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| 1 | Colonization of endophyte Acremonium sp. D212 in Panax notoginseng and rice mediated by auxin and jasmonic acid显示文摘Endophytic fungi can be beneficial to plant growth. However, the molecular mechanisms under-lying colonization of Acremonium spp. remain unclear. In this study, a novel endophytic Acremonium strain was isolated from the buds of Panax notoginseng and named Acremonium sp. D212. The Acremonium sp. D212 could colonize the roots of P. notoginseng, enhance the resistance of P. notoginseng to root rot disease, and promote root growth and saponin bio-synthesis in P. notoginseng. Acremonium sp. D212 could secrete indole-3-acetic acid (IAA) and jasmonic acid (JA), and inoculation with the fungus increased the endogenous levels of IAA and JA in P. noto-ginseng. Colonization of the Acremonium sp. D212 in the roots of the rice line Nipponbare was dependent on the concentration of methyl jasmonate (MeJA) (2–15μmol/L) and 1-naphthalenacetic acid (NAA) (10–20μmol/L). Moreover, the roots of the JA signaling-defective coi1-18 mutant were colonized by Acremonium sp. D212 to a lesser degree than those of the wild-type Nipponbare and miR393b-overexpressing lines, and the colonization was res-cued by MeJA but not by NAA. It suggests that the cross-talk between JA signaling and the auxin biosynthetic pathway plays a crucial role in the colonization of Acremonium sp. D212 in host plants. | Li Han Xuan Zhou Yiting Zhao Shusheng Zhu Lixia Wu Yunlu He Xiangrui Ping Xinqi Lu Wuying Huang Jie Qian Lina Zhang Xi Jiang Dan Zhu Chongyu Luo Saijie Li Qian Dong Qijing Fu Kaiyuan Deng Xin Wang Lei Wang Sheng Peng Jinsong Wu Weimin Li JiǐíFriml Youyong Zhu Xiahong He Yunlong Du | 2020 | Journal of Integrative Plant Biology2020，62，9： | 2 |
| 2 | Cartilage oligomeric matrix protein is an endogenous β-arrestin-2-selective allosteric modulator of AT1 receptor counteracting vascular injury显示文摘Compelling evidence has revealed that biased activation of G protein-coupled receptor(GPCR)signaling,including angiotensin II(AngII)receptor type 1(AT1)signaling,plays pivotal roles in vascular homeostasis and injury,but whether a clinically relevant endogenous biased antagonism of AT1 signaling exists under physiological and pathophysiological conditions has not been clearly elucidated.Here,we show that an extracellular matrix protein,cartilage oligomeric matrix protein(COMP),acts as an endogenous allosteric biased modulator of the AT1 receptor and its deficiency is clinically associated with abdominal aortic aneurysm(AAA)development.COMP directly interacts with the extracellular N-terminus of the AT1 via its EGF domain and inhibits AT1-β-arrestin-2 signaling,but not Gq or Gi signaling,in a selective manner through allosteric regulation of AT1 intracellular conformational states.COMP deficiency results in activation of AT1a-β-arrestin-2 signaling and subsequent exclusive AAA formation in response to AngII infusion.AAAs in COMP–/–or ApoE–/–mice are rescued by AT1a orβ-arrestin-2 deficiency,or the application of a peptidomimetic mimicking the AT1-binding motif of COMP.Explorations of the endogenous biased antagonism of AT1 receptor or other GPCRs may reveal novel therapeutic strategies for cardiovascular diseases. | Yi Fu Yaqian Huang Zhao Yang Yufei Chen Jingang Zheng Chenfeng Mao Zhiqing Li Zhixin Liu Bing Yu Tuoyi Li Meili Wang Chanjuan Xu Yiwei Zhou Guizhen Zhao Yiting Jia Wei Guo Xin Jia Tao Zhang Li Li Ziyi Liu Shengchao Guo Mingliang Ma Heng Zhang Bo Liu Junbao Du Wengong Wang Chaoshu Tang Pei Gao Qingbo Xu Xian Wang Jianfeng Liu Jinpeng Sun Wei Kong | 2021 | Cell Research2021，31，7： | 2 |
