Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway
Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohep...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kim, Hyo Jeong [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Schlagwörter: |
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| Umfang: |
11 |
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| Übergeordnetes Werk: |
Enthalten in: New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells - Wu, Zhi-Sheng ELSEVIER, 2020, the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research, New York, NY [u.a.] |
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| Übergeordnetes Werk: |
volume:110 ; year:2017 ; pages:81-91 ; extent:11 |
| Links: |
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| DOI / URN: |
10.1016/j.freeradbiomed.2017.05.026 |
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| Katalog-ID: |
ELV015232182 |
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| 245 | 1 | 0 | |a Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway |
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| 520 | |a Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. | ||
| 520 | |a Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. | ||
| 650 | 7 | |a NAFLD |2 Elsevier | |
| 650 | 7 | |a p70S6K |2 Elsevier | |
| 650 | 7 | |a HFD |2 Elsevier | |
| 650 | 7 | |a HO |2 Elsevier | |
| 650 | 7 | |a qRT-PCR |2 Elsevier | |
| 650 | 7 | |a PERK |2 Elsevier | |
| 650 | 7 | |a CO |2 Elsevier | |
| 650 | 7 | |a NASH |2 Elsevier | |
| 650 | 7 | |a ER |2 Elsevier | |
| 650 | 7 | |a MCD |2 Elsevier | |
| 650 | 7 | |a MEF |2 Elsevier | |
| 650 | 7 | |a eIF2α |2 Elsevier | |
| 650 | 7 | |a S6 RP |2 Elsevier | |
| 650 | 7 | |a TG |2 Elsevier | |
| 650 | 7 | |a SESN2 |2 Elsevier | |
| 650 | 7 | |a CORM |2 Elsevier | |
| 650 | 7 | |a AMPK |2 Elsevier | |
| 650 | 7 | |a CHOP |2 Elsevier | |
| 650 | 7 | |a Atg7 |2 Elsevier | |
| 650 | 7 | |a mTORC1 |2 Elsevier | |
| 650 | 7 | |a ATF4 |2 Elsevier | |
| 700 | 1 | |a Joe, Yeonsoo |4 oth | |
| 700 | 1 | |a Kim, Seul-Ki |4 oth | |
| 700 | 1 | |a Park, Se-Ung |4 oth | |
| 700 | 1 | |a Park, Jeongmin |4 oth | |
| 700 | 1 | |a Chen, Yingqing |4 oth | |
| 700 | 1 | |a Kim, Jin |4 oth | |
| 700 | 1 | |a Ryu, Jinhyun |4 oth | |
| 700 | 1 | |a Cho, Gyeong Jae |4 oth | |
| 700 | 1 | |a Surh, Young-Joon |4 oth | |
| 700 | 1 | |a Ryter, Stefan W. |4 oth | |
| 700 | 1 | |a Kim, Uh-Hyun |4 oth | |
| 700 | 1 | |a Chung, Hun-Taeg |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Wu, Zhi-Sheng ELSEVIER |t New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells |d 2020 |d the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research |g New York, NY [u.a.] |w (DE-627)ELV003689417 |
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10.1016/j.freeradbiomed.2017.05.026 doi GBVA2017014000025.pica (DE-627)ELV015232182 (ELSEVIER)S0891-5849(17)30610-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Kim, Hyo Jeong verfasserin aut Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. NAFLD Elsevier p70S6K Elsevier HFD Elsevier HO Elsevier qRT-PCR Elsevier PERK Elsevier CO Elsevier NASH Elsevier ER Elsevier MCD Elsevier MEF Elsevier eIF2α Elsevier S6 RP Elsevier TG Elsevier SESN2 Elsevier CORM Elsevier AMPK Elsevier CHOP Elsevier Atg7 Elsevier mTORC1 Elsevier ATF4 Elsevier Joe, Yeonsoo oth Kim, Seul-Ki oth Park, Se-Ung oth Park, Jeongmin oth Chen, Yingqing oth Kim, Jin oth Ryu, Jinhyun oth Cho, Gyeong Jae oth Surh, Young-Joon oth Ryter, Stefan W. oth Kim, Uh-Hyun oth Chung, Hun-Taeg oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:110 year:2017 pages:81-91 extent:11 https://doi.org/10.1016/j.freeradbiomed.2017.05.026 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 110 2017 81-91 11 045F 570 |
