Analytical Methods
·
2024
·Vol. 16
·期 25
·4116-4123
·
IF 2.7
Yaxing Xie,Yulei Hou,Yang Yu,Jianhong Zhang,Jinyan Long,Mengqi Chen,Xueqing Lang,Xiaolan Yang,Hui Chen
MicroRNAs (miRNAs) have been involved in many biological processes and are regarded as promising biomarkers. The short sequence, low abundance and highly homologous interference sequences greatly hinder the accurate detection of miRNAs. Here, a cascade branch migration-triggered strand displacement amplification (CBM-TSDA) strategy was developed for the first time for specific and sensitive detection of miRNA-155 (miR-155). In the presence of target miR-155, the CBM was initiated and two Y-shaped probes were eventually produced. Next, the Y-shaped probes were transformed into three-way junction (3WJ) structures and triggered the SDA to produce a large number of G-quadruplex (G4) structures. Finally, the increased fluorescence signal of G4/Thioflavin T (ThT) was used to quantify miR-155. Meanwhile, the colorimetric responses of the G4-hemin DNAzyme could be used as supplementary detection to obtain a dual-mode signal readout. This detection strategy showed high detection sensitivity, and the limit of detection was 0.28 pM in the fluorescence detection mode and 0.34 pM in the colorimetric detection mode. Notably, it showed high detection specificity, being able to discriminate the single-base mutations of the target with a high discrimination factor. The strategy also possessed excellent capacity for miR-155 detection in cell lysates and real human blood samples. The developed strategy provides a promising detection platform for miRNA, which may be applied to early clinical diagnosis.
研究领域:
生物化学
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分子生物学
·
临床诊断
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DOI
PubMed
高影响因子
CHEMICAL PAPERS
·
2022
·Vol. 76
·期 5
·2875-2882
·
IF 2.146
He Xiao-Ling,Huang Fu-Hui,Zhang Chun-Ming,Dong Zhen,Wang Bin-Quan
The larynx is an important organ of human speech, and patients with laryngeal cancer may face great pain of losing their functions. For the prevention and therapy of laryngeal carcinoma, two new Zn(II)/Cd(II) coordination polymers, namely [Zn 3 (L) 2 (4,4′-bipy)] n ·2n(DMF) ( 1 ) and [Cd 3 (L) 2 (bpp 2 ) n ·2n(H 2 O)·2n(DMF) ( 2 ) (H 3 L = 4,4′,4′′-ticarboxytriphenylamine, 4,4′-bipy = 4,4′-bipyridine, bpp = 1,3-bis(4-pyridyl)propane, DMF = N,N-dimethylformamide), were prepared. The treatment and protection activity of the new compounds against the laryngeal carcinoma was evaluated in this research, and the corresponding mechanism was explored at the same time. Firstly, CCK-8 assay was conducted to measure the inhibitory activity of compounds on the viability of laryngeal carcinoma cells. Additionally, the expression of miR-223-3P in MSC exosomes was also measured by real time RT-PCR assay.
研究领域:
肿瘤学
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药理学
·
生物化学
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DOI
高影响因子
CELLULAR AND MOLECULAR LIFE SCIENCES
·
2024
·Vol. 81
·期 1
·1-16
·
IF 6.2
Zhao Yongzhao,Chen Longting,Xiang Qian,Lin Jialiang,Jiang Shuai,Li Weishi
Background The ligamentum flavum (LF) is an important anatomical structure of the spine. Ossification of the LF (OLF) has become the leading cause of thoracic spinal stenosis. Circular RNAs (circRNAs) and N6-methyladenosine (m6A) modification are reported to be associated with several human diseases. However, the role of circRNAs and m6A modification in the pathogenesis of OLF has not been fully investigated. Here, we aimed to explore the vital function of circRNAs and m6A modification in OLF. Materials and methods We analysed the circRNA expression of 4 OLF tissues and 4 normal LF tissues using bioinformatic analysis and identified circCDK14 for further analysis. We investigated the effects of circCDK14 on the osteogenic differentiation of LF cells. We observed that circCDK14 regulated its target genes by binding to miRNAs as a miRNA sponge. Moreover, the circRNA pull-down assay indicated that RNA-binding proteins might regulate the expression of circCDK14 via m6A modification. Results CircCDK14 was significantly upregulated in OLF tissues compared to normal LF tissues. Overexpression of circCDK14 promoted the osteogenic differentiation of LF cells. Mechanistically, CircCDK14 promoted the expression of ALF transcription elongation Factor 4 (AFF4) by serving as a sponge for miR-93-5p. Moreover, Wilms tumour 1-associated protein (WTAP) increased the stability of circCDK14 via N6-methyladenosine modification. Conclusion The m6A-modified CircCDK14 binding to miR-93-5p played an important role in the osteogenesis of LF cells by targeting AFF4, providing a promising therapeutic target for OLF.
