Regulation of type I collagen expression by microRNA-29 following ionizing radiation

Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase...
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Autor*in:	Hiroyuki Yano [verfasserIn] Ryoji Hamanaka Miki Nakamura-Ota Juan Juan Zhang Noritaka Matsuo Hidekatsu Yoshioka

Format:	Artikel
Sprache:	Englisch

Erschienen:	2017

Schlagwörter:	Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction

Übergeordnetes Werk:	Enthalten in: Radiation and environmental biophysics - Berlin : Springer, 1974, (2017), Seite 1-14
Übergeordnetes Werk:	year:2017 ; pages:1-14

Links:	Volltext Link aufrufen

DOI / URN:	10.1007/s00411-017-0723-4

Katalog-ID:	OLC1998956601

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520			\|a Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF.
650		4	\|a Transforming growth factor
650		4	\|a Ions
650		4	\|a Fibrosis
650		4	\|a Transcription
650		4	\|a Ribonucleic acid--RNA
650		4	\|a Inhibition
650		4	\|a Smad protein
650		4	\|a Irradiated
650		4	\|a Nucleotides
650		4	\|a Fibroblasts
650		4	\|a Collagen
650		4	\|a Gene sequencing
650		4	\|a Gene expression
650		4	\|a Radiation
650		4	\|a Ionizing radiation
650		4	\|a Ribonucleic acids
650		4	\|a Extracellular matrix
650		4	\|a Radiation effects
650		4	\|a Smad3 protein
650		4	\|a MiRNA
650		4	\|a Collagen (type I)
650		4	\|a Signalling
650		4	\|a Signal transduction
700	0		\|a Ryoji Hamanaka \|4 oth
700	0		\|a Miki Nakamura-Ota \|4 oth
700	0		\|a Juan Juan Zhang \|4 oth
700	0		\|a Noritaka Matsuo \|4 oth
700	0		\|a Hidekatsu Yoshioka \|4 oth
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allfields	10.1007/s00411-017-0723-4 doi PQ20171228 (DE-627)OLC1998956601 (DE-599)GBVOLC1998956601 (PRQ)p576-90700e6e2655480389ffa8c9a5e5ec4b30fc3416f34235aac1f5a96bab8d6b0c0 (KEY)0050200620170000000000000001regulationoftypeicollagenexpressionbymicrorna29fol DE-627 ger DE-627 rakwb eng 18a 500 520 530 540 550 560 570 580 590 DE-101 570 AVZ BIODIV fid Hiroyuki Yano verfasserin aut Regulation of type I collagen expression by microRNA-29 following ionizing radiation 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF. Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction Ryoji Hamanaka oth Miki Nakamura-Ota oth Juan Juan Zhang oth Noritaka Matsuo oth Hidekatsu Yoshioka oth Enthalten in Radiation and environmental biophysics Berlin : Springer, 1974 (2017), Seite 1-14 (DE-627)129308528 (DE-600)124987-3 (DE-576)014507870 0301-634X nnns year:2017 pages:1-14 http://dx.doi.org/10.1007/s00411-017-0723-4 Volltext https://search.proquest.com/docview/1975465666 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-GGO GBV_ILN_70 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4277 AR 2017 1-14
spelling	10.1007/s00411-017-0723-4 doi PQ20171228 (DE-627)OLC1998956601 (DE-599)GBVOLC1998956601 (PRQ)p576-90700e6e2655480389ffa8c9a5e5ec4b30fc3416f34235aac1f5a96bab8d6b0c0 (KEY)0050200620170000000000000001regulationoftypeicollagenexpressionbymicrorna29fol DE-627 ger DE-627 rakwb eng 18a 500 520 530 540 550 560 570 580 590 DE-101 570 AVZ BIODIV fid Hiroyuki Yano verfasserin aut Regulation of type I collagen expression by microRNA-29 following ionizing radiation 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF. Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction Ryoji Hamanaka oth Miki Nakamura-Ota oth Juan Juan Zhang oth Noritaka Matsuo oth Hidekatsu Yoshioka oth Enthalten in Radiation and environmental biophysics Berlin : Springer, 1974 (2017), Seite 1-14 (DE-627)129308528 (DE-600)124987-3 (DE-576)014507870 0301-634X nnns year:2017 pages:1-14 http://dx.doi.org/10.1007/s00411-017-0723-4 Volltext https://search.proquest.com/docview/1975465666 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-GGO GBV_ILN_70 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4277 AR 2017 1-14
