ANALYTICAL CHEMISTRY
·
2026
·Vol. 98
·期 31
·23119-23129
·
IF 7.3
Zhang Lei,Liao Yuqin,Zhu Lvyun,Li Yingying,Yu Lilei,Yang Yanbing,Yuan Quan
Near-infrared II (NIR-II, 1000–1700 nm) fluorescence
imaging
enables deep-tissue analysis, but conventional “always-on”
probes suffer from high background that compromises the signal-to-background
ratio for low-abundance targets. Activatable probe strategies could
mitigate this issue, yet most existing designs rely on fluorescence
resonance energy transfer with acceptors confined to the visible region,
hampering efficient signal quenching in the NIR-II window. Here, we
present a generalizable strategy based on morphology-engineered nanometal
surface energy transfer (NSET) to construct a NIR-II core–satellite
nanoprobe for intracellular miR-21 detection. By systematically tuning
the branch aspect ratio of gold nanostars (AuNSs), their localized
surface plasmon resonance (LSPR) absorption can be red-shifted to
achieve precise spectral overlap with the NIR-II emission of Ag 2 S quantum dots. Guided by DNA self-assembly, an AuNS@Ag 2 S core–satellite structure with controllable interparticle
spacing is established, enabling an initial fluorescence quenching
efficiency of up to 88%. Upon target recognition, miR-21-triggered
strand displacement reaction induces the dissociation of Ag 2 S quantum dots from the AuNS surface, resulting in a pronounced NIR-II
fluorescence “turn-on” response. The nanoprobe exhibits
exceptional performance, including a low detection limit of 75.8 pM,
robust linearity, single-base mismatch discrimination capability,
and enables visualization of differential miR-21 expression in living
cells. Notably, high-contrast NIR-II signals are retained at penetration
depths of up to 15 mm in tissue-mimicking experiments. This work establishes
an NSET-based analytical platform through precise spectral matching
and rational structural engineering, providing a robust strategy for
high signal-to-background biosensing and in situ analysis of low-abundance
miR-21 in deep tissues.
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ANNALS OF CLINICAL AND LABORATORY SCIENCE
·
2022
·Vol. 52
·期 1
·48-59
·
IF 1.18
Guomin Lv,Yan Chen,Zhengyue Cheng,Lixiang Lin,Huasong Shen
Objective Osteoporosis is likely becoming a new disease challenge with increasing aging population. Circ_0006873 dysregulation mayserve as an event linked to osteoporosis. Thus, this study sought to evaluate the function and mechanism of circ_0006873 onosteoporosis. Methods Clinical serum samples collected from 30 osteoporosis patients were utilized to obtain circ_0006873 and miR-142-5p expressiondata. The link between circ_0006873, miR-142-5p, and phosphatase and tensin homolog (PTEN) was demonstrated via online tools(starBase, circinteractome), RNA Immunoprecipitation (RIP) and dual-Luciferase reporter assays. After knockdown or overexpression,cell counting kit-8 (CCK-8) assay measured cell viability. Alizarin red S (ARS) staining as well Alkaline phosphatase (ALP)staining detected osteoblastic differentiation levels. Quantitative real-time PCR (qRT-PCR) and western blot analyzed expressionof RNAs and proteins after transfection or during osteoblastic differentiation. Results circ_0006873 was upregulated in osteoporosis patients and decreased during osteoblastic differentiation. Following experimentsrevealed that cell viability, proliferation-related factors, osteogenic marker genes (ALP, Runx2, Bglap) and osteoblasticdifferentiation degree were promoted after circ_0006873 knockdown but inhibited after overexpression. Circ_0006873 spongedmiR-142-5p, which was downregulated in osteoporosis patients and became higher during osteoblastic differentiation. Rescueassay indicated miR-142-5p mimic could reverse the effects of circ_0006873 overexpression on cell viability and osteogenicmarkers, and also could activate Akt pathway. Furthermore, circ_0006873 can negatively target miR-142-5p via regulating PTENto inhibit osteoblastic differentiation. Conclusion Circ_0006873 sponges miR-142-5p thereby enhances PTEN expression to suppress osteoblastic differentiation via regulationof Akt signaling pathway, thus, may provide a treatment approach for osteoporosis.