研究领域:
分子生物学
·
表观遗传学
·
骨科
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生物信息学
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DOI
PubMed
高影响因子
BIOMATERIALS
·
2025
·
IF 12.9
Siting Sheng,Huiling Zhao,Lirui Liu,Dan Chen,Xingdi Wu,Chujun Liu,Xinyu Ma,Jing-Wei Xu,Jian Ji,Haijie Han,Wen Xu
Uveitis, a frequently recurrent inflammatory condition of the uvea, poses a significant risk of visual impairment and blindness, primarily due to the excessive generation of reactive oxygen species (ROS) and the activation of signaling pathways that propagate inflammatory responses. Despite the widespread use of corticosteroid eye drops as a standard treatment, these therapies are hindered by limited efficacy, adverse side effects, and poor ocular bioavailability. To address these challenges, polyethyleneimine (PEI)-modified polydopamine (PDA) carrying microRNA-132-3p (miR-132), namely PEI/PDA@miR-132, was developed to simultaneously neutralize ROS and attenuate inflammation in experimental models of acute and chronic uveitis. Mechanistically, PEI/PDA@miR-132 demonstrated remarkable efficacy by suppressing ROS production, inhibiting the pro-inflammatory polarization of macrophages, and downregulating the I κ B α /nuclear factor-kappa B (NF- κ B) p65 signaling pathway. These effects culminated in the reduction of pro-inflammatory cytokines and mitigation of apoptosis. Therapeutically, PEI/PDA@miR-132 provided significant relief from hallmark symptoms of uveitis, including iris congestion, inflammatory exudation, and retinal folds, while exhibiting superior retinal safety compared to commercially available dexamethasone. Furthermore, it showcased excellent biocompatibility, positioning it as a promising therapeutic strategy for managing oxidative stress- and inflammation-driven diseases such as acute and chronic uveitis.
研究领域:
药理学
·
眼科
·
纳米医学
·
炎症研究
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DOI
PubMed
高影响因子
ANALYST
·
2019
·Vol. 144
·期 17
·5245-5253
·
IF 4.019
Yihan Zhao,Yu Wang,Su Liu,Chonglin Wang,Jiaxu Liang,Shasha Li,Xiaonan Qu,Rufeng Zhang,Jinghua Yu,Jiadong Huang
We have formulated a rapid and high-efficiency fluorescent biosensing platform based on a target-activated triple-helix molecular switch (THMS)-conformation-change-induced exponential rolling circular amplification (RCA) strategy for the ultrasensitive detection of miR-21. In this strategy, there are several aspects that are worthwhile. First, the functionalized THMS, comprising a typical triplex structure (T-A·T), specific recognition sequence for nicking endonuclease, complementary sequence for miR-21, and RCA product-annealing sequence, was concurrently used to perform signal transduction with one fluorophore and one quencher. As compared to the traditional double-helix molecular switches or molecular beacons, one of the biggest differentiating factors is that the properties of THMSs are independent of any specific binding sequence that they may contain. As far as we know, this is the first time that an ingeniously designed THMS not only contains the primer for exponential RCA, but also functions as the tracer for fluorescence assay. In the presence of miR-21, targets can induce conformation changes in THMS with the release of the trapped DNA segment (P), which, in turn, can activate the first run of the RCA process. Meanwhile, the RCA reaction is also initiated by the formation of a similar primer (SP) as the trapped DNA through a continuous “extension-nicking” reaction. Secondly, the resultant first-generation RCA product consists of numerous tandem repeated regions that can attach to countless THMSs, resulting in the release of the trapped DNA segment (P) for initiating the second run of the RCA reaction. Significantly, a large amount of THMSs were continuously consumed to yield a remarkably strong fluorescent signal. In addition, this biosensor was demonstrated to exhibit improved sensitivity owing to the high efficiency and rapid amplification kinetics of the exponential RCA and high selectivity toward miR-21 with a limit of detection as low as 1.1 aM. Hence, the target-mediated THMS-conformation-change-initiated exponential RCA strategy presents an optimal detection performance toward analytes for potential applications in related fundamental research and clinical diagnosis.