allfields_unstemmed	10.1007/s00411-017-0723-4 doi PQ20171228 (DE-627)OLC1998956601 (DE-599)GBVOLC1998956601 (PRQ)p576-90700e6e2655480389ffa8c9a5e5ec4b30fc3416f34235aac1f5a96bab8d6b0c0 (KEY)0050200620170000000000000001regulationoftypeicollagenexpressionbymicrorna29fol DE-627 ger DE-627 rakwb eng 18a 500 520 530 540 550 560 570 580 590 DE-101 570 AVZ BIODIV fid Hiroyuki Yano verfasserin aut Regulation of type I collagen expression by microRNA-29 following ionizing radiation 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF. Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction Ryoji Hamanaka oth Miki Nakamura-Ota oth Juan Juan Zhang oth Noritaka Matsuo oth Hidekatsu Yoshioka oth Enthalten in Radiation and environmental biophysics Berlin : Springer, 1974 (2017), Seite 1-14 (DE-627)129308528 (DE-600)124987-3 (DE-576)014507870 0301-634X nnns year:2017 pages:1-14 http://dx.doi.org/10.1007/s00411-017-0723-4 Volltext https://search.proquest.com/docview/1975465666 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-GGO GBV_ILN_70 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4277 AR 2017 1-14
allfieldsGer	10.1007/s00411-017-0723-4 doi PQ20171228 (DE-627)OLC1998956601 (DE-599)GBVOLC1998956601 (PRQ)p576-90700e6e2655480389ffa8c9a5e5ec4b30fc3416f34235aac1f5a96bab8d6b0c0 (KEY)0050200620170000000000000001regulationoftypeicollagenexpressionbymicrorna29fol DE-627 ger DE-627 rakwb eng 18a 500 520 530 540 550 560 570 580 590 DE-101 570 AVZ BIODIV fid Hiroyuki Yano verfasserin aut Regulation of type I collagen expression by microRNA-29 following ionizing radiation 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF. Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction Ryoji Hamanaka oth Miki Nakamura-Ota oth Juan Juan Zhang oth Noritaka Matsuo oth Hidekatsu Yoshioka oth Enthalten in Radiation and environmental biophysics Berlin : Springer, 1974 (2017), Seite 1-14 (DE-627)129308528 (DE-600)124987-3 (DE-576)014507870 0301-634X nnns year:2017 pages:1-14 http://dx.doi.org/10.1007/s00411-017-0723-4 Volltext https://search.proquest.com/docview/1975465666 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-GGO GBV_ILN_70 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4277 AR 2017 1-14
allfieldsSound	10.1007/s00411-017-0723-4 doi PQ20171228 (DE-627)OLC1998956601 (DE-599)GBVOLC1998956601 (PRQ)p576-90700e6e2655480389ffa8c9a5e5ec4b30fc3416f34235aac1f5a96bab8d6b0c0 (KEY)0050200620170000000000000001regulationoftypeicollagenexpressionbymicrorna29fol DE-627 ger DE-627 rakwb eng 18a 500 520 530 540 550 560 570 580 590 DE-101 570 AVZ BIODIV fid Hiroyuki Yano verfasserin aut Regulation of type I collagen expression by microRNA-29 following ionizing radiation 2017 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF. Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction Ryoji Hamanaka oth Miki Nakamura-Ota oth Juan Juan Zhang oth Noritaka Matsuo oth Hidekatsu Yoshioka oth Enthalten in Radiation and environmental biophysics Berlin : Springer, 1974 (2017), Seite 1-14 (DE-627)129308528 (DE-600)124987-3 (DE-576)014507870 0301-634X nnns year:2017 pages:1-14 http://dx.doi.org/10.1007/s00411-017-0723-4 Volltext https://search.proquest.com/docview/1975465666 GBV_USEFLAG_A SYSFLAG_A GBV_OLC FID-BIODIV SSG-OLC-PHY SSG-OLC-PHA SSG-OLC-DE-84 SSG-OPC-GGO GBV_ILN_70 GBV_ILN_2018 GBV_ILN_4012 GBV_ILN_4277 AR 2017 1-14
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source	Enthalten in Radiation and environmental biophysics (2017), Seite 1-14 year:2017 pages:1-14
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topic_facet	Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction
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author	Hiroyuki Yano
spellingShingle	Hiroyuki Yano ddc 18a ddc 570 fid BIODIV misc Transforming growth factor misc Ions misc Fibrosis misc Transcription misc Ribonucleic acid--RNA misc Inhibition misc Smad protein misc Irradiated misc Nucleotides misc Fibroblasts misc Collagen misc Gene sequencing misc Gene expression misc Radiation misc Ionizing radiation misc Ribonucleic acids misc Extracellular matrix misc Radiation effects misc Smad3 protein misc MiRNA misc Collagen (type I) misc Signalling misc Signal transduction Regulation of type I collagen expression by microRNA-29 following ionizing radiation
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topic_title	18a 500 520 530 540 550 560 570 580 590 DE-101 570 AVZ BIODIV fid Regulation of type I collagen expression by microRNA-29 following ionizing radiation Transforming growth factor Ions Fibrosis Transcription Ribonucleic acid--RNA Inhibition Smad protein Irradiated Nucleotides Fibroblasts Collagen Gene sequencing Gene expression Radiation Ionizing radiation Ribonucleic acids Extracellular matrix Radiation effects Smad3 protein MiRNA Collagen (type I) Signalling Signal transduction
