Folia Biologica最新文献_第2页

A Combination of VX765 and OLT1177 Reduced Brain Injury after Intracerebral Haemorrhage via Inhibiting Inflammasome Activation. VX765联合OLT1177通过抑制炎性体激活减轻脑出血后脑损伤。

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 Epub Date: 2026-02-11 DOI: 10.14712/fb2025.0008

Lin Zhou, Adilijiang Aihemaitiniyazi, Bojun Xue, Xianglu Liu

{"title":"A Combination of VX765 and OLT1177 Reduced Brain Injury after Intracerebral Haemorrhage via Inhibiting Inflammasome Activation.","authors":"Lin Zhou, Adilijiang Aihemaitiniyazi, Bojun Xue, Xianglu Liu","doi":"10.14712/fb2025.0008","DOIUrl":"10.14712/fb2025.0008","url":null,"abstract":"Intracerebral haemorrhage (ICH) is a severe stroke subtype with high mortality and poor functional recovery. Neuroinflammation, mediated by NLRP3 inflammasome and caspase-1 (Casp1) activation, drives secondary brain injury, including oedema and cell death after ICH. We hypothesize that combining NLRP3 inhibitor OLT1177 and Casp1 inhibitor VX765 will provide enhanced neuroprotection against brain oedema and injury in experimental ICH. ICH was induced by injecting autologous blood into the basal ganglia in mouse models. Sixty-three C57Bl/6 male mice were randomly assigned to five groups: sham, vehicle, OLT1177 (dapansutrile, 200 mg/kg intraperitoneally), VX765 (75 mg/kg intraperitoneally) and combination of OLT1177 and VX765. Mice were treated for three consecutive days, starting 1 hour after ICH surgery. Behavioural tests, brain oedema, brain water content, blood-brain barrier integrity, vascular permeability, cell apoptosis, and levels of NLRP3 and its downstream proteins were measured. OLT1177 significantly reduced cerebral oedema after ICH and improved neurological function. It preserved blood-brain barrier integrity and reduced vascular leakage. Furthermore, OLT1177 prevented micro-glial morphological changes and significantly inhibited activation of Casp1 and release of IL-1β. OLT1177 also protected against neuronal loss in the affected hemisphere. Notably, the combination of OLT1177 and VX765 further attenuated brain injury after ICH by inhibiting inflammasome activation. The combination of OLT1177 and VX765 thus provided enhanced protection against brain injury by inhibiting inflammasome activation, suggesting that OLT1177 in combination with VX765 might serve as a promising therapeutic strategy for the treatment of ICH.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":" ","pages":"234-243"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical Significance of DPP10-AS1 and Its Potential Mechanism in Chronic Obstructive Pulmonary Disease through miR-34c-5p. 通过miR-34c-5p表达DPP10-AS1在慢性阻塞性肺疾病中的临床意义及其潜在机制

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025.0007

Jie Lin, Na Wang, Minyan Wang, Li Ye, Fang Lu, Cong Wang

{"title":"Clinical Significance of DPP10-AS1 and Its Potential Mechanism in Chronic Obstructive Pulmonary Disease through miR-34c-5p.","authors":"Jie Lin, Na Wang, Minyan Wang, Li Ye, Fang Lu, Cong Wang","doi":"10.14712/fb2025.0007","DOIUrl":"10.14712/fb2025.0007","url":null,"abstract":"Chronic obstructive pulmonary disease (COPD) is a leading cause of global mortality, characterized by persistent airflow limitation and chronic inflammation. Emerging evidence suggests that long non-coding RNAs (lncRNAs) play regulatory roles in COPD pathogenesis, but the function of DPP10-AS1 remains unclear. This study aimed to investigate the expression pattern, diagnostic value and functional mechanism of DPP10-AS1 in COPD, particularly its role in cigarette smoke-induced airway epithelial injury in 16HBE cells. Bioinformatic analysis of the GSE201465 dataset identified DPP10-AS1 as significantly up-regulated in COPD. Clinical validation was performed in 80 COPD patients and 80 controls. In vitro, 16HBE cells were treated with cigarette smoke extract (CSE) following DPP10-AS1 knockdown/over-expression. The interaction between DPP10-AS1 and miR-34c-5p was verified through RNA pull-down and dual-luciferase reporter assays. Functional rescue experiments with miR-34c-5p inhibitor in DPP10-AS1-silenced cells under CSE exposure were constructed. DPP10-AS1 expression was markedly elevated in COPD patients, showing a significant correlation with impaired lung function (FEV1/FVC: r = -0.743). It presented a diagnostic potential (AUC = 0.806). CSE exposure up-regulated DPP10-AS1 in 16HBE cells, which exacerbated inflammation (IL-6, IL-8 and COX-2) and fibrosis (α-SMA, Col1A1 and TGF-β1). Our research results indicated that DPP10-AS1 acts as a \"molecular sponge\" for miR-34c-5p. This mecha-nism may be of great significance for its role in COPD. We concluded that DPP10-AS1 promotes CSE-induced airway inflammation and remodelling through miR-34c-5p in 16HBE cells, suggesting its potential involvement in COPD progression. These findings combined with clinical analysis position DPP10-AS1 as a candidate diagnostic biomarker and therapeutic target.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 5-6","pages":"225-233"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147289663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Determinants of Implantation Success in Pancreatic Cancer Patient-Derived Xenografts: Role of Matrigel Application, Histological Subtype, and Time Management. 胰腺癌患者来源的异种移植物移植成功的决定因素：基质应用、组织学亚型和时间管理的作用。