研究领域:
分子生物学
·
生物化学
·
医学诊断
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2021
·
IF 6.953
Xueqin Duan,Xingxue Pan,Jing Cui,Liting Ke,Jia Liu,Xiaoping Song,Wuren Ma,Weimin Zhang,Yingqiu Liu,Yunpeng Fan
This study is to investigate the effect of microRNA-1338 (miR-1338) on the activity of Kupffer cells (KCs) and its mechanism regulated by ophiopogon polysaccharide liposome (OPL). KCs was treated with different OPL after transfected with miR-1338 mimic and miR-1338 inhibitor. The secretion of NO and iNOS, the expression of catalase (CAT) and peroxidase (POD), the phagocytic activity, the expression of CD14 and MHC II, the apoptosis and the secretion of ROS were measured. In addition, the expressions of key signal factors TLR4, IKKβ, MyD88 and NF-κB in NF-κB signaling pathway were measured by real-time PCR and Western blot (WB). The results showed that OPL could promote the secretion of iNOS, the expression of POD, the phagocytosis, the mRNA expression of TLR4, MyD88, IKKβ and NF-κB, the protein expression of TLR4 and NF-κB, and inhibit the cell apoptosis and ROS secretion after transfected with miR-1338 mimic. After transfected with miR-1338 inhibitor, OPL could promote the secretion of NO and iNOS, the expression of POD, cell migration, phagocytosis, and inhibit cell apoptosis. Meanwhile, the mRNA expression of TLR4, MyD88, IKKβ and NF-κB and the protein expression of TLR4, MyD88 and NF-κB were promoted. These results suggested that OPL could activate TLR4-NF-κB signaling pathway and thereby improve the activity of KCs by regulating miR-1338.
研究领域:
免疫学
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药理学
·
分子生物学
·
细胞生物学
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DOI
PubMed
高影响因子
MACROMOLECULAR BIOSCIENCE
·
2021
·Vol. 21
·期 5
·2100024
·
IF 4.979
Sihan Wang,Jiakai Xing,Boyu Xiong,Haobo Han,Min Hu,Quanshun Li
Emerging evidence suggests that microRNAs (miRNAs) play key roles in the regulation of multiple biological processes, including the differentiation of osteoblasts. Although miRNA-based gene therapy holds immense potential in the treatment of a variety of diseases, the intracellular delivery of miRNA remains challenging owing to the lack of efficient and safe gene carriers. In this study, a fluoropolymer (FP) is constructed through the modification of polyamidoamine (PAMAM) using heptafluorobutyric anhydride and then is used as a carrier for miR-23b transfection to induce osteocyte differentiation of osteoblasts. The derivative FP is found to facilitate miR-23b transfection due to its favorable endosomal escape from the "proton sponge" effect. Compared to PAMAM/miR-23b, the FP/miR-23b nanocomplex efficiently promotes the differentiation of osteoblasts and formation of calcified nodules, attributable to enhanced expression of various osteogenesis genes (runt-related transfection factor 2 [RUNX2], alkaline phosphatase [ALP], osteopontin [OPN], and osteocalcin [OCN]). Thus, FP-mediated miR-23b transfection may be used as an effective strategy to facilitate osteogenic differentiation.
