Quantitative microRNA (miRNA) detection is crucial for early breast cancer diagnosis and prognosis. However, quick and stable fluorescence sensing for miRNA identification is still challenging. This work developed a novel label-free detection method based on AuNPs etching for quantitatively detecting miRNA-155. A layer of AuNPs was grown on the surface of mesoporous silica nanoparticles (MSN) loaded with Rhodamine 6G (R6G) using seed-mediated growth, followed by probe attachment. In the presence of miRNA-155, the MSN@R6G@AuNP surface loses the protection of the attached probe, rendering AuNPs susceptible to etching by hydrochloric acid. This results in a significant fluorescent signal being released in the free space. The encapsulation with AuNPs effectively reduces signal leakage, while the rapid etching process shortens detection time. This strategy enables sensitive and fast detection with a detection range of 100 fM to 100 nM, a detection limit of 2.18 fM, and a detection time of 30 min. The recovery rate in normal human serum ranges from 99.02 % to 106.34 %. This work presents a simple biosensing strategy with significant potential for application in tumor diagnosis.

Objective To explore the relationship between the expression levels of microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) in the colonic mucosal tissue of patients with ulcerative colitis (UC) and the severity of the disease.Methods A total of 130 UC patients admitted to the Second Affiliated Hospital of Hebei North University from September 2021 to June 2023 were selected.According to the modified Mayo score system,the patients were assigned into an active stage group (n=85) and a remission stage group (n=45).According to the modified Truelove and Witts classification criteria,the UC patients at the active stage were assigned into a mild group (n=35),a moderate group (n=30),and a severe group (n=20).A total of 90 healthy individuals who underwent colonoscopy for physical examination or those who had normal colonoscopy results after single polypectomy and excluded other diseases were selected as the control group.The colonic mucosal tissues of UC patients with obvious lesions and the colonic mucosal tissue 20 cm away from the anus of the control group were collected.The levels of miR-155 and SOCS1 mRNA in tissues were determined by fluorescence quantitative PCR,and the expression of SOCS1 protein in tissues was determined by immunohistochemistry.The correlations of the levels of miR-155 and SOCS1 mRNA in the colonic mucosal tissue with the modified Mayo score of UC patients were analyzed.The values of the levels of miR-155 and SOCS1 mRNA in predicting the occurrence of severe illness in the UC patients at the active stage were evaluated.Results Compared with the control group and the remission stage group,the active stage group showed up-regulated expression level of miR-155,down-regulated level of SOCS1 mRNA,and decreased positive rate of SOCS1 protein in the colonic mucosal tissue (all P<0.001).The expression level of miR-155 and modified Mayo score in colonic mucosal tissues of UC patients at the active stage increased,while the mRNA level of SOCS1 was down-regulated as the disease evolved from being mild to severe (all P<0.001).The modified Mayo score was positively correlated with the miR-155 level and negative correlated with the mRNA level of SOCS1 in colonic mucosal tissues of UC patients (all P<0.001).The high miR-155 level (OR=2.762,95%CI=1.284-5.944,P=0.009),low mRNA level of SOCS1 (OR=2.617,95%CI=1.302-5.258,P=0.007),and modified Mayo score≥12 points (OR=3.232,95%CI=1.450-7.204,P=0.004) were all risk factors for severe disease in the UC patients at the active stage.The area under curve of miR-155 combined with SOCS1 mRNA in predicting severe illness in the UC patients at the active stage was 0.920.Conclusions The expression levels of miR-155 and SOCS1 mRNA were correlated with the disease severity in the UC patients at the active stage.The combination of the two indicators demonstrates good performance in predicting the occurrence of severe illness in UC patients at the active stage.
目的 探讨溃疡性结肠炎(UC)患者结肠黏膜组织微小RNA-155(miR-155)、细胞因子信号转导抑制因子1(SOCS1)表达水平与疾病严重程度的关系。方法 选取2021年9月至2023年6月河北北方学院附属第二医院收治的UC患者130例。按照改良Mayo评分系统将患者分为活动期组(n=85)和缓解期组(n=45);根据改良Truelove和Witts分型标准将UC活动期患者分为轻度组(n=35)、中度组(n=30)和重度组(n=20)。同时选取健康体检行结肠镜检查或结肠单发息肉切除术后复查结肠镜结果正常并排除其他疾病者共90例作为对照组。收集UC患者病变显著的结肠段黏膜组织和对照组距肛门20 cm处正常结肠黏膜组织。采用荧光定量PCR法测定组织中miR-155、SOCS1 mRNA表达水平,免疫组织化学法测定组织中SOCS1蛋白表达情况,分析UC患者结肠黏膜组织miR-155、SOCS1 mRNA和改良Mayo评分的相关性,评价miR-155、SOCS1 mRNA表达水平对UC活动期患者发生重度病情的预测价值。结果 与对照组和缓解期组比较,活动期组结肠黏膜组织miR-155表达水平显著升高,SOCS1 mRNA表达水平、SOCS1蛋白阳性表达率显著降低(P均<0.001)。轻、中、重度组UC活动期患者结肠黏膜组织miR-155表达水平和改良Mayo评分依次升高,SOCS1 mRNA表达水平依次降低(P均<0.001)。UC患者结肠黏膜组织miR-155与改良Mayo评分呈正相关,SOCS1 mRNA与改良Mayo评分呈负相关(P均<0.001)。miR-155高表达(OR=2.762,95%CI=1.284~5.944,P=0.009)、SOCS1 mRNA低表达(OR=2.617,95%CI=1.302~5.258,P=0.007)、改良Mayo评分≥12分(OR=3.232,95%CI=1.450~7.204,P=0.004)是影响UC活动期患者发生重度病情的危险因素。miR-155和SOCS1 mRNA联合预测UC活动期患者发生重度病情的曲线下面积为0.920。结论 miR-155、SOCS1 mRNA的表达水平与UC活动期患者的病情严重程度存在相关性,两者联合对UC活动期患者发生重度病情的预测效能较高。.