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Biomedical Materials
·
2024
·Vol. 19
·期 3
·035009
·
IF 3.9
Guancheng Zhan,Lixia Yu,Qiqi Wang,Longyang Jin,Xiaohong Yin,Xiaodong Cao,Huichang Gao
Corneal stromal injury is a common surgical disease. With the development of tissue engineering materials, many artificial corneal scaffolds have been developed to replace allograft corneal transplantation and solve the problem of corneal donor shortage. However, few researchers have paid attention to corneal stromal wound healing. Herein, a nanocomposite of amino modified mesoporous bioactive glass (MBG-NH2) and microRNA-133b (miR-133b) was introduced into the patterned collagen films to achieve corneal stromal injury repair. MBG-NH2 nanoparticles as a nano delivery carrier could efficiently load miR-133b and achieve the slow release of miR-133b. The physicochemical properties of collagen films were characterized and found the microgrooved collagen films loaded with miR-133b@MBG-NH2 nanoparticles possessed similar swelling properties, optical clarity, and biodegradability to the natural cornea. In vitro cell experiments were also conducted and proved that the patterned collagen films with miR-133b@MBG-NH2 possessed good biocompatibility, and miR-133b@MBG-NH2 nanoparticles could be significantly uptake by rabbit corneal stromal cells (RCSCs) and have a significant impact on the orientation, proliferation, migration, and gene expression of RCSCs. More importantly, the patterned collagen films with miR-133b@MBG-NH2 could effectively promote the migration of RCSCs and accelerate wound healing process, and down-regulate the expression levels of α-SMA, COL-I, and CTGF genes associated with myofibroblast differentiation of corneal stromal cells, which has a potential application prospect in the repair of corneal stromal injury.
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MICROCHEMICAL JOURNAL
·
2025
·
IF 5.1
Tingyuan Pang,Shuting Ouyang,Jia Li,Xiaorui Liu,Wenying Shu,Wenhui Gao,Junren Li,Qi Song,Jianing Huang,Jun Yang,Xiaoshun Jian,Xiaole Wang,Meimei Zhang
Cervical cancer is one common cause of cancer relative death in women worldwide, while microRNA-21 (miR-21) can serve as one upregulated miRNA in cervical cancer for early diagnosis. Chemiluminescence is a powerful assaying method, but balancing the sensitivity and selectivity is often difficult at present. For this problem, a photocatalytic chemiluminescent biosensor was developed to homogeneously assay miR-21 with good performances. Based on a base stacking principle, cooperative hybridization is employed in double DNA probes for biosensor design. After DNA probe hybridization, photocatalytic DNA-dye complex can induce luminol’s chemiluminescence signals via several processes. Here the double-probe design results in the high sensitivity to assay miR-21 with a detection limit in pM level. Meanwhile, the short probe design and cooperative principle guarantee a good selectivity to discriminate other nucleotide variants. For comparison, both a single short and long probes were also studied to show the advantages of our biosensor in assay performances. So this photocatalytic chemiluminescent biosensor via cooperative hybridization is an ideal method to assay miR-21, showing a good potential for cancer early diagnosis.
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Regenerative Medicine
·
2023
·
IF 2.7
Zhenhua Wu,Jie Geng,Yunpeng Bai,Yujuan Qi,Chao Chang,Yan Jiao,Zhigang Guo
Aim: To explore the effect of miR-125b-5p/nuclear factor of activated T cells 1 (NFAT2)/F2RL2 on myocardial infarction (MI). Method: After establishment of MI mouse model and oxygen glucose deprivation (OGD)-induced cell model, the effects of NFAT2 on the process of MI were observed, the effects of miR-125b-5p/NFAT2/F2RL2 on the cell viability, apoptosis, and inflammatory factors levels were determined. Result:NFAT2 silencing relieved MI and inhibited the inflammation in MI model mice. In OGD-induced human coronary artery endothelial cells and human cardiac microvascular endothelial cells, miR-125b-5p enhanced cell viability, yet repressed cell apoptosis and inflammatory factors and NFAT2 levels. NFAT2 overexpression reversed the effects of miR-125b-5p, while F2RL2 silencing offset the effects of NFAT2 overexpression. Conclusion: MiR-125b-5p alleviates MI injury by inhibiting NFAT2 level to reduce F2RL2 expression.
