A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics
Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma,...
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| Autor*in: |
Theodore L. Mathuram [verfasserIn] Danyelle M. Townsend [verfasserIn] Vincent J. Lynch [verfasserIn] Ilya Bederman [verfasserIn] Zhi-Wei Ye [verfasserIn] Jie Zhang [verfasserIn] Wade J. Sigurdson [verfasserIn] Erin Prendergast [verfasserIn] Raul Jobava [verfasserIn] Jonathan P. Ferruzza [verfasserIn] Mary R. D’Angelo [verfasserIn] Maria Hatzoglou [verfasserIn] Yaron Perry [verfasserIn] Anna Blumental-Perry [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Frontiers in Physiology - Frontiers Media S.A., 2011, 13(2022) |
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| Übergeordnetes Werk: |
volume:13 ; year:2022 |
| Links: |
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| DOI / URN: |
10.3389/fphys.2022.772313 |
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| Katalog-ID: |
DOAJ008013152 |
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| 520 | |a Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. | ||
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10.3389/fphys.2022.772313 doi (DE-627)DOAJ008013152 (DE-599)DOAJf5dff9159b59448badb5f7f4173eea60 DE-627 ger DE-627 rakwb eng QP1-981 Theodore L. Mathuram verfasserin aut A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. mitochondria mitochondria-to-nucleus retrograde signaling small ncRNA Krebs cycle OxPhos D-loop transcripts Physiology Danyelle M. Townsend verfasserin aut Vincent J. Lynch verfasserin aut Ilya Bederman verfasserin aut Zhi-Wei Ye verfasserin aut Jie Zhang verfasserin aut Wade J. Sigurdson verfasserin aut Erin Prendergast verfasserin aut Raul Jobava verfasserin aut Jonathan P. Ferruzza verfasserin aut Mary R. D’Angelo verfasserin aut Maria Hatzoglou verfasserin aut Yaron Perry verfasserin aut Anna Blumental-Perry verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 13(2022) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:13 year:2022 https://doi.org/10.3389/fphys.2022.772313 kostenfrei https://doaj.org/article/f5dff9159b59448badb5f7f4173eea60 kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2022.772313/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2022 |
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10.3389/fphys.2022.772313 doi (DE-627)DOAJ008013152 (DE-599)DOAJf5dff9159b59448badb5f7f4173eea60 DE-627 ger DE-627 rakwb eng QP1-981 Theodore L. Mathuram verfasserin aut A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. mitochondria mitochondria-to-nucleus retrograde signaling small ncRNA Krebs cycle OxPhos D-loop transcripts Physiology Danyelle M. Townsend verfasserin aut Vincent J. Lynch verfasserin aut Ilya Bederman verfasserin aut Zhi-Wei Ye verfasserin aut Jie Zhang verfasserin aut Wade J. Sigurdson verfasserin aut Erin Prendergast verfasserin aut Raul Jobava verfasserin aut Jonathan P. Ferruzza verfasserin aut Mary R. D’Angelo verfasserin aut Maria Hatzoglou verfasserin aut Yaron Perry verfasserin aut Anna Blumental-Perry verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 13(2022) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:13 year:2022 https://doi.org/10.3389/fphys.2022.772313 kostenfrei https://doaj.org/article/f5dff9159b59448badb5f7f4173eea60 kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2022.772313/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2022 |
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10.3389/fphys.2022.772313 doi (DE-627)DOAJ008013152 (DE-599)DOAJf5dff9159b59448badb5f7f4173eea60 DE-627 ger DE-627 rakwb eng QP1-981 Theodore L. Mathuram verfasserin aut A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. mitochondria mitochondria-to-nucleus retrograde signaling small ncRNA Krebs cycle OxPhos D-loop transcripts Physiology Danyelle M. Townsend verfasserin aut Vincent J. Lynch verfasserin aut Ilya Bederman verfasserin aut Zhi-Wei Ye verfasserin aut Jie Zhang verfasserin aut Wade J. Sigurdson verfasserin aut Erin Prendergast verfasserin aut Raul Jobava verfasserin aut Jonathan P. Ferruzza verfasserin aut Mary R. D’Angelo verfasserin aut Maria Hatzoglou verfasserin aut Yaron Perry verfasserin aut Anna Blumental-Perry verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 13(2022) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:13 year:2022 https://doi.org/10.3389/fphys.2022.772313 kostenfrei https://doaj.org/article/f5dff9159b59448badb5f7f4173eea60 kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2022.772313/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2022 |