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025.0006

Emin Gayibov, Tomáš Sychra, Alžběta Spálenková, Karolína Šeborová, Kamila Koucká, Tereza Tesařová, Kamila Kočí, Matěj Vícha, Arpád Szabó, Radka Václavíková, Zdeněk Šubrt, Pavel Souček, Martin Oliverius

{"title":"Determinants of Implantation Success in Pancreatic Cancer Patient-Derived Xenografts: Role of Matrigel Application, Histological Subtype, and Time Management.","authors":"Emin Gayibov, Tomáš Sychra, Alžběta Spálenková, Karolína Šeborová, Kamila Koucká, Tereza Tesařová, Kamila Kočí, Matěj Vícha, Arpád Szabó, Radka Václavíková, Zdeněk Šubrt, Pavel Souček, Martin Oliverius","doi":"10.14712/fb2025.0006","DOIUrl":"https://doi.org/10.14712/fb2025.0006","url":null,"abstract":"Pancreatic cancer (PC) is a growing global health concern, highlighting the need for improved preclinical models. Patient-derived xenografts (PDXs) closely replicate tumour biology and serve as a link between preclinical and clinical research. This study investigated the key factors influencing the success of PDX implantation in PC. We compared Matrigel-assisted versus Matrigel-free implantation. We also evaluated the impact of histological subtype on implantation success, analysing pancreatic ductal adenocarcinoma (PDAC), adenosquamous carcinoma (ASPC) and acinar cell carcinoma (ACC). Additionally, we assessed whether the tumour specimen culture-to-implantation period affected the take rate or tumour growth rate. A significance threshold of P < 0.05 was applied (95% confidence interval), and multivariable regression analysis was conducted to identify independent predictors of implantation success. In both NOD/SCID and NU/NU (nude) strains, Matrigel-assisted PDAC implantations achieved significantly higher take rates (75 % vs 90 %) compared to direct implantations (25 % vs 0 %) in the second generation (P = 0.02). The ASPC subtype was a significant predictor of success in the NOD/SCID strain (P = 0.04). The culture-to-implantation period did not affect the take rates. The nude strain significantly prolonged ACC engraftment (P = 0.02). In direct ACC implantations, earlier generations (F1-F5) required shorter engraftment growth duration (P < 0.0001). For ASPC, later generations demonstrated longer growth duration (P < 0.04). These findings emphasize critical variables in optimizing PC PDX protocols, particularly Matrigel use, mouse strain selection, and consideration of histological and generation-specific effects. Such refinements can optimize PDX efficiency and translational relevance.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 5-6","pages":"212-224"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147289692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Iron Must Be in Haemin to Act as a Pro-Inflammatory Stimulus in Cultured Human THP-1 Monocytes. 铁必须存在于血红蛋白中，才能在培养的人THP-1单核细胞中发挥促炎刺激作用。

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025.0001

Jan Pláteník, Peter Riško, Richard Buchal, Pavel J Kraml, Adriana Rybnikářová, Martina Čierna, Jana Potočková