MicroRNAs (miRNAs) are a class of short non-coding RNAs that play a crucial role in regulating gene expression across multiple levels. They are involved in a wide range of physiological processes, including proliferation, differentiation, apoptosis, and cell cycle control. In recent years, miRNAs have emerged as pivotal regulatory molecules in the development and progression of tumors. Among these, miR-155 has garnered significant attention due to its high expression in various diseases, particularly urologic malignancies. Since an extensive corpus of studies having focused on the roles of miR-155 in various urologic malignancies, it is essential to summarize the current evidence on this topic through a comprehensive review. Altered miR-155 expression is related to various physiological and pathological processes, including immune response, inflammation, tumor development and treatment resistance. Notably, alterations in miR-155 expression have been observed in urologic malignancies as well. The up-regulation of miR-155 expression is commonly observed in urologic malignancies, contributing to their progression by targeting specific proteins and signaling pathways. This article provides a comprehensive review of the significant role played by miR-155 in the development of urologic malignancies. Furthermore, the potential of miR-155 as a biomarker and therapeutic target in urologic malignancies is also discussed.

UNASSIGNED: Group 2 innate lymphoid cells (ILC2s) have been found to take part in type 2 inflammation by secreting TH2 cytokines. Apolipoprotein A-I (Apo-AI), a major structural and functional protein of high-density lipoproteins, has anti-inflammatory effects on neutrophils, monocytes, macrophages, and eosinophils. However, its effects on ILC2s are not well characterized.
UNASSIGNED: We aimed to investigate the effect of Apo-AI on the proliferation and function of ILC2s as well as its possible mechanism.
UNASSIGNED: The protein expression of Apo-AI and the percentage of ILC2s in peripheral blood between 20 allergic rhinitis patients and 20 controls were detected by ELISA and flow cytometry. The effect of Apo-AI and miR-155 on ILC2 proliferation and function was detected by tritiated thymidine incorporation and ELISA. Anima models were adopted to verify the effect of Apo-AI in vivo.
UNASSIGNED: Elevated expression of Apo-AI was observed in allergic rhinitis patients. Apo-AI promotes ABCA1 expression by ILC2s, which can be inhibited by anti-Apo-AI. Apo-AI decreased ILC2 proliferation and the microRNA levels of GATA3 and RORα from ILC2s. The miR-155 overexpression promoted the upregulation of GATA3 and type II cytokines from ILC2s, while the addition of Apo-AI or miR-155 inhibitor significantly inhibited expression of GATA3 and type II cytokines by ILC2s. Apo-AI-/- mice showed as enhanced allergen-induced airway inflammation. The miR-155 inhibitor can reverse the enhanced allergen-induced airway inflammation in Apo-AI-/- mice, while miR-155 mimics can reverse the decreased allergen-induced airway inflammation in Apo-AI-treated mice.
UNASSIGNED: Apo-AI suppressed the proliferation and function of ILC2s through miR-155 in allergic rhinitis. Our data provide new insights into the mechanism of allergen-induced airway inflammation.