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10.3389/fphys.2022.772313 doi (DE-627)DOAJ008013152 (DE-599)DOAJf5dff9159b59448badb5f7f4173eea60 DE-627 ger DE-627 rakwb eng QP1-981 Theodore L. Mathuram verfasserin aut A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. mitochondria mitochondria-to-nucleus retrograde signaling small ncRNA Krebs cycle OxPhos D-loop transcripts Physiology Danyelle M. Townsend verfasserin aut Vincent J. Lynch verfasserin aut Ilya Bederman verfasserin aut Zhi-Wei Ye verfasserin aut Jie Zhang verfasserin aut Wade J. Sigurdson verfasserin aut Erin Prendergast verfasserin aut Raul Jobava verfasserin aut Jonathan P. Ferruzza verfasserin aut Mary R. D’Angelo verfasserin aut Maria Hatzoglou verfasserin aut Yaron Perry verfasserin aut Anna Blumental-Perry verfasserin aut In Frontiers in Physiology Frontiers Media S.A., 2011 13(2022) (DE-627)631498788 (DE-600)2564217-0 1664042X nnns volume:13 year:2022 https://doi.org/10.3389/fphys.2022.772313 kostenfrei https://doaj.org/article/f5dff9159b59448badb5f7f4173eea60 kostenfrei https://www.frontiersin.org/articles/10.3389/fphys.2022.772313/full kostenfrei https://doaj.org/toc/1664-042X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2022 |
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A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics |
| abstract |
Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. |
| abstractGer |
Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. |
| abstract_unstemmed |
Mitochondrial malfunction is a hallmark of many diseases, including neurodegenerative disorders, cardiovascular and lung diseases, and cancers. We previously found that alveolar progenitor cells, which are more resistant to cigarette smoke-induced injury than the other cells of the lung parenchyma, upregulate the mtDNA-encoded small non-coding RNA mito-ncR-805 after exposure to smoke. The mito-ncR-805 acts as a retrograde signal between the mitochondria and the nucleus. Here, we identified a region of mito-ncR-805 that is conserved in the mammalian mitochondrial genomes and generated shorter versions of mouse and human transcripts (mmu-CR805 and hsa-LDL1, respectively), which differ in a few nucleotides and which we refer to as the “functional bit”. Overexpression of mouse and human functional bits in either the mouse or the human lung epithelial cells led to an increase in the activity of the Krebs cycle and oxidative phosphorylation, stabilized the mitochondrial potential, conferred faster cell division, and lowered the levels of proapoptotic pseudokinase, TRIB3. Both oligos, mmu-CR805 and hsa-LDL1 conferred cross-species beneficial effects. Our data indicate a high degree of evolutionary conservation of retrograde signaling via a functional bit of the D-loop transcript, mito-ncR-805, in the mammals. This emphasizes the importance of the pathway and suggests a potential to develop this functional bit into a therapeutic agent that enhances mitochondrial bioenergetics. |
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| title_short |
A Synthetic Small RNA Homologous to the D-Loop Transcript of mtDNA Enhances Mitochondrial Bioenergetics |
| url |
https://doi.org/10.3389/fphys.2022.772313 https://doaj.org/article/f5dff9159b59448badb5f7f4173eea60 https://www.frontiersin.org/articles/10.3389/fphys.2022.772313/full https://doaj.org/toc/1664-042X |
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| author2 |
Danyelle M. Townsend Vincent J. Lynch Ilya Bederman Zhi-Wei Ye Jie Zhang Wade J. Sigurdson Erin Prendergast Raul Jobava Jonathan P. Ferruzza Mary R. D’Angelo Maria Hatzoglou Yaron Perry Anna Blumental-Perry |
| author2Str |
Danyelle M. Townsend Vincent J. Lynch Ilya Bederman Zhi-Wei Ye Jie Zhang Wade J. Sigurdson Erin Prendergast Raul Jobava Jonathan P. Ferruzza Mary R. D’Angelo Maria Hatzoglou Yaron Perry Anna Blumental-Perry |
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| doi_str |
10.3389/fphys.2022.772313 |
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| up_date |
2024-07-03T15:28:25.383Z |
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