In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression

Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arteria...
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Autor*in:	Le Ribeuz, Hélène [verfasserIn] Courboulin, Audrey [verfasserIn] Ghigna, Maria-Rosa [verfasserIn] Lambert, Mélanie [verfasserIn] Hautefort, Aurélie [verfasserIn] Humbert, Marc [verfasserIn] Montani, David [verfasserIn] Cohen-Kaminsky, Sylvia [verfasserIn] Perros, Frédéric [verfasserIn] Antigny, Fabrice [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	miR-138 PAH KCNK3 Proliferation SLC45A3

Übergeordnetes Werk:	Enthalten in: Respiratory research - London : BioMed Central, 2001, 21(2020), 1 vom: 16. Juli
Übergeordnetes Werk:	volume:21 ; year:2020 ; number:1 ; day:16 ; month:07

Links:	Volltext

DOI / URN:	10.1186/s12931-020-01444-7

Katalog-ID:	SPR040373681

Internformat


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245	1	0	\|a In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression
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520			\|a Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression.
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700	1		\|a Antigny, Fabrice \|e verfasserin \|4 aut
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allfields	10.1186/s12931-020-01444-7 doi (DE-627)SPR040373681 (SPR)s12931-020-01444-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Le Ribeuz, Hélène verfasserin aut In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression. miR-138 (dpeaa)DE-He213 PAH (dpeaa)DE-He213 KCNK3 (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 SLC45A3 (dpeaa)DE-He213 Courboulin, Audrey verfasserin aut Ghigna, Maria-Rosa verfasserin aut Lambert, Mélanie verfasserin aut Hautefort, Aurélie verfasserin aut Humbert, Marc verfasserin aut Montani, David verfasserin aut Cohen-Kaminsky, Sylvia verfasserin aut Perros, Frédéric verfasserin aut Antigny, Fabrice verfasserin aut Enthalten in Respiratory research London : BioMed Central, 2001 21(2020), 1 vom: 16. Juli (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:21 year:2020 number:1 day:16 month:07 https://dx.doi.org/10.1186/s12931-020-01444-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 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 44.00 ASE AR 21 2020 1 16 07
spelling	10.1186/s12931-020-01444-7 doi (DE-627)SPR040373681 (SPR)s12931-020-01444-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Le Ribeuz, Hélène verfasserin aut In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression. miR-138 (dpeaa)DE-He213 PAH (dpeaa)DE-He213 KCNK3 (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 SLC45A3 (dpeaa)DE-He213 Courboulin, Audrey verfasserin aut Ghigna, Maria-Rosa verfasserin aut Lambert, Mélanie verfasserin aut Hautefort, Aurélie verfasserin aut Humbert, Marc verfasserin aut Montani, David verfasserin aut Cohen-Kaminsky, Sylvia verfasserin aut Perros, Frédéric verfasserin aut Antigny, Fabrice verfasserin aut Enthalten in Respiratory research London : BioMed Central, 2001 21(2020), 1 vom: 16. Juli (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:21 year:2020 number:1 day:16 month:07 https://dx.doi.org/10.1186/s12931-020-01444-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 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 44.00 ASE AR 21 2020 1 16 07
allfields_unstemmed	10.1186/s12931-020-01444-7 doi (DE-627)SPR040373681 (SPR)s12931-020-01444-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Le Ribeuz, Hélène verfasserin aut In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression. miR-138 (dpeaa)DE-He213 PAH (dpeaa)DE-He213 KCNK3 (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 SLC45A3 (dpeaa)DE-He213 Courboulin, Audrey verfasserin aut Ghigna, Maria-Rosa verfasserin aut Lambert, Mélanie verfasserin aut Hautefort, Aurélie verfasserin aut Humbert, Marc verfasserin aut Montani, David verfasserin aut Cohen-Kaminsky, Sylvia verfasserin aut Perros, Frédéric verfasserin aut Antigny, Fabrice verfasserin aut Enthalten in Respiratory research London : BioMed Central, 2001 21(2020), 1 vom: 16. Juli (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:21 year:2020 number:1 day:16 month:07 https://dx.doi.org/10.1186/s12931-020-01444-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 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 44.00 ASE AR 21 2020 1 16 07
allfieldsGer	10.1186/s12931-020-01444-7 doi (DE-627)SPR040373681 (SPR)s12931-020-01444-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Le Ribeuz, Hélène verfasserin aut In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression. miR-138 (dpeaa)DE-He213 PAH (dpeaa)DE-He213 KCNK3 (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 SLC45A3 (dpeaa)DE-He213 Courboulin, Audrey verfasserin aut Ghigna, Maria-Rosa verfasserin aut Lambert, Mélanie verfasserin aut Hautefort, Aurélie verfasserin aut Humbert, Marc verfasserin aut Montani, David verfasserin aut Cohen-Kaminsky, Sylvia verfasserin aut Perros, Frédéric verfasserin aut Antigny, Fabrice verfasserin aut Enthalten in Respiratory research London : BioMed Central, 2001 21(2020), 1 vom: 16. Juli (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:21 year:2020 number:1 day:16 month:07 https://dx.doi.org/10.1186/s12931-020-01444-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 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 44.00 ASE AR 21 2020 1 16 07
