Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways
Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wang, Lei [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020transfer abstract |
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| Umfang: |
14 |
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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:156 ; year:2020 ; day:20 ; month:08 ; pages:176-189 ; extent:14 |
| Links: |
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| DOI / URN: |
10.1016/j.freeradbiomed.2020.06.004 |
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| 520 | |a Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. | ||
| 520 | |a Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. | ||
| 650 | 7 | |a RNA sequencing |2 Elsevier | |
| 650 | 7 | |a Age-related macular degeneration |2 Elsevier | |
| 650 | 7 | |a Aging |2 Elsevier | |
| 650 | 7 | |a Innate immunity |2 Elsevier | |
| 650 | 7 | |a Differentiation |2 Elsevier | |
| 650 | 7 | |a Smoking |2 Elsevier | |
| 700 | 1 | |a Kaya, Koray D. |4 oth | |
| 700 | 1 | |a Kim, Sujung |4 oth | |
| 700 | 1 | |a Brooks, Matthew J. |4 oth | |
| 700 | 1 | |a Wang, Jie |4 oth | |
| 700 | 1 | |a Xin, Ying |4 oth | |
| 700 | 1 | |a Qian, Jiang |4 oth | |
| 700 | 1 | |a Swaroop, Anand |4 oth | |
| 700 | 1 | |a Handa, James T. |4 oth | |
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10.1016/j.freeradbiomed.2020.06.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001137.pica (DE-627)ELV051073226 (ELSEVIER)S0891-5849(20)31092-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Wang, Lei verfasserin aut Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways 2020transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. RNA sequencing Elsevier Age-related macular degeneration Elsevier Aging Elsevier Innate immunity Elsevier Differentiation Elsevier Smoking Elsevier Kaya, Koray D. oth Kim, Sujung oth Brooks, Matthew J. oth Wang, Jie oth Xin, Ying oth Qian, Jiang oth Swaroop, Anand oth Handa, James T. 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:156 year:2020 day:20 month:08 pages:176-189 extent:14 https://doi.org/10.1016/j.freeradbiomed.2020.06.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 156 2020 20 0820 176-189 14 |
| spelling |
10.1016/j.freeradbiomed.2020.06.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001137.pica (DE-627)ELV051073226 (ELSEVIER)S0891-5849(20)31092-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Wang, Lei verfasserin aut Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways 2020transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. RNA sequencing Elsevier Age-related macular degeneration Elsevier Aging Elsevier Innate immunity Elsevier Differentiation Elsevier Smoking Elsevier Kaya, Koray D. oth Kim, Sujung oth Brooks, Matthew J. oth Wang, Jie oth Xin, Ying oth Qian, Jiang oth Swaroop, Anand oth Handa, James T. 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:156 year:2020 day:20 month:08 pages:176-189 extent:14 https://doi.org/10.1016/j.freeradbiomed.2020.06.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 156 2020 20 0820 176-189 14 |
| allfields_unstemmed |
10.1016/j.freeradbiomed.2020.06.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001137.pica (DE-627)ELV051073226 (ELSEVIER)S0891-5849(20)31092-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Wang, Lei verfasserin aut Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways 2020transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. RNA sequencing Elsevier Age-related macular degeneration Elsevier Aging Elsevier Innate immunity Elsevier Differentiation Elsevier Smoking Elsevier Kaya, Koray D. oth Kim, Sujung oth Brooks, Matthew J. oth Wang, Jie oth Xin, Ying oth Qian, Jiang oth Swaroop, Anand oth Handa, James T. 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:156 year:2020 day:20 month:08 pages:176-189 extent:14 https://doi.org/10.1016/j.freeradbiomed.2020.06.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 156 2020 20 0820 176-189 14 |
| allfieldsGer |
10.1016/j.freeradbiomed.2020.06.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001137.pica (DE-627)ELV051073226 (ELSEVIER)S0891-5849(20)31092-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Wang, Lei verfasserin aut Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways 2020transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. RNA sequencing Elsevier Age-related macular degeneration Elsevier Aging Elsevier Innate immunity Elsevier Differentiation Elsevier Smoking Elsevier Kaya, Koray D. oth Kim, Sujung oth Brooks, Matthew J. oth Wang, Jie oth Xin, Ying oth Qian, Jiang oth Swaroop, Anand oth Handa, James T. 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:156 year:2020 day:20 month:08 pages:176-189 extent:14 https://doi.org/10.1016/j.freeradbiomed.2020.06.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 156 2020 20 0820 176-189 14 |
| allfieldsSound |
10.1016/j.freeradbiomed.2020.06.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001137.pica (DE-627)ELV051073226 (ELSEVIER)S0891-5849(20)31092-3 DE-627 ger DE-627 rakwb eng 620 VZ 52.57 bkl 53.36 bkl Wang, Lei verfasserin aut Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways 2020transfer abstract 14 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. RNA sequencing Elsevier Age-related macular degeneration Elsevier Aging Elsevier Innate immunity Elsevier Differentiation Elsevier Smoking Elsevier Kaya, Koray D. oth Kim, Sujung oth Brooks, Matthew J. oth Wang, Jie oth Xin, Ying oth Qian, Jiang oth Swaroop, Anand oth Handa, James T. 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:156 year:2020 day:20 month:08 pages:176-189 extent:14 https://doi.org/10.1016/j.freeradbiomed.2020.06.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 156 2020 20 0820 176-189 14 |
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Enthalten in New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells New York, NY [u.a.] volume:156 year:2020 day:20 month:08 pages:176-189 extent:14 |
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Enthalten in New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells New York, NY [u.a.] volume:156 year:2020 day:20 month:08 pages:176-189 extent:14 |
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New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells |
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retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways |
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Retinal pigment epithelium transcriptome analysis in chronic smoking reveals a suppressed innate immune response and activation of differentiation pathways |
| abstract |
Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. |
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Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. |
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Cigarette smoking, a powerful mixture of chemical oxidants, is the strongest environmental risk factor for developing age-related macular degeneration (AMD), the most common cause of blindness among the elderly in western societies. Despite intensive study, the full impact of smoking on the retinal pigment epithelium (RPE), a central cell type involved in AMD pathobiology, remains unknown. The relative contribution of the known dysfunctional pathways to AMD, at what stage they are most pathogenic, or whether other processes are relevant, is poorly understood, and furthermore, whether smoking activates them, is unknown. We performed global RNA-sequencing of the RPE from C57BL/6J mice exposed to chronic cigarette smoke for 6 months to identify potential pathogenic and cytoprotective pathways. The RPE transcriptome induced by chronic cigarette smoking exhibited a mixed response of marked suppression of the innate immune response including type I and II interferons and upregulation of cell differentiation and morphogenic gene clusters, suggesting an attempt by the RPE to maintain its differentiated state despite smoke-induced injury. Given that mice exposed to chronic smoke develop early features of AMD, these novel findings are potentially relevant to the transition from aging to AMD. |
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Kaya, Koray D. Kim, Sujung Brooks, Matthew J. Wang, Jie Xin, Ying Qian, Jiang Swaroop, Anand Handa, James T. |
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