AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1

A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random a...
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Autor*in:	Yi Tian [verfasserIn] Lan Jin [verfasserIn] Wenhong Zhang [verfasserIn] Zumeng Ya [verfasserIn] Yuan Cheng [verfasserIn] Hongyun Zhao [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Übergeordnetes Werk:	In: Genes and Diseases - KeAi Communications Co., Ltd., 2016, 6(2019), 2, Seite 185-192
Übergeordnetes Werk:	volume:6 ; year:2019 ; number:2 ; pages:185-192

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.gendis.2018.05.002

Katalog-ID:	DOAJ033955182

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520			\|a A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment
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allfields	10.1016/j.gendis.2018.05.002 doi (DE-627)DOAJ033955182 (DE-599)DOAJfa188231c2ee49a58b5027e65b286e58 DE-627 ger DE-627 rakwb eng R5-920 QH426-470 Yi Tian verfasserin aut AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment Medicine (General) Genetics Lan Jin verfasserin aut Wenhong Zhang verfasserin aut Zumeng Ya verfasserin aut Yuan Cheng verfasserin aut Hongyun Zhao verfasserin aut In Genes and Diseases KeAi Communications Co., Ltd., 2016 6(2019), 2, Seite 185-192 (DE-627)826104428 (DE-600)2821806-1 23523042 nnns volume:6 year:2019 number:2 pages:185-192 https://doi.org/10.1016/j.gendis.2018.05.002 kostenfrei https://doaj.org/article/fa188231c2ee49a58b5027e65b286e58 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352304218300631 kostenfrei https://doaj.org/toc/2352-3042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_2014 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 6 2019 2 185-192
spelling	10.1016/j.gendis.2018.05.002 doi (DE-627)DOAJ033955182 (DE-599)DOAJfa188231c2ee49a58b5027e65b286e58 DE-627 ger DE-627 rakwb eng R5-920 QH426-470 Yi Tian verfasserin aut AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment Medicine (General) Genetics Lan Jin verfasserin aut Wenhong Zhang verfasserin aut Zumeng Ya verfasserin aut Yuan Cheng verfasserin aut Hongyun Zhao verfasserin aut In Genes and Diseases KeAi Communications Co., Ltd., 2016 6(2019), 2, Seite 185-192 (DE-627)826104428 (DE-600)2821806-1 23523042 nnns volume:6 year:2019 number:2 pages:185-192 https://doi.org/10.1016/j.gendis.2018.05.002 kostenfrei https://doaj.org/article/fa188231c2ee49a58b5027e65b286e58 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352304218300631 kostenfrei https://doaj.org/toc/2352-3042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_2014 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 6 2019 2 185-192
allfields_unstemmed	10.1016/j.gendis.2018.05.002 doi (DE-627)DOAJ033955182 (DE-599)DOAJfa188231c2ee49a58b5027e65b286e58 DE-627 ger DE-627 rakwb eng R5-920 QH426-470 Yi Tian verfasserin aut AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment Medicine (General) Genetics Lan Jin verfasserin aut Wenhong Zhang verfasserin aut Zumeng Ya verfasserin aut Yuan Cheng verfasserin aut Hongyun Zhao verfasserin aut In Genes and Diseases KeAi Communications Co., Ltd., 2016 6(2019), 2, Seite 185-192 (DE-627)826104428 (DE-600)2821806-1 23523042 nnns volume:6 year:2019 number:2 pages:185-192 https://doi.org/10.1016/j.gendis.2018.05.002 kostenfrei https://doaj.org/article/fa188231c2ee49a58b5027e65b286e58 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352304218300631 kostenfrei https://doaj.org/toc/2352-3042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_2014 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 6 2019 2 185-192
allfieldsGer	10.1016/j.gendis.2018.05.002 doi (DE-627)DOAJ033955182 (DE-599)DOAJfa188231c2ee49a58b5027e65b286e58 DE-627 ger DE-627 rakwb eng R5-920 QH426-470 Yi Tian verfasserin aut AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment Medicine (General) Genetics Lan Jin verfasserin aut Wenhong Zhang verfasserin aut Zumeng Ya verfasserin aut Yuan Cheng verfasserin aut Hongyun Zhao verfasserin aut In Genes and Diseases KeAi Communications Co., Ltd., 2016 6(2019), 2, Seite 185-192 (DE-627)826104428 (DE-600)2821806-1 23523042 nnns volume:6 year:2019 number:2 pages:185-192 https://doi.org/10.1016/j.gendis.2018.05.002 kostenfrei https://doaj.org/article/fa188231c2ee49a58b5027e65b286e58 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352304218300631 kostenfrei https://doaj.org/toc/2352-3042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_2014 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 6 2019 2 185-192