研究领域:
心脏病学
·
分子生物学
·
细胞生物学
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高影响因子
Frontiers in Pharmacology
·
2023
·
IF 5.6
Jing Zhang,Juan Gao,Xianlong Li,Dengna Lin,Zhihui Li,Jialei Wang,Junfeng Chen,Zhiliang Gao,Bingliang Lin
Balancing hepatocyte death and proliferation is key to non-transplantation treatments for acute liver failure (ALF), which has a high short-term mortality rate. Small extracellular vesicles (sEVs) may act as mediators in the repair of damaged liver tissue by mesenchymal stem cells (MSCs). We aimed to investigate the efficacy of human bone marrow MSC-derived sEVs (BMSC-sEVs) in treating mice with ALF and the molecular mechanisms involved in regulating hepatocyte proliferation and apoptosis. Small EVs and sEV-free BMSC concentrated medium were injected into mice with LPS/D-GalN-induced ALF to assess survival, changes in serology, liver pathology, and apoptosis and proliferation in different phases. The results were further verified in vitro in L-02 cells with hydrogen peroxide injury. BMSC-sEV-treated mice with ALF had higher 24 h survival rates and more significant reductions in liver injury than mice treated with sEV-free concentrated medium. BMSC-sEVs reduced hepatocyte apoptosis and promoted cell proliferation by upregulating miR-20a-5p, which targeted the PTEN/AKT signaling pathway. Additionally, BMSC-sEVs upregulated the mir-20a precursor in hepatocytes. The application of BMSC-sEVs showed a positive impact by preventing the development of ALF, and may serve as a promising strategy for promoting ALF liver regeneration. miR-20a-5p plays an important role in liver protection from ALF by BMSC-sEVs.
研究领域:
干细胞生物学
·
分子生物学
·
肝病学
·
再生医学
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2020
·
IF 4.872
Rili Hao,Junlin Ge,Yongfeng Ren,Xinyu Song,Yang Jiang,Dongxiao Sun-Waterhouse,Feng Li,Dapeng Li
Cadmium (Cd), an environmental pollutant, is evidenced to cause hepatotoxicity. In this study, the potential protective effect of caffeic acid phenethyl ester (CAPE) on cadmium-induced liver damage was investigated. Forty male mice were treated daily with either CdCl 2 (1.5 mg/kg body weight (b.w.), gavage) or CAPE (10 μmol/kg b.w., gavage) or both for 4 weeks. CAPE administration significantly reduced Cd level and liver and body weight, and increased AST, ALT and ALP level. Moreover, CAPE prevented CdCl 2 -induced oxidative stress via PI3K/Akt/mTOR pathway and inhibited apoptosis by regulating apoptosis markers. CAPE also suppressed the CdCl 2 -induced inflammation by reducing the inflammatory mediators, including TNF-α, IL-6 and IL-1β. Furthermore, CAPE alleviated CdCl 2 -induced reduction of TLR4. It should be noted that this effect was achieved by targeting miR-182-5p, and CAPE improved miR-182-5p level. The improvement of the liver tissue histopathology by CAPE confirmed the biochemical data. These results show for the first time that miR-182-5p/TLR4 axis involved in CAPE's protection against CdCl 2 -induced hepatotoxicity, and may provide novel insights into the treatment of cadmium-related diseases.
