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| 1 | MicroRNA-34c-5p provokes isoprenaline-induced cardiac hypertrophy by modulating autophagy via targeting ATG4B显示文摘Pathological cardiac hypertrophy serves as a significant foundation for cardiac dysfunction and heart failure. Recently, growing evidence has revealed that microRNAs(miRNAs) play multiple roles in biological processes and participate in cardiovascular diseases. In the present research, we investigate the impact of miRNA-34 c-5 p on cardiac hypertrophy and the mechanism involved. The expression of miR-34 c-5 p was proved to be elevated in heart tissues from isoprenaline(ISO)-infused mice. ISO also promoted miR-34 c-5 p level in primary cultures of neonatal rat cardiomyocytes(NRCMs). Transfection with miR-34 c-5 p mimic enhanced cell surface area and expression levels of foetal-type genes atrial natriuretic factor(Anf) and β-myosin heavy chain(β-Mhc) in NRCMs. In contrast, treatment with miR-34 c-5 p inhibitor attenuated ISO-induced hypertrophic responses. Enforced expression of miR-34 c-5 p by tail intravenous injection of its agomir led to cardiac dysfunction and hypertrophy in mice, whereas inhibiting miR-34 c-5 p by specific antagomir could protect the animals against ISO-triggered hypertrophic abnormalities. Mechanistically, miR-34 c-5 p suppressed autophagic flux in cardiomyocytes, which contributed to the development of hypertrophy. Furthermore, the autophagy-related gene 4 B(ATG4 B) was identified as a direct target of miR-34 c-5 p, and miR-34 c-5 p was certified to interact with 3’untranslated region of Atg4 b mRNA by dual-luciferase reporter assay. miR-34 c-5 p reduced the expression of ATG4 B, thereby resulting in decreased autophagy activity and induction of hypertrophy. Inhibition of miR-34 c-5 p abolished the detrimental effects of ISO by restoring ATG4 B and increasing autophagy. In conclusion, our findings illuminate that miR-34 c-5 p participates in ISO-induced cardiac hypertrophy, at least partly through suppressing ATG4 B and autophagy. It suggests that regulation of miR-34 c-5 p may offer a new way for handling hypertrophy-related cardiac dysfunction. | Yuhong Zhang Yanqing Ding Min Li Jing Yuan Youhui Yu Xueying Bi Huiqi Hong Jiantao Ye Peiqing Liu | 2022 | Acta Pharmaceutica Sinica B2022，12，5： | 4 |
| 2 | Prediction of grindahility with multivariahle regression and neural network in Chinese coal显示文摘 | Li Peisheng Xiong Youhui Yu Dunxi Sun Xuexin | 2005 | Fuel2005，84，18： | 1 |
| 3 | Intercellular transfer of activated STING triggered by RAB22A-mediated non-canonical autophagy promotes antitumor immunity显示文摘STING,an endoplasmic reticulum(ER)transmembrane protein,mediates innate immune activation upon cGAMP stimulation and is degraded through autophagy.Here,we report that activated STING could be transferred between cells to promote antitumor immunity,a process triggered by RAB22A-mediated non-canonical autophagy.Mechanistically,RAB22A engages PI4K2A to generate PI4P that recruits the Atg12–Atg5–Atg16L1 complex,inducing the formation of ER-derived RAB22A-mediated non-canonical autophagosome,in which STING activated by agonists or chemoradiotherapy is packaged.This RAB22A-induced autophagosome fuses with RAB22A-positive early endosome,generating a new organelle that we name Rafeesome(RAB22A-mediated non-canonical autophagosome fused with early endosome).Meanwhile,RAB22A inactivates RAB7 to suppress the fusion of Rafeesome with lysosome,thereby enabling the secretion of the inner vesicle of the autophagosome bearing activated STING as a new type of extracellular vesicle that we define as R-EV(RAB22A-induced extracellular vesicle).Activated STING-containing R-EVs induce IFNβrelease from recipient cells to the tumor microenvironment,promoting antitumor immunity.Consistently,RAB22A enhances the antitumor effect of the STING agonist diABZI in mice,and a high RAB22A level predicts good survival in nasopharyngeal cancer patients treated with chemoradiotherapy.Our findings reveal that Rafeesome regulates the intercellular transfer of activated STING to trigger and spread antitumor immunity,and that the inner vesicle of non-canonical autophagosome originated from ER is secreted as R-EV,providing a new perspective for understanding the intercellular communication of organelle membrane proteins. | Ying Gao Xueping Zheng Boyang Chang Yujie Lin Xiaodan Huang Wen Wang Shirong Ding Weixiang Zhan Shang Wang Beibei Xiao Lanqing Huo Youhui Yu Yilin Chen Run Gong Yuanzhong Wu Ruhua Zhang Li Zhong Xin Wang Qiuyan Chen Song Gao Zhengfan Jiang Denghui Wei Tiebang Kang | 2022 | Cell Research2022，32，12： | 1 |
| 4 | Deciphering the high-carbonization-temperature triggered enzymatic activity of wool-derived N,S-co-doped carbon nanosheets显示文摘It is well-established that high carbonization temperature will trigger the enzyme-like activity of carbon-based materials.However,the catalytic mechanism is still ambiguous,which hinders the further rational design of nanomaterials as enzyme mimics.Hereby,N,S-rich carbonized wool nanosheets(CWs)were synthesized at different pyrolysis temperatures.As expected,only CWs treated with high-temperature possess intrinsic oxidase-and peroxidase-like activities.Meanwhile,density functional theory(DFT)calculations demonstrate that graphitic nitrogen and the co-existence of nitrogen and sulfur in the carbon matrix serve as the active sites for the enzyme-like process.More importantly,combining theoretical calculations and experimental observations,the high-temperature triggered catalytic mechanism can be ascribed to the fact that an appropriate high-temperature maximizes the graphitization degree to a certain extent,at which most of the catalytic active sites are well retained rather than evaporating.Moreover,coupling with excellent photothermal conversion efficiency and catalytic performance,CWs can be applied to photothermal-catalytic cancer therapy under near-infrared region(NIR)light irradiation.We believe this work will contribute to understanding the catalytic mechanism of carbon-based nanozymes and promote the development of new biomedical and pharmaceutical applications. | Jiachen Zhao Deshuai Yu Jianmin Chen Shihao Lin Yonghua Tang Chaoyu Fan Dongfang Zhou Youhui Lin | 2024 | Chinese Chemical Letters2024，35，3： | 0 |
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