研究领域:
生物材料
·
分子生物学
·
基因治疗
·
组织工程
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DOI
PubMed
高影响因子
EXPERIMENTAL BRAIN RESEARCH
·
2021
·Vol. 239
·期 11
·3359-3370
·
IF 1.972
Chang Jie,Zhang Yanhong,Shen Nianhong,Zhou Jingquan,Zhang Huan
Depression is a complex etiological disease with limited effective treatments. Previous studies have indicated the involvement of miRNAs in the pathophysiology of mood disorders. In this study, we focused on the role and mechanisms of miR-129-5p in depression by successfully constructing mice models of depressive-like behavior via chronic unpredictable mild stress (CUMS) exposure. Herein, miR-129-5p expression was decreased in the hippocampus of CUMS mice model. Upregulation of miR-129-5p reduced depressive-like behaviors of CUMS mice, as revealed in sucrose preference test, novelty suppressed feeding test, forced swim test, tail suspension test, social interaction test. MiR-129-5p upregulation decreased the concentrations and protein levels of proinflammatory cytokines (IL-6, IL-1β and TNF-α), indicating the inhibitory role of miR-129-5p in inflammation. Furthermore, miR-129-5p was identified to target MAPK1. MAPK1 was negatively regulated by miR-129-5p, and silencing of MAPK1 attenuated depressive-like behaviors in CUMS mice. Moreover, MAPK1 downregulation decreased inflammation in the hippocampus of CUMS mice. Upregulation of MAPK1 reversed the suppressive effects of miR-129-5p upregulation on depressive-like behaviors and inflammation in CUMS mice. In conclusion, the current study identified that miR-129-5p reduces depressive-like behaviors and suppresses inflammation by targeting MAPK1 in CUMS mice, offering a novel molecular interpretation for depression prevention.
研究领域:
神经科学
·
分子生物学
·
精神病学
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DOI
PubMed
高影响因子
MOLECULAR AND CELLULAR PROBES
·
2019
·
IF 2.511
Danning Lou,Jun Wang,Xiaohang Wang
Major depressive disorder (MDD) is one of the most prevalent psychiatric disorders worldwide and a major public health concern that is associated with grave consequences. Systemic complexity and feedback processes among diverse drivers of the depression disorder contribute to the considerable variation in responses to the treatment of depression . Dysfunctional microRNA (miRNA) is involved in MDD. miR-124 is enriched in the brain and may be critical in neuronal differentiation . Previous studies have shown the value of miRNA-124 as a putative therapeutic target and a biomarker for major depression. However, the detailed mechanism of action of miR-124 in depression remains poorly understood. Here, we observed that miR-124 was downregulated in the hippocampus of mice with chronic unpredictable mild stress (CUMS). Restoration of miR-124 expression significantly attenuated depressive-like behavior and inhibited microglial activation induced by CUMS. Mechanistically, miR-124 directly targeted signal transducer and activator of transcription 3 (STAT3) in BV2 cells; in addition, upregulation of miR-124 inhibited the increase of inducible nitric oxide synthetase and proinflammatory cytokines , including IL-6, IL-1β, TNF-α, and MCP-1, in LPS-stimulated BV2 cells. The collective data suggest that dysfunction of miR-124 may be a foundation for the development of depression by promoting microglial activation.
研究领域:
神经科学
·
分子生物学
·
精神病学
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DOI
PubMed
高影响因子
HUMAN & EXPERIMENTAL TOXICOLOGY
·
2020
·Vol. 39
·期 5
·683-695
·
IF 2.067
Y Chen,Q Zhang,Y Zhou,Z Yang,M Tan
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease with high morbidity and mortality. miR-182-5p is overexpressed in several fibrosis-related diseases but its effect in pulmonary fibrosis has not been reported yet. To investigate the function of miR-182-5p in pulmonary fibrosis, we established bleomycin (BLM)-induced fibrotic mice model and transforming growth factor-β1 (TGF-β1)-treated human embryonic lung fibroblasts model. In this study, miR-182-5p was highly expressed in pulmonary tissues of BLM-induced fibrotic mice. The content of hydroxyproline and TGF-β1 was decreased by downregulating the expression of miR-182-5p, indicating that fibrosis was alleviated in mice treated with Lentivirus-anti-miR-182-5p.Quantification of fibrosis-related proteins demonstrated that downregulation of miR-182-5p inhibited the expression of profibrotic proteins (fibronectin, α-smooth muscle actin, p-Smad2/p-Smad3) as well as enhanced the level of Smad7. In vitro assays validated that miR-182-5p was induced by TGF-β1 with the function of promoting fibrosis. In dual-luciferase reporter assay, Smad7 was demonstrated to be negatively regulated by miR-182-5p. Moreover, the effect of knocking down miR-182-5p on inhibiting fibrosis was achieved by upregulating the expression of Smad7. Therefore, miR-182-5p can be regarded as a biomarker of IPF and its inhibition may be a promising therapeutic approach in treating IPF.
