The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress

Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SD...
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Autor*in:	Huan Wang [verfasserIn] Yang Yang [verfasserIn] Haibo Chen [verfasserIn] Juhua Dan [verfasserIn] Jiali Cheng [verfasserIn] Shuyuan Guo [verfasserIn] Xin Sun [verfasserIn] Wei Wang [verfasserIn] Yiwei Ai [verfasserIn] Shuchang Li [verfasserIn] Zhixin Li [verfasserIn] Li Peng [verfasserIn] Zhen Tian [verfasserIn] Liming Yang [verfasserIn] Jichao Wu [verfasserIn] Xin Zhong [verfasserIn] Qi Zhou [verfasserIn] Peng Wang [verfasserIn] Zhiguo Zhang [verfasserIn] Wenwu Cao [verfasserIn] Ye Tian [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2014

Schlagwörter:	Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species

Übergeordnetes Werk:	In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 33(2014), 6, Seite 1789-1801
Übergeordnetes Werk:	volume:33 ; year:2014 ; number:6 ; pages:1789-1801

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000362958

Katalog-ID:	DOAJ019529813

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245	1	4	\|a The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress
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520			\|a Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in.
650		4	\|a Foam cell
650		4	\|a Apoptosis
650		4	\|a 5-aminolevulinic acid
650		4	\|a Sonodynamic therapy
650		4	\|a Mitochondria pathway
650		4	\|a ER stress
650		4	\|a Atherosclerosis
650		4	\|a Reactive oxygen species
653		0	\|a Physiology
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700	0		\|a Haibo Chen \|e verfasserin \|4 aut
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700	0		\|a Xin Sun \|e verfasserin \|4 aut
700	0		\|a Wei Wang \|e verfasserin \|4 aut
700	0		\|a Yiwei Ai \|e verfasserin \|4 aut
700	0		\|a Shuchang Li \|e verfasserin \|4 aut
700	0		\|a Zhixin Li \|e verfasserin \|4 aut
700	0		\|a Li Peng \|e verfasserin \|4 aut
700	0		\|a Zhen Tian \|e verfasserin \|4 aut
700	0		\|a Liming Yang \|e verfasserin \|4 aut
700	0		\|a Jichao Wu \|e verfasserin \|4 aut
700	0		\|a Xin Zhong \|e verfasserin \|4 aut
700	0		\|a Qi Zhou \|e verfasserin \|4 aut
700	0		\|a Peng Wang \|e verfasserin \|4 aut
700	0		\|a Zhiguo Zhang \|e verfasserin \|4 aut
700	0		\|a Wenwu Cao \|e verfasserin \|4 aut
700	0		\|a Ye Tian \|e verfasserin \|4 aut
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allfields	10.1159/000362958 doi (DE-627)DOAJ019529813 (DE-599)DOAJaabd1e797a4b478f8079ddf6ab0e0f4b DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Huan Wang verfasserin aut The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in. Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species Physiology Biochemistry Yang Yang verfasserin aut Haibo Chen verfasserin aut Juhua Dan verfasserin aut Jiali Cheng verfasserin aut Shuyuan Guo verfasserin aut Xin Sun verfasserin aut Wei Wang verfasserin aut Yiwei Ai verfasserin aut Shuchang Li verfasserin aut Zhixin Li verfasserin aut Li Peng verfasserin aut Zhen Tian verfasserin aut Liming Yang verfasserin aut Jichao Wu verfasserin aut Xin Zhong verfasserin aut Qi Zhou verfasserin aut Peng Wang verfasserin aut Zhiguo Zhang verfasserin aut Wenwu Cao verfasserin aut Ye Tian verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 6, Seite 1789-1801 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:6 pages:1789-1801 https://doi.org/10.1159/000362958 kostenfrei https://doaj.org/article/aabd1e797a4b478f8079ddf6ab0e0f4b kostenfrei http://www.karger.com/Article/FullText/362958 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 33 2014 6 1789-1801