| spelling |
10.1016/j.freeradbiomed.2017.05.026 doi GBVA2017014000025.pica (DE-627)ELV015232182 (ELSEVIER)S0891-5849(17)30610-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Kim, Hyo Jeong verfasserin aut Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. NAFLD Elsevier p70S6K Elsevier HFD Elsevier HO Elsevier qRT-PCR Elsevier PERK Elsevier CO Elsevier NASH Elsevier ER Elsevier MCD Elsevier MEF Elsevier eIF2α Elsevier S6 RP Elsevier TG Elsevier SESN2 Elsevier CORM Elsevier AMPK Elsevier CHOP Elsevier Atg7 Elsevier mTORC1 Elsevier ATF4 Elsevier Joe, Yeonsoo oth Kim, Seul-Ki oth Park, Se-Ung oth Park, Jeongmin oth Chen, Yingqing oth Kim, Jin oth Ryu, Jinhyun oth Cho, Gyeong Jae oth Surh, Young-Joon oth Ryter, Stefan W. oth Kim, Uh-Hyun oth Chung, Hun-Taeg oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:110 year:2017 pages:81-91 extent:11 https://doi.org/10.1016/j.freeradbiomed.2017.05.026 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 110 2017 81-91 11 045F 570 |
| allfields_unstemmed |
10.1016/j.freeradbiomed.2017.05.026 doi GBVA2017014000025.pica (DE-627)ELV015232182 (ELSEVIER)S0891-5849(17)30610-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Kim, Hyo Jeong verfasserin aut Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. NAFLD Elsevier p70S6K Elsevier HFD Elsevier HO Elsevier qRT-PCR Elsevier PERK Elsevier CO Elsevier NASH Elsevier ER Elsevier MCD Elsevier MEF Elsevier eIF2α Elsevier S6 RP Elsevier TG Elsevier SESN2 Elsevier CORM Elsevier AMPK Elsevier CHOP Elsevier Atg7 Elsevier mTORC1 Elsevier ATF4 Elsevier Joe, Yeonsoo oth Kim, Seul-Ki oth Park, Se-Ung oth Park, Jeongmin oth Chen, Yingqing oth Kim, Jin oth Ryu, Jinhyun oth Cho, Gyeong Jae oth Surh, Young-Joon oth Ryter, Stefan W. oth Kim, Uh-Hyun oth Chung, Hun-Taeg oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:110 year:2017 pages:81-91 extent:11 https://doi.org/10.1016/j.freeradbiomed.2017.05.026 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 110 2017 81-91 11 045F 570 |
| allfieldsGer |
10.1016/j.freeradbiomed.2017.05.026 doi GBVA2017014000025.pica (DE-627)ELV015232182 (ELSEVIER)S0891-5849(17)30610-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Kim, Hyo Jeong verfasserin aut Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. NAFLD Elsevier p70S6K Elsevier HFD Elsevier HO Elsevier qRT-PCR Elsevier PERK Elsevier CO Elsevier NASH Elsevier ER Elsevier MCD Elsevier MEF Elsevier eIF2α Elsevier S6 RP Elsevier TG Elsevier SESN2 Elsevier CORM Elsevier AMPK Elsevier CHOP Elsevier Atg7 Elsevier mTORC1 Elsevier ATF4 Elsevier Joe, Yeonsoo oth Kim, Seul-Ki oth Park, Se-Ung oth Park, Jeongmin oth Chen, Yingqing oth Kim, Jin oth Ryu, Jinhyun oth Cho, Gyeong Jae oth Surh, Young-Joon oth Ryter, Stefan W. oth Kim, Uh-Hyun oth Chung, Hun-Taeg oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:110 year:2017 pages:81-91 extent:11 https://doi.org/10.1016/j.freeradbiomed.2017.05.026 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 110 2017 81-91 11 045F 570 |
