In Situ Fe-Substituted Hexacyanoferrate for High-Performance Aqueous Potassium Ion Batteries.

The eco-friendliness, safety, and affordability of aqueous potassium batteries (AKIBs) have made them popular for large-scale energy storage devices. However, the cycling and rate performance of research materials, particularly cobalt hexacyanoferrate, have yet to meet satisfactory standards. Herein, a room-temperature drafted K1.66 Fe0.25 Co0.75 [Fe(CN)6 ]·0.83H2 O (KFCHCF) sample is reported using an in situ substitution strategy. A higher concentration of ferrocyanide ions decreases the water content and increases the potassium content, while citric acid works as a chelating agent and is responsible for Fe-substitution in the KFCHCF sample. The resultant KFCHCF sample exhibits good rate performance, and about 97% and 90.6% of discharge capacity are conserved after 400 and 1000 cycles at 100 and 200 mA g-1 , respectively. The full cell using the KFCHCF cathode and 1,4,5,8-naphthalenetetracarboxylic dianhydride-derived polyimide (PNTCDA) anode maintains ≈74.93% and 74.35% of discharge capacity at 200 mA g-1 and 1000 mA g-1 for 1000 and >10,000 cycles, respectively. Furthermore, ex situ characterizations demonstrate the high reversibility of K-ions and structural stability during the charge-discharge process. Such high performance is attributed to the fast K-ion migration and crystal structure stabilization caused by in situ Fe-substitution in the KFCHCF sample. Other hexacyanoferrates can be synthesized using this method and used in grid-scale storage systems.

MicroRNA-21 promotes proliferation, invasion and suppresses apoptosis in human osteosarcoma line MG63 through PTEN/Akt pathway.

Osteosarcoma, which accounts for 5 % of pediatric tumor, remains the major cause of death among orthopedic malignancies. However, the factors associated with its malignant biological behavior are still poorly understood. MicroRNAs are a class of small noncoding RNAs, which have been considered to associate with malignant progression including cell differentiation, proliferation, apoptosis, invasion, and distant metastasis. In our research, we found that microRNA-21 (miR-21) was significantly overexpressed in human osteosarcoma cell line MG63 compared to human fetal osteoblastic cell line hFOB1.19 by using quantitative real-time polymerase chain reaction (qRT-PCR). Moreover, miR-21 overexpression in MG63 caused a significant raise in cell proliferation and invasion and a significant reduction in cell apoptosis. However, miR-21 underexpression in MG63 caused an opposite result. Western blotting displayed that proteins related with proliferation, apoptosis, and invasion were significantly changed in different groups, respectively. Furthermore, we demonstrated that PTEN may be a potential target of miR-21 in MG63 cells and miR-21 could activate PI3K/Akt pathway by suppressing PTEN expression. In summary, our findings suggested that miR-21 played an active role in osteosarcoma and it could predict the occurrence and development of osteosarcoma.

Expression profile of circular RNAs in blood samples of Northern Chinese males with intracerebral hemorrhage shows downregulation of hsa-circ-0090829.

Circular RNAs (circRNAs) are involved in several neurological disorders; however, the mechanisms underlying their involvement remain to be clarified. We attempted to explore the expression profiles of circRNAs and their potential functions and mechanisms in the pathogenesis of intracerebral hemorrhage (ICH) in Northern Chinese males. The microarray results showed that 50 circRNAs were significantly upregulated, while 194 circRNAs were significantly downregulated in ICH patients compared with healthy controls (p < 0.05). After bioinformatics analysis, a circRNA-microRNA-messenger RNA network and a protein-protein interaction network were constructed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that the neurotrophin signaling pathway, long-term potentiation, and the mitogen-activated protein kinase pathway are potentially implicated in ICH pathophysiology. The quantitative real-time polymerase chain reaction results revealed that hsa-circ-0090829 was significantly downregulated in ICH. The receiver operating characteristic curve analysis showed that the area under the curve of hsa-circ-0090829 between ICH and healthy controls was 0.807. Furthermore, the dual-luciferase assay showed that hsa-circ-0090829 sponged miR-526b-5p. This study reports the altered expression of circRNAs and identifies the potential functions of these circRNAs in ICH. Our results may facilitate further mechanistic research on circRNAs in ICH and provide probable novel diagnostic biomarkers and therapeutic targets for ICH.