spelling	10.1159/000362958 doi (DE-627)DOAJ019529813 (DE-599)DOAJaabd1e797a4b478f8079ddf6ab0e0f4b DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Huan Wang verfasserin aut The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in. Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species Physiology Biochemistry Yang Yang verfasserin aut Haibo Chen verfasserin aut Juhua Dan verfasserin aut Jiali Cheng verfasserin aut Shuyuan Guo verfasserin aut Xin Sun verfasserin aut Wei Wang verfasserin aut Yiwei Ai verfasserin aut Shuchang Li verfasserin aut Zhixin Li verfasserin aut Li Peng verfasserin aut Zhen Tian verfasserin aut Liming Yang verfasserin aut Jichao Wu verfasserin aut Xin Zhong verfasserin aut Qi Zhou verfasserin aut Peng Wang verfasserin aut Zhiguo Zhang verfasserin aut Wenwu Cao verfasserin aut Ye Tian verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 6, Seite 1789-1801 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:6 pages:1789-1801 https://doi.org/10.1159/000362958 kostenfrei https://doaj.org/article/aabd1e797a4b478f8079ddf6ab0e0f4b kostenfrei http://www.karger.com/Article/FullText/362958 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 33 2014 6 1789-1801
allfields_unstemmed	10.1159/000362958 doi (DE-627)DOAJ019529813 (DE-599)DOAJaabd1e797a4b478f8079ddf6ab0e0f4b DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Huan Wang verfasserin aut The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in. Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species Physiology Biochemistry Yang Yang verfasserin aut Haibo Chen verfasserin aut Juhua Dan verfasserin aut Jiali Cheng verfasserin aut Shuyuan Guo verfasserin aut Xin Sun verfasserin aut Wei Wang verfasserin aut Yiwei Ai verfasserin aut Shuchang Li verfasserin aut Zhixin Li verfasserin aut Li Peng verfasserin aut Zhen Tian verfasserin aut Liming Yang verfasserin aut Jichao Wu verfasserin aut Xin Zhong verfasserin aut Qi Zhou verfasserin aut Peng Wang verfasserin aut Zhiguo Zhang verfasserin aut Wenwu Cao verfasserin aut Ye Tian verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 6, Seite 1789-1801 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:6 pages:1789-1801 https://doi.org/10.1159/000362958 kostenfrei https://doaj.org/article/aabd1e797a4b478f8079ddf6ab0e0f4b kostenfrei http://www.karger.com/Article/FullText/362958 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 33 2014 6 1789-1801
allfieldsGer	10.1159/000362958 doi (DE-627)DOAJ019529813 (DE-599)DOAJaabd1e797a4b478f8079ddf6ab0e0f4b DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Huan Wang verfasserin aut The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in. Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species Physiology Biochemistry Yang Yang verfasserin aut Haibo Chen verfasserin aut Juhua Dan verfasserin aut Jiali Cheng verfasserin aut Shuyuan Guo verfasserin aut Xin Sun verfasserin aut Wei Wang verfasserin aut Yiwei Ai verfasserin aut Shuchang Li verfasserin aut Zhixin Li verfasserin aut Li Peng verfasserin aut Zhen Tian verfasserin aut Liming Yang verfasserin aut Jichao Wu verfasserin aut Xin Zhong verfasserin aut Qi Zhou verfasserin aut Peng Wang verfasserin aut Zhiguo Zhang verfasserin aut Wenwu Cao verfasserin aut Ye Tian verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 6, Seite 1789-1801 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:6 pages:1789-1801 https://doi.org/10.1159/000362958 kostenfrei https://doaj.org/article/aabd1e797a4b478f8079ddf6ab0e0f4b kostenfrei http://www.karger.com/Article/FullText/362958 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 33 2014 6 1789-1801