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10.1016/j.freeradbiomed.2017.05.026 doi GBVA2017014000025.pica (DE-627)ELV015232182 (ELSEVIER)S0891-5849(17)30610-X DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Kim, Hyo Jeong verfasserin aut Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. NAFLD Elsevier p70S6K Elsevier HFD Elsevier HO Elsevier qRT-PCR Elsevier PERK Elsevier CO Elsevier NASH Elsevier ER Elsevier MCD Elsevier MEF Elsevier eIF2α Elsevier S6 RP Elsevier TG Elsevier SESN2 Elsevier CORM Elsevier AMPK Elsevier CHOP Elsevier Atg7 Elsevier mTORC1 Elsevier ATF4 Elsevier Joe, Yeonsoo oth Kim, Seul-Ki oth Park, Se-Ung oth Park, Jeongmin oth Chen, Yingqing oth Kim, Jin oth Ryu, Jinhyun oth Cho, Gyeong Jae oth Surh, Young-Joon oth Ryter, Stefan W. oth Kim, Uh-Hyun oth Chung, Hun-Taeg oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:110 year:2017 pages:81-91 extent:11 https://doi.org/10.1016/j.freeradbiomed.2017.05.026 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 110 2017 81-91 11 045F 570 |
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Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway |
| abstract |
Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. |
| abstractGer |
Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. |
| abstract_unstemmed |
Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome, has emerged as one of the most common causes of chronic liver disease in developed countries over the last decade. NAFLD comprises a spectrum of pathological hepatic changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, a homeostatic process for protein and organelle turnover, is decreased in the liver during the development of NAFLD. Previously, we have shown that carbon monoxide (CO), a reaction product of heme oxygenase (HO) activity, can confer protection in NAFLD, though the molecular mechanisms remain unclear. We therefore investigated the mechanisms underlying the protective effect of CO on methionine/choline-deficient (MCD) diet-induced hepatic steatosis. We found that CO induced sestrin-2 (SESN2) expression through enhanced mitochondrial ROS production and protected against MCD-induced NAFLD progression through activation of autophagy. SESN2 expression was increased by CO or CO-releasing molecule (CORM2), in a manner dependent on signaling through the protein kinase R-like endoplasmic reticulum kinase (PERK), eukaryotic initiation factor-2 alpha (eIF2α)/ activating transcription factor-4 (ATF4)-dependent pathway. CO-induced SESN2 upregulation in hepatocytes contributed to autophagy induction through activation of 5'-AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) complex I (mTORC1). Furthermore, we demonstrate that CO significantly induced the expression of SESN2 and enhanced autophagy in the livers of MCD-fed mice or in MCD-media treated hepatocytes. Conversely, knockdown of SESN2 abrogated autophagy activation and mTOR inhibition in response to CO. We conclude that CO ameliorates hepatic steatosis through the autophagy pathway induced by SESN2 upregulation. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U |
| title_short |
Carbon monoxide protects against hepatic steatosis in mice by inducing sestrin-2 via the PERK-eIF2α-ATF4 pathway |
| url |
https://doi.org/10.1016/j.freeradbiomed.2017.05.026 |
| remote_bool |
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| author2 |
Joe, Yeonsoo Kim, Seul-Ki Park, Se-Ung Park, Jeongmin Chen, Yingqing Kim, Jin Ryu, Jinhyun Cho, Gyeong Jae Surh, Young-Joon Ryter, Stefan W. Kim, Uh-Hyun Chung, Hun-Taeg |
| author2Str |
Joe, Yeonsoo Kim, Seul-Ki Park, Se-Ung Park, Jeongmin Chen, Yingqing Kim, Jin Ryu, Jinhyun Cho, Gyeong Jae Surh, Young-Joon Ryter, Stefan W. Kim, Uh-Hyun Chung, Hun-Taeg |
| ppnlink |
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| doi_str |
10.1016/j.freeradbiomed.2017.05.026 |
| up_date |
2024-07-06T17:06:41.263Z |
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