The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN
Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells...
Ausführliche Beschreibung
Autor*in: |
Wang, Jian [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2022 |
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Schlagwörter: |
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Anmerkung: |
© The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 |
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Übergeordnetes Werk: |
Enthalten in: Clinical and experimental medicine - Milano : Springer, 2001, 23(2022), 3 vom: 23. Juli, Seite 887-895 |
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Übergeordnetes Werk: |
volume:23 ; year:2022 ; number:3 ; day:23 ; month:07 ; pages:887-895 |
Links: |
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DOI / URN: |
10.1007/s10238-022-00862-9 |
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Katalog-ID: |
SPR051973154 |
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245 | 1 | 4 | |a The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN |
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520 | |a Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. | ||
650 | 4 | |a Circ_0002594 |7 (dpeaa)DE-He213 | |
650 | 4 | |a eIF4A3 |7 (dpeaa)DE-He213 | |
650 | 4 | |a PTEN |7 (dpeaa)DE-He213 | |
650 | 4 | |a Th2 cell differentiation |7 (dpeaa)DE-He213 | |
650 | 4 | |a Asthma |7 (dpeaa)DE-He213 | |
700 | 1 | |a Cheng, Yuping |4 aut | |
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10.1007/s10238-022-00862-9 doi (DE-627)SPR051973154 (SPR)s10238-022-00862-9-e DE-627 ger DE-627 rakwb eng Wang, Jian verfasserin aut The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. Circ_0002594 (dpeaa)DE-He213 eIF4A3 (dpeaa)DE-He213 PTEN (dpeaa)DE-He213 Th2 cell differentiation (dpeaa)DE-He213 Asthma (dpeaa)DE-He213 Cheng, Yuping aut Enthalten in Clinical and experimental medicine Milano : Springer, 2001 23(2022), 3 vom: 23. Juli, Seite 887-895 (DE-627)332826694 (DE-600)2054398-0 1591-9528 nnns volume:23 year:2022 number:3 day:23 month:07 pages:887-895 https://dx.doi.org/10.1007/s10238-022-00862-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 23 2022 3 23 07 887-895 |
spelling |
10.1007/s10238-022-00862-9 doi (DE-627)SPR051973154 (SPR)s10238-022-00862-9-e DE-627 ger DE-627 rakwb eng Wang, Jian verfasserin aut The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. Circ_0002594 (dpeaa)DE-He213 eIF4A3 (dpeaa)DE-He213 PTEN (dpeaa)DE-He213 Th2 cell differentiation (dpeaa)DE-He213 Asthma (dpeaa)DE-He213 Cheng, Yuping aut Enthalten in Clinical and experimental medicine Milano : Springer, 2001 23(2022), 3 vom: 23. Juli, Seite 887-895 (DE-627)332826694 (DE-600)2054398-0 1591-9528 nnns volume:23 year:2022 number:3 day:23 month:07 pages:887-895 https://dx.doi.org/10.1007/s10238-022-00862-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 23 2022 3 23 07 887-895 |
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10.1007/s10238-022-00862-9 doi (DE-627)SPR051973154 (SPR)s10238-022-00862-9-e DE-627 ger DE-627 rakwb eng Wang, Jian verfasserin aut The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. Circ_0002594 (dpeaa)DE-He213 eIF4A3 (dpeaa)DE-He213 PTEN (dpeaa)DE-He213 Th2 cell differentiation (dpeaa)DE-He213 Asthma (dpeaa)DE-He213 Cheng, Yuping aut Enthalten in Clinical and experimental medicine Milano : Springer, 2001 23(2022), 3 vom: 23. Juli, Seite 887-895 (DE-627)332826694 (DE-600)2054398-0 1591-9528 nnns volume:23 year:2022 number:3 day:23 month:07 pages:887-895 https://dx.doi.org/10.1007/s10238-022-00862-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 23 2022 3 23 07 887-895 |
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10.1007/s10238-022-00862-9 doi (DE-627)SPR051973154 (SPR)s10238-022-00862-9-e DE-627 ger DE-627 rakwb eng Wang, Jian verfasserin aut The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. Circ_0002594 (dpeaa)DE-He213 eIF4A3 (dpeaa)DE-He213 PTEN (dpeaa)DE-He213 Th2 cell differentiation (dpeaa)DE-He213 Asthma (dpeaa)DE-He213 Cheng, Yuping aut Enthalten in Clinical and experimental medicine Milano : Springer, 2001 23(2022), 3 vom: 23. Juli, Seite 887-895 (DE-627)332826694 (DE-600)2054398-0 1591-9528 nnns volume:23 year:2022 number:3 day:23 month:07 pages:887-895 https://dx.doi.org/10.1007/s10238-022-00862-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 23 2022 3 23 07 887-895 |
allfieldsSound |