| 3 | Multifunctional Gd-CuS loaded UCST polymeric micelles for MR/PA imaging-guided chemo-photothermal tumor treatment显示文摘Hepatocellular carcinoma(HCC)is a life-threatening disease for which there is no effective treatment currently.Novel theranostics simultaneously having excellent imaging and therapeutic functions are highly desired in cancer therapy.Herein,we develop the sialic acid(SA)modified polymeric micelles at an upper critical solution temperature(UCST)of 43℃(sialic acid-poly(ethylene glycol)-poly(acrylamide-co-acrylonitrile),SA-PEG-p(AAm-co-AN)),which further encapsulated with doxorubicin(DOX)and Gd-CuS nanoparticles(Gd-CuS NPs)for chemo-photothermal treatment of HCC guided by magnetic resonance(MR)/photoacoustic(PA)dual-mode imaging.The resultant SA-PEG-p(AAm-co-AN)/DOX/Gd-CuS(SPDG)had an excellent photothermal conversion efficiency,enabling SPDG with an instantaneous release behavior of DOX under near-infrared(NIR)irradiation.This study also revealed that SPDG could actively target to HCC,which was due to that SA had a high affinity with E-selectin overexpressed at the tumor site.Moreover,benefiting from the HCC-targeted ability and NIR light-controlled on-demand delivery of DOX,SPDG showed a superior potential in MR/PA dual-mode imaging-guided chemo-photothermal treatment.Overall,our study reveals that the designed SPDG may be used as an ideal multifunctional nanoplatform for cancer theranostics. | Yan Du Di Liu Mingchen Sun Gaofeng Shu Jing Qi Yuchan You Yiting Xu Kai Fan Xiaoling Xu Feiyang Jin Jun Wang Qiying Shen Luwen Zhu Xiaoying Ying Jiansong Ji Liming Wu Daren Liu Yongzhong Du | 2022 | Nano Research2022，15，3： | 0 |
| 4 | SIRT2 interacts with DDX24 to promote nasopharyngeal carcinoma growth显示文摘Background:Nasopharyngeal carcinoma(NPC)is one of the most prevalent cancers in Southeast Asia.Sirtuin 2(SIRT2)is a member of the NAD+-dependent deacetylase family and has been shown to play important roles in numerous biological processes.However,Its function in NPC remains uncertain.The primary aim of this study is to clarify the role of SIRT2 in NPC.Methods:In this research,we examined the effect of SIRT2 silencing on NPC cell proliferation and colony formation using vitro NPC cell lines.Co-immunoprecipitation and mass spectrometry was applied to identify SIRT2-interacting proteins in NPC cells.Results:In comparison to nasopharyngeal epithelial NP69 cells,SIRT2 was up-regulated in multiple NPC cell lines,particularly in CNE2 cells.SIRT2 knockdown abrogated CNE2 cell proliferation and colony formation,whereas SIRT2 overexpression promoted HNE1 cell proliferation and colony formation.The SIRT2-interacting proteins were gathered in gene expression and regulation processes including RNA processing and translation.Among the SIRT2-interacting proteins,there were multiple DEAD-box(DDX)family members.Of note,silencing of DDX24 phenocopied the effect of SIRT2 knockdown on NPC growth.Overexpression of DDX24 restored SIRT2-depleted CNE2 cells to proliferative and colony formation.Conclusions:Our study indicates that SIRT2 can interact with DDX24 to enhance NPC growth.The clinical relevance of SIRT2 and DDX24 in NPC warrants further investigation. | HAIYING YUE CHUNHUI WANG HUIJUN ZHU QINGHUA DU JIAN LI XUE OU XIANGDE LI QIULU ZHONG YITING XIE DANJING LUO YIHE LI CHUNXIAO LIANG XUEMEI XU SONGNAN DU WENQI LIU | 2023 | BIOCELL2023，47，11： | 0 |
| 5 | Spatial Distribution of Parvalbumin-Positive Fibers in the Mouse Brain and Their Alterations in Mouse Models of Temporal Lobe Epilepsy and Parkinson’s Disease显示文摘Parvalbumin interneurons belong to the major types of GABAergic interneurons.Although the distribution and pathological alterations of parvalbumin interneuron somata have been widely studied,the distribution and vulnerability of the neurites and fibers extending from parvalbumin interneurons have not been detailly interrogated.Through the Cre recombinase-reporter system,we visualized parvalbumin-positive fibers and thoroughly investigated their spatial distribution in the mouse brain.We found that parvalbumin fibers are widely distributed in the