miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway
Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or p...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Teng [verfasserIn] Wu, Dong-ming [verfasserIn] Zhang, Feng [verfasserIn] Zhang, Ting [verfasserIn] He, Miao [verfasserIn] Zhao, Yang-yang [verfasserIn] Li, Jin [verfasserIn] Li, Li [verfasserIn] Xu, Ying [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2021 |
|---|
| Übergeordnetes Werk: |
Enthalten in: International journal of radiation oncology, biology, physics - Amsterdam [u.a.] : Elsevier Science, 1975, 112, Seite 1256-1268 |
|---|---|
| Übergeordnetes Werk: |
volume:112 ; pages:1256-1268 |
| DOI / URN: |
10.1016/j.ijrobp.2021.12.003 |
|---|
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ELV007562640 |
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| 245 | 1 | 0 | |a miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway |
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| 520 | |a Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. | ||
| 700 | 1 | |a Wu, Dong-ming |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Feng |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Ting |e verfasserin |4 aut | |
| 700 | 1 | |a He, Miao |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Yang-yang |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Jin |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Li |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Ying |e verfasserin |4 aut | |
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10.1016/j.ijrobp.2021.12.003 doi (DE-627)ELV007562640 (ELSEVIER)S0360-3016(21)03238-7 DE-627 ger DE-627 rda eng 610 DE-600 44.64 bkl 44.81 bkl Liu, Teng verfasserin aut miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. Wu, Dong-ming verfasserin aut Zhang, Feng verfasserin aut Zhang, Ting verfasserin aut He, Miao verfasserin aut Zhao, Yang-yang verfasserin aut Li, Jin verfasserin aut Li, Li verfasserin aut Xu, Ying verfasserin aut Enthalten in International journal of radiation oncology, biology, physics Amsterdam [u.a.] : Elsevier Science, 1975 112, Seite 1256-1268 Online-Ressource (DE-627)306659662 (DE-600)1500486-7 (DE-576)081986319 1879-355X nnns volume:112 pages:1256-1268 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 44.64 Radiologie 44.81 Onkologie AR 112 1256-1268 |
| spelling |
10.1016/j.ijrobp.2021.12.003 doi (DE-627)ELV007562640 (ELSEVIER)S0360-3016(21)03238-7 DE-627 ger DE-627 rda eng 610 DE-600 44.64 bkl 44.81 bkl Liu, Teng verfasserin aut miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. Wu, Dong-ming verfasserin aut Zhang, Feng verfasserin aut Zhang, Ting verfasserin aut He, Miao verfasserin aut Zhao, Yang-yang verfasserin aut Li, Jin verfasserin aut Li, Li verfasserin aut Xu, Ying verfasserin aut Enthalten in International journal of radiation oncology, biology, physics Amsterdam [u.a.] : Elsevier Science, 1975 112, Seite 1256-1268 Online-Ressource (DE-627)306659662 (DE-600)1500486-7 (DE-576)081986319 1879-355X nnns volume:112 pages:1256-1268 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 44.64 Radiologie 44.81 Onkologie AR 112 1256-1268 |
| allfields_unstemmed |
10.1016/j.ijrobp.2021.12.003 doi (DE-627)ELV007562640 (ELSEVIER)S0360-3016(21)03238-7 DE-627 ger DE-627 rda eng 610 DE-600 44.64 bkl 44.81 bkl Liu, Teng verfasserin aut miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. Wu, Dong-ming verfasserin aut Zhang, Feng verfasserin aut Zhang, Ting verfasserin aut He, Miao verfasserin aut Zhao, Yang-yang verfasserin aut Li, Jin verfasserin aut Li, Li verfasserin aut Xu, Ying verfasserin aut Enthalten in International journal of radiation oncology, biology, physics Amsterdam [u.a.] : Elsevier Science, 1975 112, Seite 1256-1268 Online-Ressource (DE-627)306659662 (DE-600)1500486-7 (DE-576)081986319 1879-355X nnns volume:112 pages:1256-1268 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 44.64 Radiologie 44.81 Onkologie AR 112 1256-1268 |
| allfieldsGer |
10.1016/j.ijrobp.2021.12.003 doi (DE-627)ELV007562640 (ELSEVIER)S0360-3016(21)03238-7 DE-627 ger DE-627 rda eng 610 DE-600 44.64 bkl 44.81 bkl Liu, Teng verfasserin aut miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. Wu, Dong-ming verfasserin aut Zhang, Feng verfasserin aut Zhang, Ting verfasserin aut He, Miao verfasserin aut Zhao, Yang-yang verfasserin aut Li, Jin verfasserin aut Li, Li verfasserin aut Xu, Ying verfasserin aut Enthalten in International journal of radiation oncology, biology, physics Amsterdam [u.a.] : Elsevier Science, 1975 112, Seite 1256-1268 Online-Ressource (DE-627)306659662 (DE-600)1500486-7 (DE-576)081986319 1879-355X nnns volume:112 pages:1256-1268 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 44.64 Radiologie 44.81 Onkologie AR 112 1256-1268 |
| allfieldsSound |
10.1016/j.ijrobp.2021.12.003 doi (DE-627)ELV007562640 (ELSEVIER)S0360-3016(21)03238-7 DE-627 ger DE-627 rda eng 610 DE-600 44.64 bkl 44.81 bkl Liu, Teng verfasserin aut miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. Wu, Dong-ming verfasserin aut Zhang, Feng verfasserin aut Zhang, Ting verfasserin aut He, Miao verfasserin aut Zhao, Yang-yang verfasserin aut Li, Jin verfasserin aut Li, Li verfasserin aut Xu, Ying verfasserin aut Enthalten in International journal of radiation oncology, biology, physics Amsterdam [u.a.] : Elsevier Science, 1975 112, Seite 1256-1268 Online-Ressource (DE-627)306659662 (DE-600)1500486-7 (DE-576)081986319 1879-355X nnns volume:112 pages:1256-1268 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA GBV_ILN_31 GBV_ILN_2011 44.64 Radiologie 44.81 Onkologie AR 112 1256-1268 |