研究领域:
肺病学
·
分子生物学
·
病理学
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DOI
PubMed
高影响因子
SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
·
2026
·
IF 4.8
Yan Tu,Rongjie Yang,Shuli Li,Runhu Huang,Yueye Zhang,Qi Yang,Jinze Li,Lianqun Zhou,Wei Zhang
The microRNAs miR-34a and miR-34b are dysregulated in Alzheimer's disease (AD) and are promising diagnostic biomarkers. However, their low abundance, high sequence homology, and instability present severe challenges for accurate multiplex detection. Herein, we report a quantum dot-enhanced turn-up/down dual-miRNA FRET sensor (QDTF sensor), a platform that achieves simultaneous detection of two highly homologous miRNAs with low crosstalk via an unprecedented asymmetric dual-mode FRET strategy enhanceded by a single quantum dot 605. Among the two pairs of molecular beacons, one triggers a considerable increase in the Alexa Fluor 568 signal for miR-34a, while the other induces a decrease in the Alexa Fluor 532/Cy5 signal for miR-34b. The deliberate opposite-signaling design and spectrally well-separated dye pairs present excellent channel isolation with low crosstalk (<3.42%), even when both targets are present at high concentrations. The QDTF sensor delivers LODs of 0.96 pM (miR-34a) and 1.12 pM (miR-34b) directly in artificial cerebrospinal fluid (aCSF) without enzymes, amplification, or pretreatment, with a dynamic range spanning approximately 1 pM to 10 nM, representing a 322-fold and 203-fold sensitivity enhancement over dye-only molecular beacons, respectively. The QDTF sensor offers a simple, robust, and truly dual approach for the precise quantification of homologous miRNAs in undiluted aCSF, holding immense potential for the early clinical diagnosis of AD.
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高影响因子
International Journal of Endocrinology
·
2026
·
IF 2.5
Guoxian Zhu,Lidan Zhang,Wenbao Huang,Jiexia Ding,Lifei Yu,Xiangfei Xu
The aim of this study was to evaluate the effect and mechanism of miR‐122‐5p on hepatic injury induced by hyperthyroidism. Male Sprague Dawley rats were divided into three groups: a normal thyroid function group (sham), a levothyroxine (LT4)–induced hyperthyroidism group (T4 sodium), and a hyperthyroidism group treated with a miR‐122‐5p inhibitor (T4 sodium + antagomir‐122‐5p). Liver tissue pathology, ferroptosis and inflammatory markers, and miR‐122‐5p expression were assessed. Finally, rat hepatocytes (BRL‐3A) were treated with carbon tetrachloride (CCL4) to explore the role of the miR‐122‐5p/CCDC6 axis in hepatocyte injury. We found that miR‐122‐5p was expressed at low levels in liver tissues from hyperthyroid rats. Inhibition of miR‐122‐5p aggravated liver tissue injury. Additionally, in hyperthyroid rats, inflammatory factors, iron content, and markers of ferroptosis were upregulated by miR‐122‐5p inhibitors. Mechanistically, miR‐122‐5p was found to bind to CCDC6 and negatively regulate CCDC6 expression. Furthermore, miR‐122‐5p deletion induced hepatocyte injury by exacerbating the ferroptosis process and mitochondrial damage in CCL4‐treated hepatocytes, a process dependent on CCDC6 expression. The miR‐122‐5p/CCDC6 axis plays a protective role in hyperthyroidism‐induced liver injury and serves as a potential target for the clinical treatment of hyperthyroidism‐associated liver disease.
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高影响因子
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