brain with specific morphological characteristics in different regions,among which the cortex and thalamus exhibited the most intense parvalbumin signals.In regions such as the striatum and optic tract,even long-range thick parvalbumin projections were detected.Furthermore,in mouse models of temporal lobe epilepsy and Parkinson’s disease,parvalbumin fibers suffered both massive and subtle morphological alterations.Our study provides an overview of parvalbumin fibers in the brain and emphasizes the potential pathological implications of parvalbumin fiber alterations. | Changgeng Song Yan Zhao Jiajia Zhang Ziyi Dong Xin Kang Yuqi Pan Jinle Du Yiting Gao Haifeng Zhang Ye Xi Hui Ding Fang Kuang Wenting Wang Ceng Luo Zhengping Zhang Qinpeng Zhao Jiazhou Yang Wen Jiang Shengxi Wu Fang Gao | 2023 | Neuroscience Bulletin2023，39，11： | 0 |
| 6 | Correction:Spatial Distribution of Parvalbumin‑Positive Fibers in the Mouse Brain and Their Alterations in Mouse Models of Temporal Lobe Epilepsy and Parkinson’s Disease显示文摘In this article the wrong figure appeared as Fig.3,the figure should have appeared as shown below. | Changgeng Song Yan Zhao Jiajia Zhang Ziyi Dong Xin Kang Yuqi Pan Jinle Du Yiting Gao Haifeng Zhang Ye Xi Hui Ding Fang Kuang Wenting Wang Ceng Luo Zhengping Zhang Qinpeng Zhao Jiazhou Yang Wen Jiang Shengxi Wu Fang Gao | 2023 | Neuroscience Bulletin2023，39，11： | 0 |
| 7 | Investigation and Protection of Fishery Resources in the Middle of Bohai Sea显示文摘In May and October 2017,12 stations were set up in the Central Bohai Sea for fishery resources investigation.The results show that there are many dominant species in this area,and the inshore fishery resources are higher than those in the open sea because of the abundant nutrients from land,the high density of zooplankton and the food of swimming animals.In order to effectively protect the fishery resources in the Central Bohai Sea,this paper puts forward some suggestions,such as strengthening the protection propaganda,scientific and reasonable fishing,and strengthening the management of marine environment. | Ruijia Zhou Xiao Liu Yiting Liu Mengmeng Bao Beibei Sun Xiaoyuan Du | 2021 | Journal of Fisheries Science2021，3，2： | 0 |
| 8 | MALAT1-mediated EZH2 Recruitment to the GFER Promoter Region Curbs Normal Hepatocyte Proliferation in Acute Liver Injury显示文摘Background and Aims:The goal of this study was to investigate the mechanism by which the long noncoding RNA MALAT1 inhibited hepatocyte proliferation in acute liver injury(ALI).Methods:Lipopolysaccharide(LPS)was used to induce an ALI cellular model in HL7702 cells,in which lentivirus vectors containing MALAT1/EZH2/GFER overexpression or knockdown were introduced.A series of experiments were performed to determine their roles in liver injury,oxidative stress injury,and cell biological processes.The interaction of MALAT1 with EZH2 and enrichment of EZH2 and H3K27me3 in the GFER promoter region were identified.Rats were treated with MALAT1 knockdown or GFER overexpression before LPS induction to verify the results derived from the in vitro assay.Results:MALAT1 levels were elevated and GFER levels were reduced in ALI patients and the LPS-induced cell model.MALAT1 knockdown or GFER overexpression suppressed cell apoptosis and oxidative stress injury induced cell proliferation,and reduced ALI.Functionally,MALAT1 interacted directly with EZH2 and increased the enrichment of EZH2 and H3K27me3 in the GFER promoter region to reduce GFER expression.Moreover,MALAT1/EZH2/GFER was activated the AMPK/mTOR signaling pathway.Conclusion:Our study highlighted the inhibitory role of reduced MALAT1 in ALI through the modulation of EZH2-mediated GFER. | Li Chen Xintong Kang Xiujuan Meng Liang Huang Yiting Du Yilan Zeng Chunfeng Liao | 2023 | Journal of Clinical and Translational Hepatology2023，11，1： | 0 |
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