Acute lung injury (ALI) is an acute inflammatory process that can result in life-threatening consequences. Programmable DNA nanostructures have emerged as excellent nanoplatforms for microRNA-based therapeutics, offering potential nanomedicines for ALI treatment. Nonetheless, the traditional systematic administration of nanomedicines is constrained by low delivery efficiency, poor pharmacokinetics, and nonspecific side effects. Here, we identify macrophage microRNA-155 as a novel therapeutic target using the magnetic bead sorting technique. We further construct a DNA nanotubular nucleic acid drug antagonizing microRNA-155 (NT-155) for ALI treatment through intratracheal administration. Flow cytometry results demonstrate that NT-155, when inhaled, is taken up much more effectively by macrophages and dendritic cells in the bronchoalveolar lavage fluid of ALI mice. Furthermore, NT-155 effectively silences the overexpressed microRNA-155 in macrophages and exerts excellent inflammation inhibition effects in vitro and ALI mouse models. Mechanistically, NT-155 suppresses microRNA-155 expression and activates its target gene SOCS1, inhibiting the p-P65 signaling pathway and suppressing proinflammatory cytokine secretion. The current study suggests that deliberately designed nucleic acid drugs are promising nanomedicines for ALI treatment and the local administration may open up new practical applications of DNA in the future.

Atopic dermatitis (AD) is a common inflammatory skin condition and the leading cause of morbidity associated with skin conditions worldwide. For the majority of patients, AD is a lifelong disease that cannot be cured completely. Therefore, in the present study, differentially expressed genes (DEGs) in the epidermal immune microenvironment were screened using bioinformatic techniques. Subsequently, an in vitro cellular model was constructed to investigate the role of microRNA (miR)-155 in immune infiltration during AD. In the present study, two datasets (GSE121212 and GSE157194) were downloaded from Gene Expression Omnibus, before the DEGs were screened and subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functional enrichment analyses. miRNet was used to predict the possible target genes of miR-155 among the differentially expressed genes found. Consequently, peptidase inhibitor 3 (PI3), FOS-like 1, AP-1 transcription factor subunit (FOSL1), C-X-C motif chemokine ligand (CXCL)1 and CXCL8 were selected to be the potential target genes of miR-155 in the epidermal immune microenvironment of patients with AD. Concurrently, an inflammatory cell model using HaCaT cells was constructed by TNF-α and IFN-γ treatment. The effects of miR-155 on HaCaT cell proliferation and secretion of IL-1β, IL-6, IL-10, IL-15, PI3, FOSL1, CXCL1 and CXCL8 under inflammatory and non-inflammatory conditions were then analyzed. The results showed that after the HaCaT cells were transfected with miR-155, miR-155 inhibited HaCaT cell proliferation and decreased the mRNA expression levels of PI3 and CXCL8, increased the mRNA levels of FOSL1 and secretion levels of IL-1β, IL-6, IL-15 and CXCL1. By contrast, miR-155 decreased the secretion levels of IL-10 and CXCL8. In the inflammatory cell model of HaCaT cells, miR-155 was found to significantly inhibit the proliferation of HaCaT cells during inflammation whilst significantly increasing the secretion of IL-1β, IL-6, IL-10 and IL-15. In addition, miR-155 increased the mRNA expression and secretion levels of CXCL1 and CXCL8, whilst also increasing the mRNA expression levels of PI3. Results from the current study suggest that miR-155 can stimulate keratinocytes to produce inflammatory cytokines and proteins to enhance the inflammatory response in AD.

MicroRNA-155 (miR-155) is a multifunctional miRNA whose expression is known to be involved in a range of physiological and pathological processes. Its association with several oral diseases has been established. However, the specific role of miR-155 in orthodontic tooth movement remains unclear. In this study, we investigated the impact of miR-155 on osteoclast differentiation and orthodontic tooth movement models, aiming to explore the underlying mechanisms.
In this experiment, we utilized various agents including miR-155 mimic, miR-155 inhibitor, as well as non-specific sequences (NC mimic & NC inhibitor) to treat murine BMMNCs. Subsequently, osteoclast induction (OC) was carried out to examine the changes in the differentiation ability of monocytes under different conditions. To assess these changes, we employed RT-PCR, Western blotting, and TRAP staining techniques. For the orthodontic tooth movement model in mice, the subjects were divided into two groups: the NaCl group (injected with saline solution) and the miR-155 inhibitor group (injected with AntagomiR-155). We observed the impact of orthodontic tooth movement using stereoscopic microscopy, micro-CT, and HE staining. Furthermore, we performed RT-PCR and Western blotting analyses on the tissues surrounding the moving teeth. Additionally, we employed TargetScan to predict potential target genes of miR-155.
During osteoclast induction of BMMNCs, the expression of miR-155 exhibited an inverse correlation with osteoclast-related markers. Overexpression of miR-155 led to a decrease in osteoclast-related indexes, whereas underexpression of miR-155 increased those indexes. In the mouse orthodontic tooth movement model, the rate of tooth movement was enhanced following injection of the miR-155 inhibitor, leading to heightened osteoclast activity. TargetScan analysis identified SOCS1 as a target gene of miR-155.
Our results suggest that miR-155 functions as an inhibitor of osteoclast differentiation, and it appears to regulate osteoclasts during orthodontic tooth movement. The regulatory mechanism of miR-155 in this process involves the targeting of SOCS1.

