Akam-Baxter Eman, Chen Howard H, Boukhalfa Asma, Yu Ada, Ling Lauren A, Kung Andrew H, Bulnes Rodriguez Susana, Yuan Hushan, Josephson Lee, Sosnovik David E
Cardiovascular Research Center, Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02129, USA.
Institute for Innovation in Imaging, Massachusetts General Hospital, Boston, MA, 02129, USA.
Small. 2025 Feb;21(6):e2407915. doi: 10.1002/smll.202407915. Epub 2024 Dec 26.
Autophagy is a key biological process that has proven extremely difficult to detect noninvasively. To address this, an autophagy detecting nanoparticle (ADN) was recently developed, consisting of an iron oxide nanoparticle decorated with cathepsin-cleavable arginine-rich peptides bound to the near-infrared fluorochrome Cy5.5. Activation of the probe in autophagolysosomes results in the emission of Cy5.5 fluorescence and provides a measure of autophagosome flux. However, in the early autophagosome ADN fluorescence is silent due to fluorochrome stacking. Here, we introduce to ADN a second non-cleavable fluorophore that allows the probe to be tracked through all stages of autophagy. The nature of the secondary/tracking fluorophore has a profound effect on the activation of ADN and the emission of Cy5.5 fluorescence. The lead candidate, ADN2 (featuring AZDye546 as the secondary fluorophore) has the highest activation rate and change in Cy5.5 fluorescence. Absorbance and fluorescence spectrophotometry methods show that the negatively charged AZDye546 interacts with the positively charged polyarginine motifs of the Cy5.5-polyArg activatable fluorophore, resulting in enhanced baseline quenching of the Cy5.5 signal in the nanoprobe. Flow cytometry shows that the activation of ADN2 remains specific for autophagy and is strongly modulated by classical regulators of autophagy (starvation, bafilomycin) and genetic deletion of key autophagy proteins (ATG5, ATG7). ADN2 co-localized strongly with LC3-GFP positive autophagosomes and provided readouts of in vivo probe delivery and activation in the hearts of fed/starved mice. ADN2 enhances the ability to image autophagy without genetic transfection of cells/animals and underscores the possible effects for unanticipated interactions between fluorochromes and other moieties on the surface of decorated nanoparticles.
自噬是一个关键的生物学过程,已证明极难进行非侵入性检测。为了解决这个问题,最近开发了一种自噬检测纳米颗粒(ADN),它由一个氧化铁纳米颗粒组成,该纳米颗粒装饰有与近红外荧光染料Cy5.5结合的组织蛋白酶可裂解的富含精氨酸的肽。自噬溶酶体中探针的激活导致Cy5.5荧光的发射,并提供自噬体通量的一种度量。然而,在早期自噬体中,由于荧光染料堆积,ADN荧光是沉默的。在这里,我们向ADN引入了第二种不可裂解的荧光团,它使探针能够在自噬的所有阶段被追踪。二级/追踪荧光团的性质对ADN的激活和Cy5.5荧光的发射有深远影响。主要候选物ADN2(以AZDye546作为二级荧光团)具有最高的激活率和Cy5.5荧光变化。吸光度和荧光分光光度法表明,带负电荷的AZDye546与Cy5.5-聚精氨酸可激活荧光团的带正电荷的聚精氨酸基序相互作用,导致纳米探针中Cy5.5信号的基线猝灭增强。流式细胞术表明,ADN2的激活对自噬仍然具有特异性,并且受到自噬的经典调节剂(饥饿、巴弗洛霉素)和关键自噬蛋白(ATG5、ATG7)的基因缺失的强烈调节。ADN2与LC3-GFP阳性自噬体强烈共定位,并提供了体内探针在喂食/饥饿小鼠心脏中的递送和激活的读数。ADN2增强了在不进行细胞/动物基因转染的情况下对自噬成像的能力,并强调了荧光染料与修饰纳米颗粒表面其他部分之间意外相互作用的可能影响。