Clinical features of myasthenia gravis with neurological and systemic autoimmune diseases.

Multiple reports on the co-existence of autoimmune diseases and myasthenia gravis (MG) have raised considerable concern. Therefore, we reviewed autoimmune diseases in MG to explore their clinical presentations and determine whether the presence of autoimmune diseases affects the disease severity and treatment strategies for MG. We reviewed all the major immune-mediated coexisting autoimmune conditions associated with MG. PubMed, Embase and Web of Science were searched for relevant studies from their inception to January 2023. There is a higher frequency of concomitant autoimmune diseases in patients with MG than in the general population with a marked risk in women. Most autoimmune comorbidities are linked to AChR-MG; however, there are few reports of MuSK-MG. Thyroid disorders, systemic lupus erythematosus, and vitiligo are the most common system autoimmune diseases associated with MG. In addition, MG can coexist with neurological autoimmune diseases, such as neuromyelitis optica (NMO), inflammatory myopathy (IM), multiple sclerosis (MS), and autoimmune encephalitis (AE), with NMO being the most common. Autoimmune diseases appear to develop more often in early-onset MG (EOMG). MS coexists more commonly with EOMG, while IM coexists with LOMG. In addition, MG complicated by autoimmune diseases tends to have mild clinical manifestations, and the coexistence of autoimmune diseases does not influence the clinical course of MG. The clinical course of neurological autoimmune diseases is typically severe. Autoimmune diseases occur most often after MG or as a combined abnormality; therefore, timely thymectomy followed by immunotherapy could be effective. In addition, thymoma-associated AChR MG is associated with an increased risk of AE and IM, whereas NMO and MS are associated with thymic hyperplasia. The co-occurrence of MG and autoimmune diseases could be attributed to similar immunological mechanisms with different targets and common genetic factor predisposition. This review provides evidence of the association between MG and several comorbid autoimmune diseases.

Effect of Low Nesquehonite Addition on the Hydration Product and Pore Structure of Reactive Magnesia Paste.

Reactive magnesia cement is considered an eco-efficient binder due to its low synthesis temperature and CO2 absorption properties. However, the hydration of pure MgO-H2O mixtures cannot produce strong Mg(OH)2 pastes. In this study, nesquehonite (Nes, MgCO3·3H2O) was added to the MgO-H2O system to improve its strength properties, and its hydration products and pore structure were analyzed. The experimental results showed that the hydration product changed from small plate-like Mg(OH)2 crystals to interlaced sheet-like crystals after the addition of a small amount of Nes. The porosity increased from 36.3% to 64.6%, and the total pore surface area increased from 4.6 to 118.5 m2/g. At the same time, most of the pores decreased in size from the micron scale to the nanometer scale, which indicated that Nes had a positive effect on improving the pore structure and enhancing the compressive strength. Combined with an X-ray diffractometer (XRD), a Fourier transform infrared spectrometer (FTIR), and a simultaneous thermal analyzer (TG/DSC), the hydration product of the sample after Nes addition could be described as xMgCO3·Mg(OH)2·yH2O. When Nes was added at 7.87 and 14.35 wt%, the x-values in the chemical formula of the hydration products were 0.025 and 0.048, respectively. These small x-values resulted in lattice and property parameters of the hydration products that were similar to those of Mg(OH)2.