OBJECTIVE: Acute kidney injury (AKI) is a common complication in patients with sepsis, and early detection and timely treatment are crucial. This article aims to explore the clinical role of microRNA-155 (miR-155) in early diagnosis and prognosis evaluation of septic patients with acute kidney injury.
METHODS: We collected the blood samples of septic patients and measured the relative expression of serum miR-155 by RT-qPCR, and drew the receiver operating characteristic (ROC) curves to evaluate its early diagnosis for septic AKI.
RESULTS: The relative expression of miR-155 in the septic AKI was significantly higher than that in the septic non-AKI, and increased with the aggravation of renal function damage. The ROC curve of miR-155 for the diagnosis of septic AKI was 1.91 (95% CI: 1.61-2.19). When the optimal cut-off value of miR-155 expression was 2.37, its sensitivity for diagnosing septic AKI was 91.12% (95% CI: 80.41-95.07%), and its specificity was 84.52% (95% CI: 71.74-89.36%). Furthermore, the severity of kidney injury, SOFA score, APACHE II score and miR-155 were the risk factors affecting the prognosis of septic patients with AKI.
CONCLUSIONS: Serum miR-155 can be used as a novel biomarker for the early diagnosis of septic AKI, and also has important clinical value in the prognosis evaluation of septic patients with AKI.

Parkinson\'s disease(PD)is the second most common neurodegenerative disease after Alzheimer\'s disease,with high morbidity and high disability rate.Since the early symptoms of PD are not typical and often similar to those of normal aging or other diseases.It is easy to missed diagnosis and misdiagnosis,which seriously affects the diagnosis and treatment of this disease and aggravetes the burden on the patients\' life.MicroRNAs(miRNA)are a class of endogenous non-coding RNAs that are involved in post-transcriptional regulation by binding to target messenger RNAs(mRNA).They are highly conserved,short,easy to obtain,and can stably exist in peripheral body fluids.They have been used as biomarkers for a variety of diseases.Recent studies have demonstrated that miRNA play an important role in the development of PD.This paper reviews the recent research progress of miR-7/124/155,three mature miRNA in PD,aiming to provide reference for clarifying the pathogenesis and guiding the diagnosis and treatment of PD.
帕金森病(PD)是继阿尔茨海默病之后的全球第二大神经退行性疾病,具有高发病率及高致残率,早期症状不典型,常与正常的老化或其他疾病表现类似,容易漏诊和误诊,严重影响该病的诊治,加重患病人群的生活负担。微小RNA(miRNA)是一类内源性的非编码RNA,通过结合信使RNA进行转录后调节,具有高度保守、短小、简单易获取等特点,并且可以在外周体液中稳定存在,已经被作为多种疾病的生物标志物。最新研究表明,miRNA在PD的发生发展中起重要作用。本文综述近年来国内外学者对miR-7/124/155这三种研究相对成熟的miRNA在PD中的研究进展,旨在为阐明PD的发病机制、指导PD的诊断及治疗提供参考。.

Intervertebral disc degeneration (IDD) is associated with low back pain, yet its inherent mechanism remains obscure. Hypercholesteremia was regarded as a risk factor for IDD, and our previous study showed that cholesterol accumulation could elicit matrix degradation in the nucleus pulposus (NP). MicroRNA-155 (miR-155) was substantiated as protective in IDD, but its role in cholesterol-induced IDD was unclear. The present study investigated whether miR-155 could mediate cholesterol-related IDD and its internal mechanisms. In vivo experiments revealed high-fat diet-induced hypercholesteremia in wild-type (WT) mice along with the occurrence of IDD, whereas Rm155LG transgenic mice showed milder NP degeneration, as evidenced by Saffron O-fast green (SF) staining and immunohistochemistry (IHC). Meanwhile, IHC showed that NLRP3 and Bax expression was also suppressed in Rm155LG mice. In vitro studies using Western blotting (WB) and immunofluorescence (IF) confirmed that the miR-155 mimic could alleviate cholesterol-induced matrix degradation, apoptosis and pyroptosis in NP. Moreover, RORα was upregulated in severely degenerated NP compared to mild IDD. It was also noted that RORα was suppressed in Rm155LG mice. In this study, we demonstrated that miR-155 could target RORα and that inhibition of RORα could prevent cholesterol-induced matrix degradation, apoptosis, and pyroptosis in NP, indicating the protective effect of miR-155 in cholesterol-induced IDD by targeting RORα.