研究领域:
毒理学
·
分子生物学
·
肝脏研究
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ARCHIVES OF TOXICOLOGY
·
2020
·Vol. 94
·期 3
·857-871
·
IF 5.059
Ling Yuhang,Sun Limei,Wang Danting,Jiang Jiahui,Sun Wenjing,Ai Weiming,Wang Xuedong,Wang Huili
Triclosan (TCS) is ubiquitous in a wide range of personal care and consumer products, and it is acute/chronic exposure may result in several nervous system disorders. Previous studies demonstrated TCS-induced abnormal expression of miRNAs, but no investigations focused on upstream changes of miRNAs and associated molecular mechanisms. Herein, phenotype observation and behavioral analysis confirmed that TCS exposure (0, 62.5, 125, 250 μg/L) led to developmental neurotoxicity in zebrafish larvae, especially for oligodendrocyte precursor cells (OPCs). High-throughput sequencing demonstrated the critical role of miR-219 in the differentiation of OPCs. Larvae with miR-219 depletion showed the same phenotype caused by TCS. Functional tests with miR-219 knock-down and over-expression showed that miR-219 promoted differentiation of OPCs by acting on myelination inhibitors. The miR-219 also protected against TCS-induced inhibition of cell differentiation. Several epigenetic features were identified to reveal potential upstream regulatory mechanisms of miR-219. In particular, five CpG islands hyper-methylated with increasing TCS concentrations in the promoter region of miR-219. TCS inhibited OPC differentiation by influencing epigenetic effects on miR-219-related pathways, contributing to severe neurotoxicity. These findings enhance our understanding of epigenetic mechanisms affecting demyelination diseases due to TCS exposure, and also provide theoretical guidance for early intervention and gene therapy of environmentally induced diseases.
研究领域:
毒理学
·
神经科学
·
分子生物学
·
表观遗传学
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Artificial Cells Nanomedicine and Biotechnology
·
2020
·Vol. 48
·期 1
·584-593
·
IF 3.343
Li X,Zhang Q,Yang Z
Hsa_circ_0058124 was reported to possess the capacity of enhancing tumorigenesis and invasiveness. This investigation explored the effects of hsa_circ_0058124 on human lung cancer. qRT-PCR was employed for assessing the expression of hsa_circ_0058124 and miR-1297. Cell transfection was conducted for altering the expression of hsa_circ_0058124 and miR-1297. Dual-luciferase reporter gene assay was employed for exploring the relationship between hsa_circ_0058124 and miR-1297. CCK-8 assay, colony formation, flow cytometry, western blot and transwell assay were respectively conducted for exploring the effects of hsa_circ_0058124 silencing and miR-1297 inhibition. The expression of proteins participated in PTEN/AKT and Wnt/β-catenin pathways were determined for exploring the underlying mechanism. Hsa_circ_0058124 was highly expressed in human lung tumour tissues. Besides, hsa_circ_0058124 silencing suppressed cell viability, colony formation, migration and invasion, while enhanced cell apoptosis, which were respectively verified by the regulation of apoptosis-associated and metastasis-related proteins. Additionally, hsa_circ_0058124 silencing inhibited the expression of proteins involved in PTEN/AKT and Wnt/β-catenin pathways including p/t-AKT and β-catenin. miR-1297 was lowly expressed in patients' tumour tissues and was a target of hsa_circ_0058124. Moreover, the above mentioned effects were prominently abrogated by miR-1297 inhibition. This research verified that hsa_circ_0058124 silencing might achieve its anti-tumour roles via inactivation of PTEN/AKT and Wnt/β-catenin pathways through elevating miR-1297 expression.
研究领域:
分子生物学
·
肿瘤学
·
细胞生物学
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MEDIATORS OF INFLAMMATION
·
2023
·
IF 4.6
Zhousheng Yang,Tianyu Li,Chunyan Wang,Mingyu Meng,Shenglan Tan,Lei Chen
Dihydromyricetin (DMY), a natural flavonoid compound extracted from the stems and leaves of Ampelopsis grossedentata, has been found as a potential therapeutic chemical for treating atherosclerosis. This study explores the underlying mechanism of DMY repressing M1 macrophage polarization in atherosclerosis. We showed that DMY treatment markedly decreased M1 macrophage markers (e.g., Tnf-α and IL-1β) and p65-positive macrophage numbers in the vessel wall of Apoe-deficient (Apoe–/–) mice. Overexpression of miR-9 or knockdown of SIRT1 in macrophages reversed the effect of DMY on M1 macrophage polarization. The data we presented in the study indicate that the miR-9-mediated SIRT1/NF-κB pathway plays a pivotal role in M1 macrophage polarization and is one of the molecular mechanisms underlying the anti-atherosclerosis effects of DMY. We provide new solid evidence that DMY may be explored as a potential therapeutic adjuvant for treating atherosclerosis.