Inflammatory regulation by restraining M2 microglial polarization: Neurodestructive effects of Kallikrein-related peptidase 8 activation in intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a cerebrovascular disease. Kallikrein-related peptidase 8 (KLK8) is a serine peptidase, while its role in ICH remains unclarified. Western blot (WB) showed that KLK8 was upregulated in rat perihematomal tissues 24 h following autologous blood injection. KLK8 overexpression aggravated behavioral deficits and increased water content and Fluoro-Jade B (FJB)-positive neuron numbers in brain tissue of rats. Immunofluorescence (IF) assay showed that overexpressed-KLK8 promoted Iba-1 and iNOS expression in perihematomal tissue of rats. Overexpressed-KLK8 increased COX-2, iNOS, and Arg-1 expression and the content of IL-6, IL-1ß, and TNF-α in perihematomal tissue of rats, confirmed by WB and ELISA. IF staining confirmed the expression of CCR5 was co-expressed with Iba-1, and the WB results shown increased CCR5 expression and decreased p-PKA and p-CREB expression in perihematomal tissue. Maraviroc (MVC, CCR5 inhibitor) administration rescued KLK8-induced behavioral deficits and brain injury (decreased water content and FJB-positive neuron numbers) in rats. Additionally, MVC suppressed p-PKA and p-CREB expression and the content of IL-6, IL-1ß, and TNF-α in perihematomal tissue, induced by overexpressed-KLK8. Co-IP confirmed the binding of CCR5 and CCL14 in HMC3 cells. Transwell assay shown that KLK8 plus CCL4 promoted the chemotactic activity of cells, which was rescued by MVC. The biological function of KLK8/CCL14/CCR5 axis in ICH injury was also proved by MVC administration in HMC3 cells. Overall, our work revealed that KLK8 overexpression aggravated ICH process and involved in microglial activation. KLK8 might activate CCL14 thereby turning on downstream CCR5/PKA/CREB pathway, providing a theoretical basis for future therapy.

Neurodegeneration and Glial Activation Related CSF Biomarker as the Diagnosis of Alzheimer's Disease: A Systematic Review and an Updated Meta- analysis.

OBJECTIVE: Recently, neuron specific enolase (NSE), Visinin-like protein-1 (VLP-1), neurogranin (Ng), and YKL-40 have been identified as candidates for neuronal degeneration and glial activation biomarkers. Therefore, we perform a comprehensive meta-analysis to assess the diagnostic value of CSF NSE, VLP-1, Ng and YKL-40 in Alzheimer's disease (AD). METHODS: We searched Pubmed, MEDLINE, EMBASE databases for research about the levels of CSF NSE, VLP-1, Ng and YKL-40 in AD patients compared with controls or other dementia diseases until Dec 2020. RESULTS: The present meta-analysis contained a total of 51 studies comprising 6248 patients with dementia disorders and 3861 controls. Among them, there were 3262 patients with AD, 2456 patients with mild cognitive impairment (MCI), 173 patients with vascular dementia (VaD), 221 patients with frontotemporal dementia (FTD), and 136 with Lewy bodies dementia (DLB). Our study demonstrated that CSF NSE, VLP-1, Ng and YKL-40 levels were increased in AD as compared to healthy controls. We also observed that the CSF NSE level was higher in AD than VaD, suggesting CSF NSE might act as a key role in distinguishing between AD and VaD. Interestingly, there was a higher VLP-1 expression in AD, and a lower expression in DLB patients. Moreover, we found the CSF Ng level was increased in AD than MCI, implying CSF Ng might be a biomarker for identifying the progression of AD. Additionally, a significantly higher CSF YKL-40 level was detected not only in AD, but also in FTD, DLB, VaD, signifying YKL-40 was not sensitive in the diagnosis of AD. CONCLUSION: Our study confirmed that CSF levels of NSE, VLP-1, and Ng could be valuable biomarkers for identifying patients who are more susceptible to AD and distinguishing AD from other neurodegenerative dementia disorders.

Identification of Novel Key Genes and Pathways in Multiple Sclerosis Based on Weighted Gene Coexpression Network Analysis and Long Noncoding RNA-Associated Competing Endogenous RNA Network.