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Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wu, Dong-ming</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Feng</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Ting</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Miao</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhao, Yang-yang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Jin</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Li</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xu, Ying</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">International journal of radiation oncology, biology, physics</subfield><subfield code="d">Amsterdam [u.a.] : Elsevier Science, 1975</subfield><subfield code="g">112, Seite 1256-1268</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)306659662</subfield><subfield code="w">(DE-600)1500486-7</subfield><subfield code="w">(DE-576)081986319</subfield><subfield code="x">1879-355X</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:112</subfield><subfield code="g">pages:1256-1268</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_31</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_2011</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.64</subfield><subfield code="j">Radiologie</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.81</subfield><subfield code="j">Onkologie</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">112</subfield><subfield code="h">1256-1268</subfield></datafield></record></collection>
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Liu, Teng ddc 610 bkl 44.64 bkl 44.81 miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway |
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610 DE-600 44.64 bkl 44.81 bkl miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway |
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miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway |
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miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway |
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mir-142a-3p enhances flaa n/c protection against radiation-mediated intestinal injury by modulating the irak1/nf-κb signaling pathway |
| title_auth |
miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway |
| abstract |
Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. |
| abstractGer |
Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. |
| abstract_unstemmed |
Purpose: Our purpose was to investigate the role of recombinant protein flagellin A N/C (FlaA N/C) protein-mediated pyroptosis inhibition and related miRNA in radiation protection.Methods and Materials: Mice received 10 Gy irradiation after FlaA N/C pretreatment, IRAK-1/4 Inhibitor I treatment, or pyrrolidine dithiocarbamate treatment. Human intestinal epithelial cells (HIEC) received 10 Gy irradiation after FlaA N/C pretreatment, overexpressed miR-142a-3p with miR-142a-3p mimics, or inhibited miR-142a-3p with miR-142a-3p inhibitor. Mouse & Rat miRNA OneArray determined the change in relevant miRNA after FlaA N/C pretreatment; real-time polymerase chain reaction detected IRAK1 and miR-142a-3p expression; a CCK-8 assay evaluated cell viability; LDH release analyzed cytotoxicity; caspase-1 activity assay, interleukin-1β level, and flow cytometry analyzed pyroptosis in cells; hematoxylin-eosin staining evaluated the damage to intestinal tissue; CO-IP detected the inflammation activation; immunohistochemistry, Western blot analysis, and immunofluorescence analyzed activation of pyroptosis-related proteins and the activation of NF-kB signaling pathways; and luciferase reporter assay and fluorescence in situ hybridization detected the interaction between miR-142a-3p and IRAK1.Results: FlaA N/C reduced radiation-induced pyroptosis in vivo and in vitro, and miR-142a-3p expression increased after FlaA N/C pretreatment. Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. Inhibiting the NF-kB signaling pathway can reduce radiation-mediated pyroptosis in mice intestines.Conclusions: Our findings indicated this new radioprotectant protein regulates miR-142a-3p, effectively inhibiting radiation-induced pyroptosis mediated by the IRAK1/NF-κB signaling pathway in intestinal cells. |
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miR-142a-3p Enhances FlaA N/C Protection Against Radiation-Mediated Intestinal Injury by Modulating the IRAK1/NF-κB Signaling Pathway |
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Upregulating the expression of miR-142a-3p inhibited radiation-induced pyroptosis in HIEC, and downregulating the expression of miR-142a-3p led to radiation-induced pyroptosis in HIEC after FlaA N/C pretreatment. IRAK1 was a direct target of miR-142a-3p and played an important role in radiation-induced pyroptosis in HIEC. Inhibiting IRAK1 reduced radiation-mediated pyroptosis in mice intestines. miR-142a-3p downregulated IRAK1 and suppressed the NF-kB pathway. 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