Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease

Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial proge...
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Autor*in:	Kato, Ryo [verfasserIn] Mizuno, Shiro Kadowaki, Maiko Shiozaki, Kohei Akai, Masaya Nakagawa, Ken Oikawa, Taku Iguchi, Masaharu Osanai, Kazuhiro Ishizaki, Takeshi Voelkel, Norbert F Toga, Hirohisa

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	miR-34a miR-126 p53 Sirt1

Anmerkung:	© The Author(s). 2016

Übergeordnetes Werk:	Enthalten in: Respiratory research - London : BioMed Central, 2001, 17(2016), 1 vom: 27. Okt.
Übergeordnetes Werk:	volume:17 ; year:2016 ; number:1 ; day:27 ; month:10

Links:	Volltext

DOI / URN:	10.1186/s12931-016-0452-2

Katalog-ID:	SPR028521765

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520			\|a Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD.
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700	1		\|a Mizuno, Shiro \|0 (orcid)0000-0002-5552-2215 \|4 aut
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700	1		\|a Voelkel, Norbert F \|4 aut
700	1		\|a Toga, Hirohisa \|4 aut
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Indexfelder

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matchkey_str	article:1465993X:2016----::itepesoiascaewtc3epesoibodelfoptetwtcrn
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publishDate	2016
allfields	10.1186/s12931-016-0452-2 doi (DE-627)SPR028521765 (SPR)s12931-016-0452-2-e DE-627 ger DE-627 rakwb eng Kato, Ryo verfasserin aut Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. miR-34a (dpeaa)DE-He213 miR-126 (dpeaa)DE-He213 p53 (dpeaa)DE-He213 Sirt1 (dpeaa)DE-He213 Mizuno, Shiro (orcid)0000-0002-5552-2215 aut Kadowaki, Maiko aut Shiozaki, Kohei aut Akai, Masaya aut Nakagawa, Ken aut Oikawa, Taku aut Iguchi, Masaharu aut Osanai, Kazuhiro aut Ishizaki, Takeshi aut Voelkel, Norbert F aut Toga, Hirohisa aut Enthalten in Respiratory research London : BioMed Central, 2001 17(2016), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:17 year:2016 number:1 day:27 month:10 https://dx.doi.org/10.1186/s12931-016-0452-2 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 AR 17 2016 1 27 10
spelling	10.1186/s12931-016-0452-2 doi (DE-627)SPR028521765 (SPR)s12931-016-0452-2-e DE-627 ger DE-627 rakwb eng Kato, Ryo verfasserin aut Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. miR-34a (dpeaa)DE-He213 miR-126 (dpeaa)DE-He213 p53 (dpeaa)DE-He213 Sirt1 (dpeaa)DE-He213 Mizuno, Shiro (orcid)0000-0002-5552-2215 aut Kadowaki, Maiko aut Shiozaki, Kohei aut Akai, Masaya aut Nakagawa, Ken aut Oikawa, Taku aut Iguchi, Masaharu aut Osanai, Kazuhiro aut Ishizaki, Takeshi aut Voelkel, Norbert F aut Toga, Hirohisa aut Enthalten in Respiratory research London : BioMed Central, 2001 17(2016), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:17 year:2016 number:1 day:27 month:10 https://dx.doi.org/10.1186/s12931-016-0452-2 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 AR 17 2016 1 27 10
allfields_unstemmed	10.1186/s12931-016-0452-2 doi (DE-627)SPR028521765 (SPR)s12931-016-0452-2-e DE-627 ger DE-627 rakwb eng Kato, Ryo verfasserin aut Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. miR-34a (dpeaa)DE-He213 miR-126 (dpeaa)DE-He213 p53 (dpeaa)DE-He213 Sirt1 (dpeaa)DE-He213 Mizuno, Shiro (orcid)0000-0002-5552-2215 aut Kadowaki, Maiko aut Shiozaki, Kohei aut Akai, Masaya aut Nakagawa, Ken aut Oikawa, Taku aut Iguchi, Masaharu aut Osanai, Kazuhiro aut Ishizaki, Takeshi aut Voelkel, Norbert F aut Toga, Hirohisa aut Enthalten in Respiratory research London : BioMed Central, 2001 17(2016), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:17 year:2016 number:1 day:27 month:10 https://dx.doi.org/10.1186/s12931-016-0452-2 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 AR 17 2016 1 27 10
allfieldsGer	10.1186/s12931-016-0452-2 doi (DE-627)SPR028521765 (SPR)s12931-016-0452-2-e DE-627 ger DE-627 rakwb eng Kato, Ryo verfasserin aut Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. miR-34a (dpeaa)DE-He213 miR-126 (dpeaa)DE-He213 p53 (dpeaa)DE-He213 Sirt1 (dpeaa)DE-He213 Mizuno, Shiro (orcid)0000-0002-5552-2215 aut Kadowaki, Maiko aut Shiozaki, Kohei aut Akai, Masaya aut Nakagawa, Ken aut Oikawa, Taku aut Iguchi, Masaharu aut Osanai, Kazuhiro aut Ishizaki, Takeshi aut Voelkel, Norbert F aut Toga, Hirohisa aut Enthalten in Respiratory research London : BioMed Central, 2001 17(2016), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:17 year:2016 number:1 day:27 month:10 https://dx.doi.org/10.1186/s12931-016-0452-2 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 AR 17 2016 1 27 10
allfieldsSound	10.1186/s12931-016-0452-2 doi (DE-627)SPR028521765 (SPR)s12931-016-0452-2-e DE-627 ger DE-627 rakwb eng Kato, Ryo verfasserin aut Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2016 Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. miR-34a (dpeaa)DE-He213 miR-126 (dpeaa)DE-He213 p53 (dpeaa)DE-He213 Sirt1 (dpeaa)DE-He213 Mizuno, Shiro (orcid)0000-0002-5552-2215 aut Kadowaki, Maiko aut Shiozaki, Kohei aut Akai, Masaya aut Nakagawa, Ken aut Oikawa, Taku aut Iguchi, Masaharu aut Osanai, Kazuhiro aut Ishizaki, Takeshi aut Voelkel, Norbert F aut Toga, Hirohisa aut Enthalten in Respiratory research London : BioMed Central, 2001 17(2016), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:17 year:2016 number:1 day:27 month:10 https://dx.doi.org/10.1186/s12931-016-0452-2 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 AR 17 2016 1 27 10