allfieldsSound	10.1186/s12931-020-01444-7 doi (DE-627)SPR040373681 (SPR)s12931-020-01444-7-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Le Ribeuz, Hélène verfasserin aut In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression. miR-138 (dpeaa)DE-He213 PAH (dpeaa)DE-He213 KCNK3 (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 SLC45A3 (dpeaa)DE-He213 Courboulin, Audrey verfasserin aut Ghigna, Maria-Rosa verfasserin aut Lambert, Mélanie verfasserin aut Hautefort, Aurélie verfasserin aut Humbert, Marc verfasserin aut Montani, David verfasserin aut Cohen-Kaminsky, Sylvia verfasserin aut Perros, Frédéric verfasserin aut Antigny, Fabrice verfasserin aut Enthalten in Respiratory research London : BioMed Central, 2001 21(2020), 1 vom: 16. Juli (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:21 year:2020 number:1 day:16 month:07 https://dx.doi.org/10.1186/s12931-020-01444-7 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 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 44.00 ASE AR 21 2020 1 16 07
language	English
source	Enthalten in Respiratory research 21(2020), 1 vom: 16. Juli volume:21 year:2020 number:1 day:16 month:07
sourceStr	Enthalten in Respiratory research 21(2020), 1 vom: 16. Juli volume:21 year:2020 number:1 day:16 month:07
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	miR-138 PAH KCNK3 Proliferation SLC45A3
dewey-raw	610
isfreeaccess_bool	true
container_title	Respiratory research
authorswithroles_txt_mv	Le Ribeuz, Hélène @@aut@@ Courboulin, Audrey @@aut@@ Ghigna, Maria-Rosa @@aut@@ Lambert, Mélanie @@aut@@ Hautefort, Aurélie @@aut@@ Humbert, Marc @@aut@@ Montani, David @@aut@@ Cohen-Kaminsky, Sylvia @@aut@@ Perros, Frédéric @@aut@@ Antigny, Fabrice @@aut@@
publishDateDaySort_date	2020-07-16T00:00:00Z
hierarchy_top_id	326646485
dewey-sort	3610
id	SPR040373681
language_de	englisch
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MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. 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author	Le Ribeuz, Hélène
spellingShingle	Le Ribeuz, Hélène ddc 610 bkl 44.00 misc miR-138 misc PAH misc KCNK3 misc Proliferation misc SLC45A3 In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression
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topic_title	610 ASE 44.00 bkl In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression miR-138 (dpeaa)DE-He213 PAH (dpeaa)DE-He213 KCNK3 (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 SLC45A3 (dpeaa)DE-He213
topic	ddc 610 bkl 44.00 misc miR-138 misc PAH misc KCNK3 misc Proliferation misc SLC45A3
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title	In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression
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title_full	In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression
author_sort	Le Ribeuz, Hélène
journal	Respiratory research
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author_browse	Le Ribeuz, Hélène Courboulin, Audrey Ghigna, Maria-Rosa Lambert, Mélanie Hautefort, Aurélie Humbert, Marc Montani, David Cohen-Kaminsky, Sylvia Perros, Frédéric Antigny, Fabrice
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author-letter	Le Ribeuz, Hélène
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author2-role	verfasserin
title_sort	in vivo mir-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary kcnk3 and slc45a3 expression
title_auth	In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression
abstract	Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression.
abstractGer	Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression.
abstract_unstemmed	Background The pathogenesis of pulmonary arterial hypertension (PAH) involves many signalling pathways. MicroRNAs are potential candidates involved in simultaneously coordinating multiple genes under such multifactorial conditions. Methods and results MiR-138-5p is overexpressed in pulmonary arterial smooth muscle cells (PASMCs) from PAH patients and in lungs from rats with monocrotaline-induced pulmonary hypertension (MCT-PH). MiR-138-5p is predicted to regulate the expression of the potassium channel KCNK3, whose loss is associated with the development and progression of PAH. We hypothesized that, in vivo, miR-138-5p inhibition would restore KCNK3 lung expression and subsequently alleviate PAH. Nebulization-based delivery of anti-miR-138-5p to rats with established MCT-PH significantly reduced the right ventricular systolic pressure and significantly improved the pulmonary arterial acceleration time (PAAT). These haemodynamic improvements were related to decrease pulmonary vascular remodelling, lung inflammation and pulmonary vascular cell proliferation in situ. In vivo inhibition of miR-138-5p restored KCNK3 mRNA expression and SLC45A3 protein expression in the lungs. Conclusions We confirmed that in vivo inhibition of miR-138-5p reduces the development of PH in experimental MCT-PH. The possible curative mechanisms involve at least the normalization of lung KCNK3 as well as SLC45A3 expression.
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container_issue	1
title_short	In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression
url	https://dx.doi.org/10.1186/s12931-020-01444-7
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author2	Courboulin, Audrey Ghigna, Maria-Rosa Lambert, Mélanie Hautefort, Aurélie Humbert, Marc Montani, David Cohen-Kaminsky, Sylvia Perros, Frédéric Antigny, Fabrice
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up_date	2024-07-03T15:34:46.332Z
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In vivo miR-138-5p inhibition alleviates monocrotaline-induced pulmonary hypertension and normalizes pulmonary KCNK3 and SLC45A3 expression

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