ATF3，全稱為Activating Transcription Factor 3，是一種具有轉(zhuǎn)錄調(diào)控功能的蛋白質(zhì)。它主要通過(guò)調(diào)節(jié)基因的表達(dá)，參與了細(xì)胞增殖、細(xì)胞衰老、細(xì)胞死亡、DNA損傷修復(fù)等多個(gè)重要的生物學(xué)過(guò)程。然而，最近的研究發(fā)現(xiàn)，ATF3在我們的身心健康和成功取得方面也發(fā)揮著關(guān)鍵作用。
廣州醫(yī)科大學(xué)在Circulation Research雜志有新的文獻(xiàn)研究，《Spatiotemporal ATF3 Expression DeterminesVSMC Fate in Abdominal Aortic Aneurysm》，該研究表明ATF3的時(shí)空表達(dá)決定腹主動(dòng)脈瘤VSMC的命運(yùn)。研究結(jié)果顯示，在Ang II誘導(dǎo)的AAA小鼠和AAA患者中，動(dòng)脈瘤組織中ATF3表達(dá)降低，主動(dòng)脈病變組織中ATF3表達(dá)升高。血管平滑肌細(xì)胞中ATF3的缺乏促進(jìn)了Ang II誘導(dǎo)的AAA小鼠的AAA形成。PDGFRB(血小板衍生生長(zhǎng)因子受體β)被確定為ATF3的靶點(diǎn)，ATF3在AAA早期響應(yīng)TNF-α(腫瘤壞死因子-α)介導(dǎo)血管平滑肌細(xì)胞增殖，ATF3通過(guò)上調(diào)其直接靶點(diǎn)BCL2抑制晚期線粒體依賴性凋亡。染色質(zhì)免疫沉淀結(jié)果還表明，NFκB1和P300/BAF/H3K27ac復(fù)合物募集到ATF3啟動(dòng)子上，通過(guò)增強(qiáng)子激活誘導(dǎo)ATF3轉(zhuǎn)錄。NFKB1抑制劑(穿心蓮內(nèi)酯)通過(guò)阻斷募集者NFκB1和ATF3增強(qiáng)子到達(dá)ATF3啟動(dòng)子區(qū)域，從而抑制ATF3的表達(dá)，最終導(dǎo)致AAA的發(fā)展。該研究結(jié)果表明，ATF3在AAA的發(fā)生和發(fā)展中發(fā)揮了以前未被認(rèn)識(shí)到的作用，ATF3可能作為AAA的一種新的治療和預(yù)后標(biāo)志物。Transmission eleetron microseopy (TEM)The TEM were supported by Wuhan PinuofeiBiological Co, Ltd. Briefly, to detect the ultrastructural internalization of mitochondrial damage in VSMCs, fresh abdominalaortas were harvested and then fixed with 2.5% glutaraldehyde for more than 2 hoursThen tissues embedded in Epon resin (EMbed-812 resin) after rinsed, fixed, anddehydrated in ethanol series, stained with uranyl acetate and lead citrate, ultrathinsections (100 nm) were examined by the transmission electron microscope FEI CM100(Japan Electron Optics Laboratory). Images were recorded with an Advantage CCDcamera using iTEM software (Olympus)。武漢市皮諾飛生物科技有限公司完成了該論文的透射電鏡方面的工作，所做數(shù)據(jù)如下：
