.org/10.3389/fcvm.2023.1092555 kostenfrei https://doaj.org/article/962ac1dea1284d8ebe20808f17cf4d72 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2023.1092555/full kostenfrei https://doaj.org/toc/2297-055X 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_2003 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 10 2023
spelling	10.3389/fcvm.2023.1092555 doi (DE-627)DOAJ08858917X (DE-599)DOAJ962ac1dea1284d8ebe20808f17cf4d72 DE-627 ger DE-627 rakwb eng RC666-701 Weilai Fu verfasserin aut Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis. abdominal aortic aneurysm protein inhibitor of activated STAT3 inflammation macrophage animal model Diseases of the circulatory (Cardiovascular) system Weilai Fu verfasserin aut Haole Liu verfasserin aut Panpan Wei verfasserin aut Panpan Wei verfasserin aut Congcong Xia verfasserin aut Congcong Xia verfasserin aut Qingqing Yu verfasserin aut Kangli Tian verfasserin aut Yankui Li verfasserin aut Enqi Liu verfasserin aut Baohui Xu verfasserin aut Masaaki Miyata verfasserin aut Rong Wang verfasserin aut Sihai Zhao verfasserin aut Sihai Zhao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 10(2023) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:10 year:2023 https://doi.org/10.3389/fcvm.2023.1092555 kostenfrei https://doaj.org/article/962ac1dea1284d8ebe20808f17cf4d72 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2023.1092555/full kostenfrei https://doaj.org/toc/2297-055X 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_2003 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 10 2023
allfields_unstemmed	10.3389/fcvm.2023.1092555 doi (DE-627)DOAJ08858917X (DE-599)DOAJ962ac1dea1284d8ebe20808f17cf4d72 DE-627 ger DE-627 rakwb eng RC666-701 Weilai Fu verfasserin aut Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis. abdominal aortic aneurysm protein inhibitor of activated STAT3 inflammation macrophage animal model Diseases of the circulatory (Cardiovascular) system Weilai Fu verfasserin aut Haole Liu verfasserin aut Panpan Wei verfasserin aut Panpan Wei verfasserin aut Congcong Xia verfasserin aut Congcong Xia verfasserin aut Qingqing Yu verfasserin aut Kangli Tian verfasserin aut Yankui Li verfasserin aut Enqi Liu verfasserin aut Baohui Xu verfasserin aut Masaaki Miyata verfasserin aut Rong Wang verfasserin aut Sihai Zhao verfasserin aut Sihai Zhao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 10(2023) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:10 year:2023 https://doi.org/10.3389/fcvm.2023.1092555 kostenfrei https://doaj.org/article/962ac1dea1284d8ebe20808f17cf4d72 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2023.1092555/full kostenfrei https://doaj.org/toc/2297-055X 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_2003 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 10 2023
allfieldsGer	10.3389/fcvm.2023.1092555 doi (DE-627)DOAJ08858917X (DE-599)DOAJ962ac1dea1284d8ebe20808f17cf4d72 DE-627 ger DE-627 rakwb eng RC666-701 Weilai Fu verfasserin aut Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis. abdominal aortic aneurysm protein inhibitor of activated STAT3 inflammation macrophage animal model Diseases of the circulatory (Cardiovascular) system Weilai Fu verfasserin aut Haole Liu verfasserin aut Panpan Wei verfasserin aut Panpan Wei verfasserin aut Congcong Xia verfasserin aut Congcong Xia verfasserin aut Qingqing Yu verfasserin aut Kangli Tian verfasserin aut Yankui Li verfasserin aut Enqi Liu verfasserin aut Baohui Xu verfasserin aut Masaaki Miyata verfasserin aut Rong Wang verfasserin aut Sihai Zhao verfasserin aut Sihai Zhao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 10(2023) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:10 year:2023 https://doi.org/10.3389/fcvm.2023.1092555 kostenfrei https://doaj.org/article/962ac1dea1284d8ebe20808f17cf4d72 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2023.1092555/full kostenfrei https://doaj.org/toc/2297-055X 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_2003 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 10 2023
allfieldsSound	10.3389/fcvm.2023.1092555 doi (DE-627)DOAJ08858917X (DE-599)DOAJ962ac1dea1284d8ebe20808f17cf4d72 DE-627 ger DE-627 rakwb eng RC666-701 Weilai Fu verfasserin aut Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis. abdominal aortic aneurysm protein inhibitor of activated STAT3 inflammation macrophage animal model Diseases of the circulatory (Cardiovascular) system Weilai Fu verfasserin aut Haole Liu verfasserin aut Panpan Wei verfasserin aut Panpan Wei verfasserin aut Congcong Xia verfasserin aut Congcong Xia verfasserin aut Qingqing Yu verfasserin aut Kangli Tian verfasserin aut Yankui Li verfasserin aut Enqi Liu verfasserin aut Baohui Xu verfasserin aut Masaaki Miyata verfasserin aut Rong Wang verfasserin aut Sihai Zhao verfasserin aut Sihai Zhao verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 10(2023) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:10 year:2023 https://doi.org/10.3389/fcvm.2023.1092555 kostenfrei https://doaj.org/article/962ac1dea1284d8ebe20808f17cf4d72 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2023.1092555/full kostenfrei https://doaj.org/toc/2297-055X 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_2003 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 10 2023
