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| 1 | Mycorrhizal symbiosis modulates the rhizosphere microbiota to promote rhizobia–legume symbiosis显示文摘Plants establish symbioses with mutualistic fungi,such as arbuscular mycorrhizal(AM)fungi,and bacteria,such as rhizobia,to exchange key nutrients and thrive.Plants and symbionts have coevolved and represent vital components of terrestrial ecosystems.Plants employ an ancestral AM signaling pathway to establish intracellular symbioses,including the legume–rhizobia symbiosis,in their roots.Nevertheless,the relationship between the AM and rhizobial symbioses in native soil is poorly understood.Here,we examined how these distinct symbioses affect root-associated bacterial communities in Medicago truncatula by performing quantitative microbiota profiling(QMP)of 16S rRNA genes.We found that M.truncatula mutants that cannot establish AM or rhizobia symbiosis have an altered microbial load(quantitative abundance)in the rhizosphere and roots,and in particular that AM symbiosis is required to assemble a normal quantitative root-associated microbiota in native soil.Moreover,quantitative microbial co-abundance network analyses revealed that AM symbiosis affects Rhizobiales hubs among plant microbiota and benefits the plant holobiont.Through QMP of rhizobial rpoB and AM fungal SSU rRNA genes,we revealed a new layer of interaction whereby AM symbiosis promotes rhizobia accumulation in the rhizosphere of M.truncatula.We further showed that AM symbiosis-conditioned microbial communities within the M.truncatula rhizosphere could promote nodulation in different legume plants in native soil.Given that the AM and rhizobial symbioses are critical for crop growth,our findings might inform strategies to improve agricultural management.Moreover,our work sheds light on the co-evolution of these intracellular symbioses during plant adaptation to native soil conditions. | Xiaolin Wang Huan Feng Yayu Wang Mingxing Wang Xingguang Xie Huizhong Chang Like Wang Jicheng Qu Kai Sun Wei He Chunyan Wang Chuanchao Dai Zhaohui Chu Changfu Tian Nan Yu Xuebin Zhang Huan Liu Ertao Wang | 2021 | Molecular Plant2021，14，3： | 6 |
| 2 | Mesenchymal stem cell treatment improves outcome of COVID-19 patients via multiple immunomodulatory mechanisms显示文摘The infusion of coronavirus disease 2019(COVID-19)patients with mesenchymal stem cells(MSCs)potentially improves clinical symptoms,but the underlying mechanism remains unclear.We conducted a randomized,single-blind,placebo-controlled(29 patients/group)phase II clinical trial to validate previous findings and explore the potential mechanisms.Patients treated with umbilical cord-derived MSCs exhibited a shorter hospital stay(P=0.0198)and less time required for symptoms remission(P=0.0194)than those who received placebo.Based on chest images,both severe and critical patients treated with MSCs showed improvement by day 7(P=0.0099)and day 21(P=0.0084).MSC-treated patients had fewer adverse events.MSC infusion reduced the levels of C-reactive protein,proinflammatory cytokines,and neutrophil extracellular traps(NETs)and promoted the maintenance of SARS-CoV-2-specific antibodies.To explore how MSCs modulate the immune system,we employed single-cell RNA sequencing analysis on peripheral blood.Our analysis identified a novel subpopulation of VNN2+hematopoietic stem/progenitorlike(HSPC-like)cells expressing CSF3R and PTPRE that were mobilized following MSC infusion.Genes encoding chemotaxis factors—CX3CR1 and L-selectin—were upregulated in various immune cells.MSC treatment also regulated B cell subsets and increased the expression of costimulatory CD28 in T cells in vivo and in vitro.In addition,an in vivo mouse study confirmed that MSCs suppressed NET release and reduced venous thrombosis by upregulating kindlin-3 signaling.Together,our results underscore the role of MSCs in improving COVID-19 patient outcomes via maintenance of immune homeostasis. | Rongjia Zhu Tingdong Yan Yingmei Feng Yan Liu Hongcui Cao Gongxin Peng