Objective: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system characterized by chronic inflammation and demyelination. This study is aimed at identifying crucial genes and molecular pathways involved in MS pathogenesis. Methods: Raw data in GSE52139 were collected from the Gene Expression Omnibus. The top 50% expression variants were subjected to weighted gene coexpression network analysis (WGCNA), and the key module associated with MS occurrence was identified. A long noncoding RNA- (lncRNA-) associated competing endogenous RNA (ceRNA) network was constructed in the key module. The hub gene candidates were subsequently verified in an individual database. Results: Of the 18 modules obtained, the cyan module was designated as the key module. The established ceRNA network was composed of seven lncRNAs, 45 mRNAs, and 21 microRNAs (miRNAs), and the FAM13A-AS1 was the lncRNA with the highest centrality. Functional assessments indicated that the genes in the cyan module primarily gathered in ribosome-related functional terms. Interestingly, the targeted mRNAs of the ceRNA network enriched in diverse categories. Moreover, highly expressed CYBRD1, GNG12, and SMAD1, which were identified as hub genes, may be associated with "valine leucine and isoleucine degradation," "base excision repair," and "fatty acid metabolism," respectively, according to the results of single gene-based genomes and gene set enrichment analysis (GSEA). Conclusions: Combined with the WGCNA and ceRNA network, our findings provide novel insights into the pathogenesis of MS. The hub genes discovered herein might also serve as novel biomarkers that correlate with the development and management of MS.

Comprehensive analysis of immune-related biomarkers and pathways in intracerebral hemorrhage using weighted gene co-expression network analysis and competing endogenous ribonucleic acid.

The immune response is an important part of secondary brain injury following intracerebral hemorrhage (ICH), and is related to neurological deficits and prognosis. The mechanisms underlying the immune response and inflammation are of great significance for brain injury and potential functional restoration; however, the immune-related biomarkers and competing endogenous ribonucleic acid (RNA) (ceRNA) networks in the peripheral blood of ICH patients have not yet been constructed. We collected the peripheral blood from ICH patients and controls to assess their ceRNA profiles using LCHuman ceRNA microarray, and to verify their expression with qRT-PCR. Two-hundred-eleven DElncRNAs and one-hundred-one DEmRNAs were detected in the ceRNA microarray of ICH patients. The results of functional enrichment analysis showed that the immune response was an important part of the pathological process of ICH. Twelve lncRNAs, ten miRNAs, and seven mRNAs were present in our constructed immune-related ceRNA network, combining weighted gene co-expression network analysis (WGCNA). Our study was the first to establish the network of the immune-related ceRNAs derived from WGCNA, and to identify leukemia inhibitory factor (LIF) and B cell lymphoma 2-like 13 (BCL2L13) as pivotal immune-related biomarkers in the peripheral blood of ICH patients, which are likely associated with PI3K-Akt, the MAPK signaling pathway, and oxidative phosphorylation. The MOXD2P-miR-211-3p -LIF and LINC00299-miR-198-BCL2L13 axes were indicated to participate in the immune regulatory mechanism of ICH. The goal of our study was to offer innovative insights into the underlying immune regulatory mechanism and to identify possible immune intervention targets for ICH.

Oxidized low-density lipoprotein receptor 1: a novel potential therapeutic target for intracerebral hemorrhage.

Oxidized low-density lipoprotein receptor 1 (OLR1) is upregulated in neurons and participates in hypertension-induced neuronal apoptosis. OLR1 deletion exerts protective effects on cerebral damage induced by hypertensive-induced stroke. Therefore, OLR1 is likely involved in the progress of intracerebral hemorrhage. In this study, we examined the potential role of OLR1 in intracerebral hemorrhage using a rat model. OLR1 small interfering RNA (10 µL; 50 pmol/µL) was injected into the right basal ganglia to knock down OLR1. Twenty-four hours later, 0.5 U collagenase type VII was injected to induce intracerebral hemorrhage. We found that knockdown of OLR1 attenuated neurological behavior impairment in rats with intracerebral hemorrhage and reduced hematoma, neuron loss, inflammatory reaction, and oxidative stress in rat brain tissue. We also found that silencing of OLR1 suppressed ferroptosis induced by intracerebral hemorrhage and the p38 signaling pathway. Therefore, silencing OLR1 exhibits protective effects against secondary injury of intracerebral hemorrhage. These findings suggest that OLR1 may be a novel potential therapeutic target for intracerebral hemorrhage.