allfieldsSound	10.1159/000362958 doi (DE-627)DOAJ019529813 (DE-599)DOAJaabd1e797a4b478f8079ddf6ab0e0f4b DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Huan Wang verfasserin aut The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in. Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species Physiology Biochemistry Yang Yang verfasserin aut Haibo Chen verfasserin aut Juhua Dan verfasserin aut Jiali Cheng verfasserin aut Shuyuan Guo verfasserin aut Xin Sun verfasserin aut Wei Wang verfasserin aut Yiwei Ai verfasserin aut Shuchang Li verfasserin aut Zhixin Li verfasserin aut Li Peng verfasserin aut Zhen Tian verfasserin aut Liming Yang verfasserin aut Jichao Wu verfasserin aut Xin Zhong verfasserin aut Qi Zhou verfasserin aut Peng Wang verfasserin aut Zhiguo Zhang verfasserin aut Wenwu Cao verfasserin aut Ye Tian verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 33(2014), 6, Seite 1789-1801 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:33 year:2014 number:6 pages:1789-1801 https://doi.org/10.1159/000362958 kostenfrei https://doaj.org/article/aabd1e797a4b478f8079ddf6ab0e0f4b kostenfrei http://www.karger.com/Article/FullText/362958 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 33 2014 6 1789-1801
language	English
source	In Cellular Physiology and Biochemistry 33(2014), 6, Seite 1789-1801 volume:33 year:2014 number:6 pages:1789-1801
sourceStr	In Cellular Physiology and Biochemistry 33(2014), 6, Seite 1789-1801 volume:33 year:2014 number:6 pages:1789-1801
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species Physiology Biochemistry
isfreeaccess_bool	true
container_title	Cellular Physiology and Biochemistry
authorswithroles_txt_mv	Huan Wang @@aut@@ Yang Yang @@aut@@ Haibo Chen @@aut@@ Juhua Dan @@aut@@ Jiali Cheng @@aut@@ Shuyuan Guo @@aut@@ Xin Sun @@aut@@ Wei Wang @@aut@@ Yiwei Ai @@aut@@ Shuchang Li @@aut@@ Zhixin Li @@aut@@ Li Peng @@aut@@ Zhen Tian @@aut@@ Liming Yang @@aut@@ Jichao Wu @@aut@@ Xin Zhong @@aut@@ Qi Zhou @@aut@@ Peng Wang @@aut@@ Zhiguo Zhang @@aut@@ Wenwu Cao @@aut@@ Ye Tian @@aut@@
publishDateDaySort_date	2014-01-01T00:00:00Z
hierarchy_top_id	300189702
id	DOAJ019529813
language_de	englisch
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Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Foam cell</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Apoptosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">5-aminolevulinic acid</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Sonodynamic therapy</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Mitochondria pathway</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">ER stress</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Atherosclerosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Reactive oxygen species</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Physiology</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Biochemistry</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yang Yang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Haibo Chen</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Juhua Dan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Jiali Cheng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Shuyuan Guo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" 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callnumber-first	Q - Science
author	Huan Wang
spellingShingle	Huan Wang misc QP1-981 misc QD415-436 misc Foam cell misc Apoptosis misc 5-aminolevulinic acid misc Sonodynamic therapy misc Mitochondria pathway misc ER stress misc Atherosclerosis misc Reactive oxygen species misc Physiology misc Biochemistry The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress
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topic_title	QP1-981 QD415-436 The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress Foam cell Apoptosis 5-aminolevulinic acid Sonodynamic therapy Mitochondria pathway ER stress Atherosclerosis Reactive oxygen species
topic	misc QP1-981 misc QD415-436 misc Foam cell misc Apoptosis misc 5-aminolevulinic acid misc Sonodynamic therapy misc Mitochondria pathway misc ER stress misc Atherosclerosis misc Reactive oxygen species misc Physiology misc Biochemistry
topic_unstemmed	misc QP1-981 misc QD415-436 misc Foam cell misc Apoptosis misc 5-aminolevulinic acid misc Sonodynamic therapy misc Mitochondria pathway misc ER stress misc Atherosclerosis misc Reactive oxygen species misc Physiology misc Biochemistry