Yanlei Yang Zhen Xu Jingqi Liu Wei Hou Xiaoyue Wang Zhe Li Luchan Deng Shihua Wang Jing Li Qin Han Hongling Li Guangliang Shan Yinghao Cao Xingyan An Jianshe Yan Zhonghui Zhang Huafei Li Xuebin Qu Jiaqi Zhu Shumin Zhou Jiao Wang Fengchun Zhang Jinming Gao Ronghua Jin Dayong Xu Yan-Qing Ma Tao Huang Shuang Peng Zhi Zheng Ilia Stambler Eric Gilson Lee Wei Lim Alexey Moskalev Antonio Cano Sasanka Chakrabarti Brun Ulfhake Huanxing Su Haoying Xu Sihuan Xu Feng Wei Holly MBrown-Borg Kyung-Jin Min Georgina Ellison-Hughes Calogero Caruso Kunlin Jin Robert Chunhua Zhao | 2021 | Cell Research2021，31，12： | 5 |
| 3 | The circular RNA circINPP4B acts as a sponge of miR-30a to regulate Th17 cell differentiation during progression of experimental autoimmune encephalomyelitis显示文摘Circular RNAs(circRNAs)regulate gene expression and participate in various biological and pathological processes.However,little is known about the effects of specific circRNAs on T helper cell 17(Th17)differentiation and related autoimmune diseases,such as multiple sclerosis(MS).Here,using transcriptome microarray analysis at different stages of experimental autoimmune encephalomyelitis(EAE),we identified the EAE progression-related circINPP4B,which showed upregulated expression in Th17 cells from mice with EAE and during Th17 differentiation in vitro.Silencing of circINPP4B inhibited Th17 differentiation and alleviated EAE,characterized by less demyelination and Th17 infiltration in the spinal cord.Mechanistically,circINPP4B served as a sponge that directly targeted miR-30a to regulate Th17 differentiation.Furthermore,circINPP4B levels were associated with the developing phases of clinical relapsing-remitting MS patients.Our results indicate that circINPP4B plays an important role in promoting Th17 differentiation and progression of EAE by targeting miR-30a,which provides a potential diagnostic and therapeutic target for Th17-mediated MS. | Jingjing Han Wei Zhuang Wanhua Feng Fuxing Dong Fang Hua Ruiqin Yao Xuebin Qu | 2021 | Cellular & Molecular Immunology2021，18，9： | 2 |
| 4 | MicroRNA-100 regulates osteogenic differentiation of human adipose-derived mesenchymal stem cells by targeting BMPR2显示文摘 | Yang Zeng Xuebin Qu Hongling Li Shan Huang Shihua Wang Qilin Xu Ruizhu Lin Qin Han Jing Li Robert Chunhua Zhao | 2012 | FEBS Letters2012，，16： | 2 |
| 5 | Mesenchymal stem cells hold promise for regenerative medicine显示文摘Regenerative medicine is an emerging interdisciplinary field of research that uses several technological approaches including stem cells to repair tissues.Mesenchymal stem cells(MSCs),a type of adult stem cell,have generated a great amount of interest over the past decade in this field.Numerous studies have explored the role of MSCs in tissue repair and modulation of allogeneic immune responses.The mechanisms through which MSCs exert their therapeutic potential rely on some key properties of the cells as follows:the capacity to differentiate into osteoblasts,chondrocytes,adipocytes,cardiomyocytes,hepatocytes,endothelial,and neuronal cells;the ability to secrete multiple bioactive molecules capable of stimulating the recovery of injured cells and inhibiting inflammation;the lack of immunogenicity;and the ability to perform immunomodulatory functions.In the present review,we focus on these three aspects upon which the therapeutic effects of MSCs are mainly based.Furthermore,some pathological conditions under which the application of MSCs should be done with caution are also mentioned. | Shihua Wang Xuebin Qu Robert Chunhua Zhao | 2011 | Frontiers of Medicine2011，5，4： | 1 |
| 6 | Quercetin improves hypoxia-ischemia induced cognitive deficits via promoting remyelination in neonatal rat显示文摘 | Xuebin Qu Dashi Qi Fuxing Dong | 2014 | Brain Res2014，1553，： | 1 |
| 7 | Mesenchymal stem cells play a potential role in regulating the establishmentand maintenance of epithelial-mesenchymal transition in MCF7 human breast cancercells by paracrine and induced autocrine TGF-β显示文摘 | Qilin Xu Liang Wang Hongling Li Qin Han Jing Li Xuebin Qu Shan Huang Robert Zhao | 2012 | International Journal of Oncology2012，，3： | 1 |