language	English
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authorswithroles_txt_mv	Weilai Fu @@aut@@ Haole Liu @@aut@@ Panpan Wei @@aut@@ Congcong Xia @@aut@@ Qingqing Yu @@aut@@ Kangli Tian @@aut@@ Yankui Li @@aut@@ Enqi Liu @@aut@@ Baohui Xu @@aut@@ Masaaki Miyata @@aut@@ Rong Wang @@aut@@ Sihai Zhao @@aut@@
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callnumber-first	R - Medicine
author	Weilai Fu
spellingShingle	Weilai Fu misc RC666-701 misc abdominal aortic aneurysm misc protein inhibitor of activated STAT3 misc inflammation misc macrophage misc animal model misc Diseases of the circulatory (Cardiovascular) system Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms
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topic_title	RC666-701 Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms abdominal aortic aneurysm protein inhibitor of activated STAT3 inflammation macrophage animal model
topic	misc RC666-701 misc abdominal aortic aneurysm misc protein inhibitor of activated STAT3 misc inflammation misc macrophage misc animal model misc Diseases of the circulatory (Cardiovascular) system
topic_unstemmed	misc RC666-701 misc abdominal aortic aneurysm misc protein inhibitor of activated STAT3 misc inflammation misc macrophage misc animal model misc Diseases of the circulatory (Cardiovascular) system
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title	Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms
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title_full	Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms
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title_sort	genetic deficiency of protein inhibitor of activated stat3 suppresses experimental abdominal aortic aneurysms
callnumber	RC666-701
title_auth	Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms
abstract	AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis.
abstractGer	AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis.
abstract_unstemmed	AimSignal transducer and activator of transcription (STAT) signaling is critical for the pathogenesis of abdominal aortic aneurysms (AAAs). Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis.
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title_short	Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms
url	https://doi.org/10.3389/fcvm.2023.1092555 https://doaj.org/article/962ac1dea1284d8ebe20808f17cf4d72 https://www.frontiersin.org/articles/10.3389/fcvm.2023.1092555/full https://doaj.org/toc/2297-055X
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author2	Weilai Fu Haole Liu Panpan Wei Congcong Xia Qingqing Yu Kangli Tian Yankui Li Enqi Liu Baohui Xu Masaaki Miyata Rong Wang Sihai Zhao
author2Str	Weilai Fu Haole Liu Panpan Wei Congcong Xia Qingqing Yu Kangli Tian Yankui Li Enqi Liu Baohui Xu Masaaki Miyata Rong Wang Sihai Zhao
ppnlink	793951607
callnumber-subject	RC - Internal Medicine
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doi_str	10.3389/fcvm.2023.1092555
callnumber-a	RC666-701
up_date	2024-07-03T18:30:21.399Z
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Though protein inhibitor of activated STAT3 (PIAS3) negatively modulates STAT3 activity, but its role in AAA disease remains undefined.MethodAAAs were induced in PIAS3 deficient (PIAS3−/−) and wild type (PIAS3+/+) male mice via transient intra-aortic elastase infusion. AAAs were assessed by in situ measurements of infrarenal aortic external diameters prior to (day 0) and 14 days after elastase infusion. Characteristic aneurysmal pathologies were evaluated by histopathology.ResultsFourteen days following elastase infusion, aneurysmal aortic diameter was reduced by an approximately 50% in PIAS3−/− as compared to PIAS3+/+ mice. On histological analyses, PIAS3−/− mice showed less medial elastin degradation (media score: 2.5) and smooth muscle cell loss (media score: 3.0) than those in PIAS3+/+ mice (media score: 4 for both elastin and SMC destruction). Aortic wall leukocyte accumulation including macrophages, CD4+ T cells, CD8+ T cells and B cells as well as mural neovessel formation were significantly reduced in PIAS3−/− as compared to PIAS3+/+ mice. Additionally, PIAS3 deficiency also downregulated the expression levels of matrix metalloproteinases 2 and 9 by 61% and 70%, respectively, in aneurysmal lesion.ConclusionPIAS3 deficiency ameliorated experimental AAAs in conjunction with reduced medial elastin degradation and smooth muscle cell depletion, mural leukocyte accumulation and angiogenesis.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">abdominal aortic aneurysm</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">protein inhibitor of activated STAT3</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">inflammation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">macrophage</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">animal model</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) 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Genetic deficiency of protein inhibitor of activated STAT3 suppresses experimental abdominal aortic aneurysms

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