Solid-solution reaction suppresses the Jahn-Teller effect of potassium manganese hexacyanoferrate in potassium-ion batteries.

Potassium manganese hexacyanoferrate (KMnHCF) suffers from poor cycling stability in potassium-ion batteries due to the Jahn-Teller effect, and experiences destabilizing asymmetric expansions and contractions during cycling. Herein, hollow nanospheres consisting of ultrasmall KMnHCF nanocube subunits (KMnHCF-S) are developed by a facile strategy. In situ XRD analysis demonstrates that the traditional phase transition for KMnHCF is replaced by a single-phase solid-solution reaction for KMnHCF-S, which effectively suppresses the Jahn-Teller effect. From DFT calculations, it was found that the calculated reaction energy for K+ extraction in the solid-solution reaction is much lower than that in the phase transition, indicating easier K+ extraction during the solid-solution reaction. KMnHCF-S delivers high capacity, outstanding rate capability, and superior cycling performance. Impressively, the K-ion full cell composed of the KMnHCF-S cathode and graphite anode also displays excellent cycling stability. The solid-solution reaction not only suppresses the Jahn-Teller effect of KMnHCF-S but also provides a strategy to enhance the electrochemical performance of other electrodes which undergo phase transitions.

PANX2 and brain lower grade glioma genesis: A bioinformatic analysis.

PANX2 forms large-pore channels mediating ATP release in response to physiological and pathological stimuli. Although PANX2 shows involvements in glioma genesis, the underlying mechanism remains unclear. PANX2 mRNA expression was analyzed via Oncomine and was confirmed via Gene Expression Profiling Interactive Analysis (GEPIA). The influence of PANX2 on overall survival (OS) of glioma was evaluated using LinkedOmics and further assessed through Cox regression analysis. The correlated genes with PANX2 acquired from LinkedOmics were validated through GEPIA and cBioPortal. Protein-protein interaction (PPI) of these genes was then obtained using Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape with MCODE plug-in. All the PANX2-related genes underwent Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The correlation between PANX2 and cancer immune infiltrates was evaluated via Tumor Immune Estimation Resource (TIMER). A higher expression of PANX2 only revealed a better OS in brain low grade glioma (LGG). PANX2-related genes in LGG functionally enriched in neuroactive ligand-receptor interaction, synaptic vesicle cycle, and calcium signaling. The hub genes from highest module of PPI were mainly linked to chemical synaptic transmission, plasma membrane, neuropeptide, and the pathway of neuroactive ligand-receptor interaction. Besides, PANX2 expression was negatively associated with infiltrating levels of macrophage, dendritic cells, and CD4+ T cells. This study demonstrated that PANX2 likely participated in LGG pathogenesis by affecting multiple molecular pathways and immune-related processes. PANX2 was associated with LGG prognosis and might become a promising therapeutic target of LGG.

Assessment of Weighted Gene Co-Expression Network Analysis to Explore Key Pathways and Novel Biomarkers in Muscular Dystrophy.

PURPOSE: This study aimed to explore the key molecular pathways involved in Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) and thereby identify hub genes to be potentially used as novel biomarkers using a bioinformatics approach. METHODS: Raw GSE109178 data were collected from the Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was conducted on the top 50% of altered genes. The key modules associated with the clinical features of DMD and BMD were identified. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed using the DAVID website. A protein-protein interaction (PPI) network was constructed using the STRING website. MCODE, together with the Cytohubba plug-ins of Cytoscape, screened out the potential hub genes, which were subsequently verified via receiver operating characteristic (ROC) curves in other datasets. RESULTS: Among the 11 modules obtained, the black module was predominantly associated with pathology and DMD, whereas the light-green module was primarily related to age and BMD. Functional enrichment assessments indicated that the genes in the black module were primarily clustered in "immune response" and "phagosome," whereas the ones in the light-green module were chiefly enriched in "protein polyubiquitination". Eleven essential genes were eventually identified, including VCAM1, TYROBP, CD44, ITGB2, CSF1R, LCP2, C3AR1, CCL2, and ITGAM for DMD, along with UBA5 and UBR2 for BMD. CONCLUSION: Overall, our findings may be useful for investigating the mechanisms underlying DMD and BMD. In addition, the hub genes discovered might serve as novel molecular markers correlated with dystrophinopathies.