| 8 | MiR-3Oa-centered molecular crosstalk regulates STh17 differentiation显示文摘Recently,there has been growing interest in the specific role of Th17 cells in the pathogenesis of neuroinflammation-related degenerative diseases,including Alzheimer’s disease(AD),Parkinson’s disease(PD),amyotrophic lateral sclerosis(ALS),and multiple sclerosis(MS)[1].The Th17-mediated autoimmune response is a key determinant of these pathological outcomes.Interleukin-17(IL-17),the most important cytokine of activated Th17 cells,is considered a pivotal agent of autoimmunity because of its proinflammatory effect and migration-promoting ability.Although the specific mechanism of Th17/IL-17 is still controversial,exploring the molecular pathways of Th17/IL-17 in neurodegeneration will facilitate the identification of suitable targets to modulate these cellular processes.Th17 differentiation is directed by lineage-specific transcription factors,including RORγt and RORα,and is controlled by the coordinated activity of a series of positive and negative regulators,as well as additional signals from different cytokines to maintain and stabilize the proinflammatory features of Th17 cells[2,3]. | Jingjing Han Wanhua Feng Ruiqin Yao Liucai Yang Xuebin Qu | 2022 | Cellular & Molecular Immunology2022，19，8： | 1 |
| 9 | Conditional Deletion of Foxg1 Alleviates Demyelination and Facilitates Remyelination via the Wnt Signaling Pathway in Cuprizone-Induced Demyelinated Mice显示文摘The massive loss of oligodendrocytes caused by various pathological factors is a basic feature of many demyelinating diseases of the central nervous system(CNS). Based on a variety of studies, it is now well established that impairment of oligodendrocyte precursor cells(OPCs) to differentiate and remyelinate axons is a vital event in the failed treatment of demyelinating diseases. Recent evidence suggests that Foxg1 is essential for the proliferation of certain precursors and inhibits premature neurogenesis during brain development. To date, very little attention has been paid to the role of Foxg1 in the proliferation and differentiation of OPCs in demyelinating diseases of the CNS. Here, for the first time, we examined the effects of Foxg1 on demyelination and remyelination in the brain using a cuprizone(CPZ)-induced mouse model. In this work, 7-week-old Foxg1 conditional knockout and wild-type(WT) mice were fed a diet containing 0.2% CPZ w/w for 5 weeks, after which CPZ was withdrawn to enable remyelination. Our results demonstrated that, compared with WT mice, Foxg1-knockout mice exhibited not only alleviated demyelination but also accelerated remyelination of the demyelinated corpus callosum. Furthermore, we found that Foxg1 knockout decreased the proliferation of OPCs and accelerated their differentiation into mature oligodendrocytes both in vivo and in vitro. Wnt signaling plays a critical role in development and in a variety of diseases. GSK-3 b, a key regulatory kinase in the Wnt pathway, regulates the ability of b-catenin to enter nuclei, where it activates the expression of Wnt target genes. We then used SB216763,a selective inhibitor of GSK-3 b activity, to further demonstrate the regulatory mechanism by which Foxg1 affects OPCs in vitro. The results showed that SB216763 clearly inhibited the expression of GSK-3 b, which abolished the effect of the proliferation and differentiation of OPCs caused by the knockdown of Foxg1. These results suggest that Foxg1 is involved in the proliferation and differentiation of OPCs through the Wnt signaling pathway. The present experimental results are some of the first to suggest that Foxg1 is a new therapeutic target for the treatment of demyelinating diseases of the CNS. | Fuxing Dong Dajin Liu Feiyu Jiang Yaping Liu Xiuxiang Wu Xuebin Qu Jing Liu Yan Chen Hongbin Fan Ruiqin Yao | 2021 | Neuroscience Bulletin2021，37，1： | 0 |
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