研究领域:
药理学
·
免疫学
·
心血管疾病
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BIOLOGICAL CHEMISTRY
·
2023
·
IF 3.7
Peng Sun,Yusong Luan,Xuhao Cai,Qi Liu,Peide Ren,Panxin Peng,Yonggang Yu,Bolun Song,Yangyang Wang,Huijing Chang,Haoyue Ma,Yinggang Chen
Hepatic metastasis is a major cause of colorectal cancer (CRC)-related deaths. Presently, the role of long non-coding RNAs (lncRNAs) in hepatic metastases from CRC is elusive. We dissected possible interplay between LINC00858/miR-132-3p/IGF2BP1 via bioinformatics approaches. Subsequently we analyzed mRNA expression of LINC00858, miR-132-3p and IGF2BP1 through qRT-PCR. Western blot was used to detect protein expression of IGF2BP1. RNA immunoprecipitation chip and dual-luciferase assay validated interaction between LINC00858 and miR-132-3p, as well as miR-132-3p and IGF2BP1. Cell viability, invasion, and migration were examined via CCK-8, colony formation, transwell and wound healing assays. Effect of LINC00858 on CRC hepatic metastases was validated via in vivo assay. Upregulated LINC00858 and IGF2BP1, and downregulated miR-132-3p were predicted in tumor tissues of patients with hepatic metastases from CRC. There were targeting relationships between LINC00858 and miR-132-3p, as well as miR-132-3p and IGF2BP1. Besides, LINC00858 facilitated progression of CRC cells. Rescue assay suggested that silencing LINC00858 suppressed CRC cell progression, while further silencing miR-132-3p or overexpressing IGF2BP1 reversed such effects. LINC00858 could facilitate CRC tumor growth and hepatic metastases. LINC00858 induced CRC hepatic metastases via regulating miR-132-3p/ IGF2BP1, and this study may deliver a new diagnostic marker for the disease.
研究领域:
肿瘤学
·
分子生物学
·
癌症研究
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EXPERIMENTAL ANIMALS
·
2021
·
IF 2.319
Lili TAN,Limin LIU,Jian YAO,Chenghao PIAO
Myocardial ischemia-reperfusion (I/R) injury is a common complication following reperfusion therapy that involves a series of immune or apoptotic reactions. Studies have revealed the potential roles of miRNAs in I/R injury. Herein, we established a myocardial I/R model in rats and a hypoxia/reoxygenation (H/R) model in H9c2 cells and investigated the effect of miR-145-5p on myocardial I/R injury. After 3 h or 24 h of reperfusion, LVESP, EF, and FS were obviously decreased, and LVEDP was increased. Meanwhile, I/R induced an increase in myocardial infarction area. Moreover, a decrease in miR-145-5p and increase in NOH-1 were observed following I/R injury. With this in mind, we performed a luciferase reporter assay and demonstrated that miR-145-5p directly bound to NOH-1 3’ UTR. Furthermore, miR-145-5p mimics decreased the levels of TNF-α, IL-1β, and IL-6 via OGD/R stimulation. Upregulation of miR-145-5p increased cell viability and reduced apoptosis accompanied by downregulation of Bax, cleaved caspase-3, cleaved PARP and upregulation of Bcl2. In addition, miR-145-5p overexpression increased SOD activity and reduced ROS and MDA content under OGD/R stress. Notably, NOH-1 could significantly abrogate the above effects, suggesting that it is involved in miR-145-5p-regulated I/R injury. In summary, our findings indicated that miR-145-5p/NOH-1 has a protective effect on myocardial I/R injury by inhibiting the inflammatory response and apoptosis.
研究领域:
心脏病学
·
分子生物学
·
炎症
·
细胞凋亡
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高影响因子
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