10.1007/s10238-022-00862-9 doi (DE-627)SPR051973154 (SPR)s10238-022-00862-9-e DE-627 ger DE-627 rakwb eng Wang, Jian verfasserin aut The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. Circ_0002594 (dpeaa)DE-He213 eIF4A3 (dpeaa)DE-He213 PTEN (dpeaa)DE-He213 Th2 cell differentiation (dpeaa)DE-He213 Asthma (dpeaa)DE-He213 Cheng, Yuping aut Enthalten in Clinical and experimental medicine Milano : Springer, 2001 23(2022), 3 vom: 23. Juli, Seite 887-895 (DE-627)332826694 (DE-600)2054398-0 1591-9528 nnns volume:23 year:2022 number:3 day:23 month:07 pages:887-895 https://dx.doi.org/10.1007/s10238-022-00862-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_711 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 23 2022 3 23 07 887-895 |
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Enthalten in Clinical and experimental medicine 23(2022), 3 vom: 23. Juli, Seite 887-895 volume:23 year:2022 number:3 day:23 month:07 pages:887-895 |
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Enthalten in Clinical and experimental medicine 23(2022), 3 vom: 23. Juli, Seite 887-895 volume:23 year:2022 number:3 day:23 month:07 pages:887-895 |
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Circ_0002594 eIF4A3 PTEN Th2 cell differentiation Asthma |
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Clinical and experimental medicine |
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Wang, Jian @@aut@@ Cheng, Yuping @@aut@@ |
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2022-07-23T00:00:00Z |
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Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. 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author |
Wang, Jian |
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Wang, Jian misc Circ_0002594 misc eIF4A3 misc PTEN misc Th2 cell differentiation misc Asthma The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN |
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The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN Circ_0002594 (dpeaa)DE-He213 eIF4A3 (dpeaa)DE-He213 PTEN (dpeaa)DE-He213 Th2 cell differentiation (dpeaa)DE-He213 Asthma (dpeaa)DE-He213 |
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The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN |
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The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN |
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interaction of hsa_circ_0002594 and eif4a3 promotes t-helper 2 cell differentiation by the regulation of pten |
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The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN |
abstract |
Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 |
abstractGer |
Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 |
abstract_unstemmed |
Abstract T helper (Th) 2 cell-medicated immune response participates in various immune diseases, especially in asthma. Circ_0002594 has been reported to be up-regulated in asthmatic patients, and was higher in Th2-high subgroups, but the specific mechanisms by which circ_0002594 regulating Th2 cells were still unclear. Here, we found that circ_0002594 was significantly up-regulated in $ CD4^{+} $ T cells of asthmatic patients. Circ_0002594 overexpression elevated Th2-related cytokine IL-4 production and reduced Th1-related cytokine INF-γ production, promoting Th2 cell differentiation, while circ_0002594 loss resulted in the opposite results. Additionally, eIF4A3 overexpression reversed the effects of circ_0002594 on the production of INF-γ, IL-4 and Th1/Th2 ratio by interacting with circ_0002594. Moreover, circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, thus down-regulating PTEN mRNA expression. Furthermore, eIF4A3 overexpression markedly reversed the significant down-regulation of PTEN protein level and the activation of PI3K/AKT/mTOR pathway in $ CD4^{+} $ T cells transfected with Lv-circ_0002594, suggesting the involvement of circ_0002594/eIF4A3/PTEN axis in the activation of PI3K/AKT/mTOR pathway. Also, rapamycin (the mTOR inhibitor) dramatically reversed the promotion effects of circ_0002594 overexpression on Th2 cells. In conclusion, our study demonstrated that circ_0002594 interacted with eIF4A3 to reduce PTEN mRNA stability, down-regulating PTEN expression, thereby activating the PI3K/AKT/mTOR pathway to promote Th2 cell differentiation. Our work may highlight novel insights into the molecular mechanism of circ_0002594 in regulating Th2 cell differentiation in asthma. © The Author(s), under exclusive licence to Springer Nature Switzerland AG 2022 |
collection_details |
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container_issue |
3 |
title_short |
The interaction of hsa_circ_0002594 and eIF4A3 promotes T-helper 2 cell differentiation by the regulation of PTEN |
url |
https://dx.doi.org/10.1007/s10238-022-00862-9 |
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up_date |
2024-07-04T00:42:01.510Z |
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score |
7.4009943 |