CELLULAR SIGNALLING
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2022
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IF 4.85
Yutong Wu,Hongbo Ai,Yuchi Zou,Qiankun Yang,Ce Dou,Jianzhong Xu
Small extracellular vesicles (sEVs) are considered to play critical roles in intercellular communications during normal and pathological processes since they are enriched with miRNAs and other signal molecules. In bone remodeling , osteoclasts generate large amounts of sEVs. However, there is very few research studying whether and how osteoclast-derived sEVs (OC-sEVs) affect surrounding cells. In our study, microarray analysis identified miR-106a-5p as highly enriched in OC-sEV. Further experiments confirmed that OC-sEVs inhibited Fam134a through miR-106a-5p and significantly promoted bone mesenchymal stem cell (BMSC) osteogenic mineralization in vitro . Next, we prepared an sEV-modified demineralized bone matrix (DBM) as scaffold treating calvarial defect mouse model to evaluate the pro-osteogenic activities of the scaffold. In vivo results indicated that DBM modified with miR-106a-5p-sEVs showed an enhanced capacity for bone regeneration . This important finding further emphasizes that sEV-mediated miR-106a-5p transfer plays a critical role in osteogenesis and indicates a novel communication mode between osteoclasts and BMSCs.
研究领域:
骨骼生物学
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干细胞研究
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再生医学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Biomedical Optics Express
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2025
·Vol. 16
·期 5
·2033-2046
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IF 3.2
Binbin Zeng,Huaiwu Fu,Cong Wu,Xudong Zhang,Tianran Li,Qiong Xu,Yayun Qian,Yayun Qian,Ruirui Yang,Ruirui Yang
In this study, we constructed a SERS assay platform that can be used for the ultrasensitive detection of cerebral infarction (CI)-associated miR-106a-5p based on the recognition competition strategy and the highly efficient catalytic activity of Au@Pt NRs nanoenzymes. When the target miR-106a-5p is present in the detection solution, it binds to the nucleic acid aptamer (cDNA), leading to the detachment of its complementary strand (H1) carrying Au@Pt NRs from the surface of AuNHs, and the oxidation of TMB is reduced, resulting in the decrease of SERS signal. In addition, this method enables single-step, ultrasensitive detection of target miRNAs in patient serum with a limit of detection (LOD) of 0.96 fM, which is consistent with the results of real-time quantitative polymerase chain reaction (qRT-PCR) and fluorescence. This method provides a novel approach for the effective detection of miRNAs, which is of great clinical value for the early detection of CI.
研究领域:
生物传感器
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纳米技术
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分子诊断学
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生物医学工程
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RNA检测
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产品关联
DOI
高影响因子
Bioengineered
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2021
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IF 3.269
Xinyue Zhou,Zhenyu Chen,Lipeng Pei,Jingli Sun
Emerging evidence has exhibited an obvious decreased expression of miR-106a-5p in the ectopic endometrial tissue of endometriosis (EMS) patients. Thus far, the pathophysiological function of miR-106a-5p in EMS is unknown. A previous study showed an increased FOXC1 expression in the ectopic endometrial tissue of patients with EMS. Moreover, we found that there was a binding site of miR-106a-5p on the 3ʹUTR of FOXC1 through bioinformatics predictions. Hence, we speculated that miR-106a-5p might affect the development of EMS via targeting FOXC1. We first showed a decreased level of miR-106a-5p and an increased level of FOXC1 mRNA in ectopic endometrial tissues compared with normal tissues. Functionally, we transfected ectopic endometrial stromal cells (ESCs) with miR-106a-5p mimics or NC mimics and indicated an inhibitory role of miR-106a-5p on ESC proliferation, invasion, and migration. Mechanistically, FOXC1 was found to be a target gene of miR-106a-5p. To confirm whether miR-106a-5p exerted an inhibitory activity in ESCs via targeting FOXC1, miR-106a-5p mimic was co-transfected into ESCs with the FOXC1-plasmid or vector. We found that FOXC1 overexpression evidently reversed the results caused by a miR-106a-5p mimic in ESCs. Additionally, our results demonstrated that miR-106a-5p mimic inhibited the expression of p-Akt and p-PI3K. Collectively, these results revealed that miR-106a-5p inhibited the proliferative, migratory, and invasive ability of ESCs via directly binding to FOXC1, likely through the suppression of the PI3K and its downstream signaling pathway, which offered a potential and novel therapeutic strategy for EMS treatment.
研究领域:
妇科学
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分子生物学
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细胞生物学
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病理生理学
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产品关联
DOI
PubMed
高影响因子
Clinical Interventions in Aging
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2022
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IF 3.829
Bao Hai,Yunlong Ma,Xiaoyu Pan,Lei Yong,Chen Liang,Guanping He,Chenlong Yang,Bin Zhu,Xiaoguang Liu
Background Disc degeneration (DD) is one of the common diseases worldwide, which deeply influences normal life and leads to excruciating pain. However, an effective treatment for DD is still not identified.Method The present study systemically examined the effect of melatonin on annulus fibrosus (AF) cells of patients with DD.Results Melatonin had the effect of promoting proliferation, inducing autophagy, and suppressing apoptosis on AF cells of patients with DD. Moreover, melatonin contributed to the translation and transcription of autophagy-related protein ATG7 and inhibited the function of miR-106a-5p in AF cells. In addition, the results suggested that miR-106a-5p mediated the expression of ATG7 by directly binding to its 3′UTR in AF cells.Conclusion This research not only gained a deep insight of melatonin mode of action, but also indicated its potential target signaling pathway in AF cells.
研究领域:
神经病学
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细胞生物学
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分子生物学
✓ 已验证
DOI
PubMed
高影响因子