allfieldsSound	10.1016/j.gendis.2018.05.002 doi (DE-627)DOAJ033955182 (DE-599)DOAJfa188231c2ee49a58b5027e65b286e58 DE-627 ger DE-627 rakwb eng R5-920 QH426-470 Yi Tian verfasserin aut AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment Medicine (General) Genetics Lan Jin verfasserin aut Wenhong Zhang verfasserin aut Zumeng Ya verfasserin aut Yuan Cheng verfasserin aut Hongyun Zhao verfasserin aut In Genes and Diseases KeAi Communications Co., Ltd., 2016 6(2019), 2, Seite 185-192 (DE-627)826104428 (DE-600)2821806-1 23523042 nnns volume:6 year:2019 number:2 pages:185-192 https://doi.org/10.1016/j.gendis.2018.05.002 kostenfrei https://doaj.org/article/fa188231c2ee49a58b5027e65b286e58 kostenfrei http://www.sciencedirect.com/science/article/pii/S2352304218300631 kostenfrei https://doaj.org/toc/2352-3042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_70 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_2014 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 6 2019 2 185-192
language	English
source	In Genes and Diseases 6(2019), 2, Seite 185-192 volume:6 year:2019 number:2 pages:185-192
sourceStr	In Genes and Diseases 6(2019), 2, Seite 185-192 volume:6 year:2019 number:2 pages:185-192
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topic_facet	Medicine (General) Genetics
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authorswithroles_txt_mv	Yi Tian @@aut@@ Lan Jin @@aut@@ Wenhong Zhang @@aut@@ Zumeng Ya @@aut@@ Yuan Cheng @@aut@@ Hongyun Zhao @@aut@@
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callnumber-first	R - Medicine
author	Yi Tian
spellingShingle	Yi Tian misc R5-920 misc QH426-470 misc Medicine (General) misc Genetics AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1
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topic_title	R5-920 QH426-470 AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1
topic	misc R5-920 misc QH426-470 misc Medicine (General) misc Genetics
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title	AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1
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title_full	AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1
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author_browse	Yi Tian Lan Jin Wenhong Zhang Zumeng Ya Yuan Cheng Hongyun Zhao
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title_sort	amf sirna treatment of keloid through inhibition signaling pathway of rhoa/rock1
callnumber	R5-920
title_auth	AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1
abstract	A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment
abstractGer	A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment
abstract_unstemmed	A keloid (KD) is a benign dermal fibrotic tumor. Treatment of KDs is challenging and the recurrence rate is high; thus, there is an unmet need to explore new target sites and new treatment methods. As a tumor-associated cytokine, autocrine motility factor (AMF) can effectively stimulate the random and directional movement of cells. We first found that AMF was overexpressed in keloid fibroblasts (KFs) and the proliferation and migration of KFs were promoted by AMF stimulation. After treatment with Y-27632, RhoA kinase inhibitor, the proliferation and migration capacity of KFs declined significantly, and type I collagen protein, active RhoA and ROCK1 also were downregulated. In addition, a KD transplantation model was established under the skin of nude mice, with KD intramural injection AMF siRNA, we found that the weight of the KD was smaller than in the control group (P < 0.05), KD tissue sections stained by HE and Masson showed that fibers became loose and the blood vessels were visibly reduced. In conclusion, AMF siRNA is expected to be a novel strategy to treat KD by inhibiting signaling pathway of RhoA/ROCK1. keywords: Autocrine motility factor, Keloid, RhoA, SIRNA, Treatment
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title_short	AMF siRNA treatment of keloid through inhibition signaling pathway of RhoA/ROCK1
url	https://doi.org/10.1016/j.gendis.2018.05.002 https://doaj.org/article/fa188231c2ee49a58b5027e65b286e58 http://www.sciencedirect.com/science/article/pii/S2352304218300631 https://doaj.org/toc/2352-3042
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author2	Lan Jin Wenhong Zhang Zumeng Ya Yuan Cheng Hongyun Zhao
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up_date	2024-07-03T20:34:40.419Z
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