topic	ddc 18a ddc 570 fid BIODIV misc Transforming growth factor misc Ions misc Fibrosis misc Transcription misc Ribonucleic acid--RNA misc Inhibition misc Smad protein misc Irradiated misc Nucleotides misc Fibroblasts misc Collagen misc Gene sequencing misc Gene expression misc Radiation misc Ionizing radiation misc Ribonucleic acids misc Extracellular matrix misc Radiation effects misc Smad3 protein misc MiRNA misc Collagen (type I) misc Signalling misc Signal transduction
topic_unstemmed	ddc 18a ddc 570 fid BIODIV misc Transforming growth factor misc Ions misc Fibrosis misc Transcription misc Ribonucleic acid--RNA misc Inhibition misc Smad protein misc Irradiated misc Nucleotides misc Fibroblasts misc Collagen misc Gene sequencing misc Gene expression misc Radiation misc Ionizing radiation misc Ribonucleic acids misc Extracellular matrix misc Radiation effects misc Smad3 protein misc MiRNA misc Collagen (type I) misc Signalling misc Signal transduction
topic_browse	ddc 18a ddc 570 fid BIODIV misc Transforming growth factor misc Ions misc Fibrosis misc Transcription misc Ribonucleic acid--RNA misc Inhibition misc Smad protein misc Irradiated misc Nucleotides misc Fibroblasts misc Collagen misc Gene sequencing misc Gene expression misc Radiation misc Ionizing radiation misc Ribonucleic acids misc Extracellular matrix misc Radiation effects misc Smad3 protein misc MiRNA misc Collagen (type I) misc Signalling misc Signal transduction
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title	Regulation of type I collagen expression by microRNA-29 following ionizing radiation
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title_full	Regulation of type I collagen expression by microRNA-29 following ionizing radiation
author_sort	Hiroyuki Yano
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title_sort	regulation of type i collagen expression by microrna-29 following ionizing radiation
title_auth	Regulation of type I collagen expression by microRNA-29 following ionizing radiation
abstract	Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF.
abstractGer	Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF.
abstract_unstemmed	Radiation-induced fibrosis (RIF) is thought to involve the excessive accumulation of collagen and other extracellular matrix components; previously, we reported that ionizing radiation increased the type I collagen expression and that transforming growth factor (TGF)-β was involved in this increase through activating its downstream mediator, Smad3. A recent study found that microRNAs (miRNAs)—small, noncoding sequences approximately 20 nucleotides long—negatively regulate the gene expression posttranscriptionally, and it has been suggested that miRNAs play essential roles in cellular processes, including fibrosis. However, their role in the development of RIF remains unexplored. In the present study, we examined the effects of miRNA on the expression of type I collagen induced by ionizing radiation and the mechanisms underlying the miRNA expression observed following ionizing radiation. We analyzed the regulation of miRNA following ionizing radiation by an miRNA real-time PCR, and found that miR-29 family members were downregulated in irradiated mouse fibroblasts and directly targeted type I collagen genes by specifically binding to the 3ʹ untranslated region. We also found that the overexpression of miR-29 inhibited the ionizing radiation-induced expression of type I collagen, whereas the knockdown of miR-29 enhanced it. In addition, TGF-β/Smad-signaling significantly decreased the transcription of miR-29, whereas the inhibition of this signaling pathway cancelled this decrease. In conclusion, miR-29 was involved in the regulation of type I collagen expression through the TGF-β/Smad-signaling pathway in irradiated cells, suggesting that miR-29 may be an important regulator of RIF.
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title_short	Regulation of type I collagen expression by microRNA-29 following ionizing radiation
url	http://dx.doi.org/10.1007/s00411-017-0723-4 https://search.proquest.com/docview/1975465666
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author2	Ryoji Hamanaka Miki Nakamura-Ota Juan Juan Zhang Noritaka Matsuo Hidekatsu Yoshioka
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