language	English
source	Enthalten in Respiratory research 17(2016), 1 vom: 27. Okt. volume:17 year:2016 number:1 day:27 month:10
sourceStr	Enthalten in Respiratory research 17(2016), 1 vom: 27. Okt. volume:17 year:2016 number:1 day:27 month:10
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	miR-34a miR-126 p53 Sirt1
isfreeaccess_bool	true
container_title	Respiratory research
authorswithroles_txt_mv	Kato, Ryo @@aut@@ Mizuno, Shiro @@aut@@ Kadowaki, Maiko @@aut@@ Shiozaki, Kohei @@aut@@ Akai, Masaya @@aut@@ Nakagawa, Ken @@aut@@ Oikawa, Taku @@aut@@ Iguchi, Masaharu @@aut@@ Osanai, Kazuhiro @@aut@@ Ishizaki, Takeshi @@aut@@ Voelkel, Norbert F @@aut@@ Toga, Hirohisa @@aut@@
publishDateDaySort_date	2016-10-27T00:00:00Z
hierarchy_top_id	326646485
id	SPR028521765
language_de	englisch
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Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. 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author	Kato, Ryo
spellingShingle	Kato, Ryo misc miR-34a misc miR-126 misc p53 misc Sirt1 Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease
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topic_title	Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease miR-34a (dpeaa)DE-He213 miR-126 (dpeaa)DE-He213 p53 (dpeaa)DE-He213 Sirt1 (dpeaa)DE-He213
topic	misc miR-34a misc miR-126 misc p53 misc Sirt1
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title	Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease
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title_full	Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease
author_sort	Kato, Ryo
journal	Respiratory research
journalStr	Respiratory research
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author_browse	Kato, Ryo Mizuno, Shiro Kadowaki, Maiko Shiozaki, Kohei Akai, Masaya Nakagawa, Ken Oikawa, Taku Iguchi, Masaharu Osanai, Kazuhiro Ishizaki, Takeshi Voelkel, Norbert F Toga, Hirohisa
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title_sort	sirt1 expression is associated with cd31 expression in blood cells from patients with chronic obstructive pulmonary disease
title_auth	Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease
abstract	Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. © The Author(s). 2016
abstractGer	Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. © The Author(s). 2016
abstract_unstemmed	Background Cigarette smoke induced oxidative stress has been shown to reduce silent information regulator 1 (Sirt1) levels in lung tissue from smokers and patients with COPD patients. Sirt1 is known to inhibit endothelial senescence and may play a protective role in vascular cells. Endothelial progenitor cells (EPCs) are mobilized into circulation under various pathophysiological conditions, and are thought to play an important role in tissue repair in chronic obstructive lung disease (COPD). Therefore, Sirt1 and EPC-associated mRNAs were measured in blood samples from patients with COPD and from cultured $ CD34^{+} $ progenitor cells to examine whether these genes are associated with COPD development. Methods This study included 358 patients with a smoking history of more than 10 pack-years. RNA was extracted from blood samples and from $ CD34^{+} $ progenitor cells treated with cigarette smoke extract (CSE), followed by assessment of CD31, CD34, Sirt1 mRNA, miR-34a, and miR-126-3p expression by real-time RT-PCR. Results The expression of CD31, CD34, Sirt1 mRNAs, and miR-126-3p decreased and that of miR-34a increased in moderate COPD compared with that in control smokers. However, no significant differences in these genes were observed in blood cells from patients with severe COPD compared with those in control smokers. CSE significantly decreased Sirt1 and increased miR-34a expression in cultured progenitor cells. Conclusion Sirt1 expression in blood cells from patients with COPD could be a biomarker for disease stability in patients with moderate COPD. MiR-34a may participate in apoptosis and/or senescence of EPCs in smokers. Decreased expression of CD31, CD34, and miR-126-3p potentially represents decreased numbers of EPCs in blood cell from patients with COPD. © The Author(s). 2016
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title_short	Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease
url	https://dx.doi.org/10.1186/s12931-016-0452-2
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author2	Mizuno, Shiro Kadowaki, Maiko Shiozaki, Kohei Akai, Masaya Nakagawa, Ken Oikawa, Taku Iguchi, Masaharu Osanai, Kazuhiro Ishizaki, Takeshi Voelkel, Norbert F Toga, Hirohisa
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up_date	2024-07-03T19:58:06.307Z
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Sirt1 expression is associated with CD31 expression in blood cells from patients with chronic obstructive pulmonary disease

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