Identification of Candidate Blood mRNA Biomarkers in Intracerebral Hemorrhage Using Integrated Microarray and Weighted Gene Co-expression Network Analysis.

PURPOSE: Intracerebral hemorrhage (ICH) is a serious public health hazard due to its high morbidity, disability, and mortality. Currently, the exact molecular mechanisms of ICH are unknown. We tried to identify the ICH-related candidate blood messenger RNA (mRNA) biomarkers by microarray analysis and weighted gene co-expression network analysis (WGCNA). MATERIALS AND METHODS: We collected the blood samples from patients with ICH (n = 4) and from vascular risk factor (VRF) controls (n = 4) and analyzed the mRNA expression profiles by competitive endogenous RNA (ceRNA) microarray. Differentially expressed genes (DEGs) were identified and then a weighted gene co-expression network was constructed. Modules with clinical significance were distinguished. Then, we downloaded two Gene Expression Omnibus (GEO) datasets (GSE24265 and GSE125512). Candidate mRNAs were identified by taking the intersection of the DEGs in our microarray, the interesting genes in the key module, and the DEGs in GSE24265. Functional analysis involving Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) and construction of a protein-protein interaction (PPI) network were conducted. RESULTS: A total of 340 DEGs in our microarray were identified between the ICH group and the control group. Among the eight gene modules established by WGCNA, the yellow module containing 191 genes was the most strongly associated with ICH. Four candidate mRNAs (C3AR1, PAWR, ARNTL2, and LDLRAD4) were identified. In the early stage of ICH (within 24 h), C3AR1, PAWR, and ARNTL2 were highly expressed in the perihematomal tissue, but with low expressions in peripheral blood; in the late stage (72 h after the first blood draw), an obvious upward trend of C3AR1 and PAWR in peripheral blood was seen. Functional analysis showed that candidate mRNAs were concerned with multiple pathways, such as the Wnt signaling pathway and calcium signaling pathway. They might affect the process of ICH through neuroinflammation, cell apoptosis, and pyroptosis. CONCLUSION: We identified four candidate blood mRNAs (C3AR1, PAWR, ARNTL2, and LDLRAD4) related to ICH. They showed different expression patterns in peripheral blood and perihematomal tissues and changed with time. They might play important roles in ICH through neuroinflammation, cell apoptosis, and pyroptosis and might shed new light to novel biomarkers or therapeutic targets in ICH.

Comprehensive Analysis of Long Non-coding RNA-Associated Competing Endogenous RNA Network in Duchenne Muscular Dystrophy.

Duchenne muscular dystrophy (DMD) is one of the most severe neuromuscular disorders. Long non-coding RNAs (lncRNAs) are a group of non-coding transcripts, which could regulate messenger RNA (mRNA) by binding the mutual miRNAs, thus acting as competing endogenous RNAs (ceRNAs). So far, the role of lncRNA in DMD pathogenesis remains unclear. In the current study, expression profile from a total of 33 DMD patients and 12 healthy people were downloaded from Gene Expression Omnibus (GEO) database (GSE38417 and GSE109178). Differentially expressed (DE) lncRNAs were discovered and targeted mRNAs were predicted. The ceRNA network of lncRNAs-miRNAs-mRNAs was then constructed. Genome Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses of the putative mRNAs in the ceRNA network were performed through Database for Annotation, Visualization and Integration Discovery (DAVID) website. Topological property of the network was analyzed using Cytoscape to disclose the hub lncRNAs. According to our assessments, 19 common DElncRNAs and 846 common DEmRNAs were identified in DMD compared to controls. The created ceRNA network contained 6 lncRNA nodes, 69 mRNA nodes, 27 miRNA nodes and 102 edges, while four hub lncRNAs (XIST, AL132709, LINC00310, ALDH1L1-AS2) were uncovered. In conclusion, our latest bioinformatic analysis demonstrated that lncRNA is likely involved in DMD. This work highlights the importance of lncRNA and provides new insights for exploring the molecular mechanism of DMD. The created ceRNA network contained 6 lncRNA nodes, 69 mRNA nodes, 27 miRNA nodes and 102 edges, while four hub lncRNAs (XIST, AL132709, LINC00310, ALDH1L1-AS2) were uncovered. Remarkably, KEGG analysis indicated that targeted mRNAs in the network were mainly enriched in "microRNAs in cancer" and "proteoglycans in cancer". Our study may offer novel perspectives on the pathogenesis of DMD from the point of lncRNAs. This work might be also conducive for exploring the molecular mechanism of increased incidence of tumorigenesis reported in DMD patients and experimental models.