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title	The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress
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title_full	The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress
author_sort	Huan Wang
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author_browse	Huan Wang Yang Yang Haibo Chen Juhua Dan Jiali Cheng Shuyuan Guo Xin Sun Wei Wang Yiwei Ai Shuchang Li Zhixin Li Li Peng Zhen Tian Liming Yang Jichao Wu Xin Zhong Qi Zhou Peng Wang Zhiguo Zhang Wenwu Cao Ye Tian
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title_sort	predominant pathway of apoptosis in thp-1 macrophage-derived foam cells induced by 5-aminolevulinic acid-mediated sonodynamic therapy is the mitochondria-caspase pathway despite the participation of endoplasmic reticulum stress
callnumber	QP1-981
title_auth	The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress
abstract	Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in.
abstractGer	Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in.
abstract_unstemmed	Background: In advanced atherosclerosis, chronic endoplasmic reticulum (ER) stress induces foam cells apoptosis and generates inflammatory reactions. Methods: THP-1 macrophage-derived foam cells (FC) were incubated with 1 mM 5-aminolevulinic acid (ALA). After ALA mediated sonodynamic therapy (ALA-SDT), apoptosis of FC was assayed by Annexin V-PI staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential were detected by staining with CellROX® Green Reagent and jc-1. Pretreatment of FC with N-acetylcysteine (NAC), Z-VAD-FMK or 4-phenylbutyrate (4-PBA), mitochondria apoptotic pathway associated proteins and C/EBP-homologous (CHOP) expressions were assayed by wertern blotting. Results: Burst of apoptosis of FC was observed at 5-hour after ALA-SDT with 6-hour incubation of ALA and 0.4 W/cm2 ultrasound. After ALA-SDT, intracellular ROS level increased and mitochondrial membrane potential collapsed. Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. Conclusion: The mitochondria-caspase pathway is predominant in the apoptosis of FC induced by ALA-SDT though ER stress participates in.
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title_short	The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress
url	https://doi.org/10.1159/000362958 https://doaj.org/article/aabd1e797a4b478f8079ddf6ab0e0f4b http://www.karger.com/Article/FullText/362958 https://doaj.org/toc/1015-8987 https://doaj.org/toc/1421-9778
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author2	Yang Yang Haibo Chen Juhua Dan Jiali Cheng Shuyuan Guo Xin Sun Wei Wang Yiwei Ai Shuchang Li Zhixin Li Li Peng Zhen Tian Liming Yang Jichao Wu Xin Zhong Qi Zhou Peng Wang Zhiguo Zhang Wenwu Cao Ye Tian
author2Str	Yang Yang Haibo Chen Juhua Dan Jiali Cheng Shuyuan Guo Xin Sun Wei Wang Yiwei Ai Shuchang Li Zhixin Li Li Peng Zhen Tian Liming Yang Jichao Wu Xin Zhong Qi Zhou Peng Wang Zhiguo Zhang Wenwu Cao Ye Tian
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up_date	2024-07-03T23:54:37.275Z
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Translocations of cytochrome c from mitochondria into cytosol and Bax from cytosol into mitochondria, cleaved caspase 9, cleaved caspase 3, upregulation of CHOP, as well as downregulation of Bcl-2 after ALA-SDT were detected, which could be suppressed by NAC. Activation of mitochondria-caspase pathway could not be inhibited by 4-PBA. Cleaved caspase 9 and caspase 3 as well as apoptosis induced by ALA-SDT could be inhibited by Z-VAD-FMK. 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The Predominant Pathway of Apoptosis in THP-1 Macrophage-Derived Foam Cells Induced by 5-Aminolevulinic Acid-Mediated Sonodynamic Therapy is the Mitochondria-Caspase Pathway Despite the Participation of Endoplasmic Reticulum Stress

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