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[1]陳婷,陳麗娟,陳銀河.Smad泛素化調(diào)節(jié)因子2對(duì)人胚胎眼鞏膜成纖維細(xì)胞TGF-β1/Smads信號(hào)通路和I型膠原表達(dá)的影響[J].福建醫(yī)藥雜志,2022,44(02):110-113.
 CHEN Ting,CHEN Lijuan,CHEN Yinhe.Effect of Smad ubiquitination regulator factor 2(Smurf 2)on TGF-β1/Smads signal pathway andexpression of type I collagen in human fetal scleral fibroblasts(HFSFs)cells[J].FUJIAN MEDICAL JOURNAL,2022,44(02):110-113.
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Smad泛素化調(diào)節(jié)因子2對(duì)人胚胎眼鞏膜成纖維細(xì)胞TGF-β1/Smads信號(hào)通路和I型膠原表達(dá)的影響()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
44
期數(shù):
2022年02期
頁(yè)碼:
110-113
欄目:
基礎(chǔ)研究
出版日期:
2022-04-15

文章信息/Info

Title:
Effect of Smad ubiquitination regulator factor 2(Smurf 2)on TGF-β1/Smads signal pathway andexpression of type I collagen in human fetal scleral fibroblasts(HFSFs)cells
文章編號(hào):
1002-2600(2022)02-0110-04
作者:
陳婷陳麗娟1陳銀河2
福建醫(yī)科大學(xué)附屬第二醫(yī)院眼科(泉州 362000)
Author(s):
CHEN Ting CHEN Lijuan CHEN Yinhe
Department of Ophthalmology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian 362000, China
關(guān)鍵詞:
Smad泛素化調(diào)節(jié)因子2(Smurf2) 人胚胎眼鞏膜成纖維細(xì)胞(HFSFs細(xì)胞) TGF-β1/Smad通路 近視
Keywords:
Smad ubiquitination regulatory factor 2(Smurf2) human fetal scleral fibroblasts(HFSFs)cells transforming growth factor-β1(TGF-β1) Smad pathway myopia
分類(lèi)號(hào):
R778.1
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 探討Smad泛素化調(diào)節(jié)因子2(Smurf2)在轉(zhuǎn)化生長(zhǎng)因子-β1(TGF-β1)誘導(dǎo)后對(duì)人胚胎眼鞏膜成纖維細(xì)胞(HFSFs)分泌Smads蛋白、I型膠原α1(COLIA1)的影響,探討泛素化在鞏膜重塑中的作用。方法 HFSFs復(fù)蘇并穩(wěn)定傳代后,免疫組化(IHC)法檢測(cè)細(xì)胞中Smurf2的表達(dá)。將HFSFs細(xì)胞分別設(shè)空白對(duì)照組、TGF-β1 組(加入10 ng/mL TGF-β1)、Control siRNA轉(zhuǎn)染組(10 ng/mL TGF-β1+Control siRNA)及Smurf2 siRNA轉(zhuǎn)染組(10ng/mL TGF-β1+Smurf2 siRNA)。Western Blot法檢測(cè)COLIA1蛋白表達(dá)水平。RT-PCR法檢測(cè)各組細(xì)胞中Smurf2、Smad2、Smad3和Smad7的mRNA表達(dá)水平。結(jié)果 IHC結(jié)果顯示,HFSFs中有Smurf2蛋白表達(dá)。TGF-β1誘導(dǎo)HFSFs中COLIA1蛋白顯著性高表達(dá),而當(dāng)Smurf2被抑制時(shí),COLIA1蛋白表達(dá)受抑制。與空白對(duì)照組比較,Smad7 mRNA表達(dá)水平呈上升趨勢(shì),差異有統(tǒng)計(jì)意義(P<0.05),但Smad7蛋白表達(dá)水平與PCR結(jié)果不完全相同; 各培養(yǎng)組中Smad2和Smad3 mRNA和蛋白表達(dá)水平,與對(duì)照組比較,差異均無(wú)統(tǒng)計(jì)學(xué)意義(P>0.05)。結(jié)論 Smurf2表達(dá)于HFSFs細(xì)胞中,且隨著Smurf2表達(dá)減少,HFSFs細(xì)胞中Smad7蛋白含量呈上升趨勢(shì),COLIA1含量呈下降趨勢(shì)。提示Smurf2可能通過(guò)作用于TGF-β1/Smads信號(hào)通路參與了鞏膜重塑過(guò)程。
Abstract:
Objective To explore the effect of Smad ubiquitination regulator factor 2(Smurf2)on the secretion of Smads protein and Collagen type I α1(COLIA1)by human fetal scleral fibroblasts(HFSFs)after induction by transforming growth factor-β1(TGF-β1).Methods After recovery and stable passage of HFSFs,expression of Smurt2 in cells was detected by immunohistochemistry(IHC).The HFSFs were set up as control group, TGF-β1 group(10ng/mL TGF-β1), control siRNA transfection group(10 ng/mL TGF-β1+control siRNA)and Smurf2 siRNA transfection group(10 ng/mL TGF -β1+Smurf2 siRNA).Western Blot method was used to detect the expression level of COLIA1.The mRNA expression levels of Smurf2, Smad2, Smad3 and Smad7 in each group were detected by RT-PCR.Results IHC showed the expression of Smurf2 in HFSFs.The COLIA1 of HFSFs induced by TGF-β1 was highly expressed.When Smurf2 was inhibited, the expression of COLIA1 decreased significantly.Compared with the control group, the mRNA expression level of Smad7 showed an upward trend, and the difference was statistically significant(P<0.05).However, the Smad7 protein expression level was not exactly the same as the PCR result.Compared with the control group, the mRNA and protein expression levels of Smad2 and Smad3 in the other three groups were not statistically significant(P>0.05).Conclusion Smurf2 is expressed in HFSFs, and as the expression of Smurf2 decreases, the protein content of Smad7 in HFSFs shows an upward trend, while the content of COLIA1 shows a downward trend.The Smurf2 may be involved in the pathological process of scleral remodeling by acting on the TGF-β1/Smads signaling pathway.

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備注/Memo

備注/Memo:
基金項(xiàng)目:福建省教育廳中青年教師教育科研項(xiàng)目(JAT170249)
1 漳州衛(wèi)生職業(yè)學(xué)院醫(yī)學(xué)技術(shù)系眼視光教研室; 2 通信作者,泉州市婦幼保健院·兒童醫(yī)院眼科,Email:[email protected]
更新日期/Last Update: 2022-04-15