MicroRNA-26a-5p alleviates neuronal apoptosis and brain injury in intracerebral hemorrhage by targeting RAN binding protein 9.

Emerging evidence has unraveled the important implications of microRNAs (miRNAs/miRs) in intracerebral hemorrhage (ICH). The aim of the present study was to assess the possible regulatory role of miR-26a-5p in ICH both in vivo and in vitro. ICH model of rats was constructed using stereotactic injection of VII collagenase, and ICH condition of PC-12 cells was stimulated by hemin. Exogenous overexpression of miR-26a-5p was achieved utilizing the transfection with miR-26a-5p agomir or miR-26a-5p mimics. We detected decreased miR-26a-5p and increased RAN binding protein 9 (RANBP9) levels in perihematomal tissues of ICH rats and in PC-12 cells following ICH. While miR-26a-5p overexpression alleviated behavioral deficits and neuronal apoptosis of rats with ICH. Apoptosis-related proteins Bax, Bcl-2 and cleaved caspase-3 in perihematomal region were also measured to further confirm the inhibitory effect of miR-26a-5p on neuronal apoptosis. In ICH models in vitro, we found that miR-26a-5p overexpression significantly decreased hemin-stimulated apoptosis of PC-12 cells. Additionally, RANBP9 knockdown could suppress the apoptosis of PC-12 cells, similar to the effects of PC-12 cells transfected with miR-26a-5p mimics. With dual-luciferase reporter assay, we identified that miR-26a-5p directly targeted RANBP9. In conclusion, exogenous miR-26a-5p alleviated neuronal apoptosis and brain injury partially by targeting RANBP9, and miR-26a-5p/RANBP9 axis may be a potential target for ICH treatment.

Role and mechanism of microRNA-21 in H2O2-induced apoptosis in bone marrow mesenchymal stem cells.

microRNA-21 (miR-21) contributes to anti-apoptosis, proliferation and migration in many cells, but its role in inhibiting apoptosis in bone marrow mesenchymal stem cells (BMSC) remains unclear. The aim of this study was to determine the role of miR-21 in H2O2-induced BMSC apoptosis. We used quantitative real time-polymerase chain reaction (RT-PCR) to demonstrate the level of miR-21 after treatment of BMSC with H2O2. BMSC apoptosis was induced by different concentrations of H2O2 and was decreased in miR-21-upregulated cells. The expression of PTEN, a functional target gene of miR-21 in BMSC, was regulated by miR-21. The RT-PCR results indicated that miR-21 was significantly up-regulated, and western blot analysis indicated that Bcl-2 was up-regulated, whereas the apoptosis-related genes caspase 3/9 and Bax were down-regulated in miR-21-up-regulated cells. The miR-21-up-regulated cells had significantly enhanced Akt phosphorylation, as measured by western blot analysis. LY294002, an inhibitor of Akt activation, abolished the protective effects of miR-21-up-regulated cells. These results suggest that miR-21 contributes to inhibition of apoptosis in BMSC by down-regulating PTEN, potentially via the PI3K/Akt pathway.