{"title":"Iron Must Be in Haemin to Act as a Pro-Inflammatory Stimulus in Cultured Human THP-1 Monocytes.","authors":"Jan Pláteník, Peter Riško, Richard Buchal, Pavel J Kraml, Adriana Rybnikářová, Martina Čierna, Jana Potočková","doi":"10.14712/fb2025.0001","DOIUrl":"https://doi.org/10.14712/fb2025.0001","url":null,"abstract":"Cardiovascular diseases due to atherosclerosis remain a dominant medical problem. Macro-phages play a crucial role in both atherosclerosis progression and recycling of body iron. Epidemio-logical data point to elevation of body iron stores as one of non-classical cardiovascular risk factors, and we know that iron must be contained within macrophages to be atherogenic. Presumably, iron already contained within circulating monocytes turns cells to a more pro-inflammatory and hence atherogenic phenotype, but experimental evidence for such relationship remains limited. In this study, human monocytic THP-1 cells were loaded with micromolar iron in the forms of transferrin, ferric-ammonium citrate (FAC) and haemin for 2 and 24 hours. Only haemin was cytotoxic. All kinds of iron elevated the labile iron pool at 2 hours, as well as ferritin expression at 24 hours. Expression of scavenger receptors A and B, pro-inflammatory as well as anti-inflammatory cytokines, haem oxygenase and haptoglobin receptor were measured by quantitative PCR. Very few changes, none pro-inflammatory, were observed in response to transferrin or FAC. Haemin suppressed the expression of scavenger receptors, increased the expression of pro-inflammatory, and variably, anti-inflammatory cytokines, and dramatically induced haem oxygenase. The effects of haemin were not prevented by apotransferrin. We conclude that iron must be in the haemin form to act as a pro-inflammatory stimulus in THP-1 monocytes. Non-haem iron might require the presence of other factors to be atherogenic. Haemin treatment of THP-1 cells may represent a convenient experimental model to study the pro-inflammatory effects of haem that are observed in late stages of atherosclerosis.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 4","pages":"149-161"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nerol Activates Ca2+-Dependent Oxidative Eryptosis and Haemolysis-like Cell Death via Caspase/PKC/RIP1/p38 MAPK/CK1α, Energy Depletion and Ceramide Accumulation. 橙花醇通过Caspase/PKC/RIP1/p38 MAPK/CK1α、能量消耗和神经酰胺积累激活Ca2+依赖性氧化凋亡和溶血样细胞死亡。

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025.0004

Mohrah A Alalshaikh, Jawaher Alsughayyir, Sabiha Fatima, Mohammad A Alfhili

{"title":"Nerol Activates Ca2+-Dependent Oxidative Eryptosis and Haemolysis-like Cell Death via Caspase/PKC/RIP1/p38 MAPK/CK1α, Energy Depletion and Ceramide Accumulation.","authors":"Mohrah A Alalshaikh, Jawaher Alsughayyir, Sabiha Fatima, Mohammad A Alfhili","doi":"10.14712/fb2025.0004","DOIUrl":"10.14712/fb2025.0004","url":null,"abstract":"Nerol (NRL), a monoterpene in essential oils of various plants, exhibits anticancer activity, albeit with contrasting effects on normal cells. Because anaemia is induced by anticancer drugs, this study was initiated to profile the cytotoxic mechanisms of NRL in human erythrocytes. Cells were treated with NRL (0.01-0.1 %) for 24 h at 37 °C in Ringer buffers. Lytic cell death was measured photometrically and eryptosis was examined by flow cytometry using forward scatter, annexin V-affinity assay, H2DCFDA, and Fluo4/AM to evaluate cell volume, phosphatidylserine (PS) externalization, oxidative stress, and Ca2+, respectively. Small molecule inhibitors were used to probe the molecular mechanisms governing NRL-induced cytotoxicity. NRL led to eryptotic volume loss associa-ted with increased PS externalization and lysis through oxidative stress and Ca2+ nucleation. Ca2+ deprivation and K+ gradient dissipation, along with glucose, guanosine and sucrose, significantly blunted NRL-induced eryptosis and lytic death. Notably, both forms of cell death were inhibited by staurosporine, necrostatin 2 and myriocin, whereas urea, Z-VAD-FMK, SB205830 and D4476 only attenuated eryptosis. Furthermore, while lytic death was inhibited by polyethylene glycol, it was potentiated by Ca2+ deprivation and heparin, whereas eryptosis was aggravated by uric acid. In conclusion, NRL triggers cation channel- and redox-mediated eryptosis and lytic death through energy deprivation and activation of protein kinase C, receptor-interacting protein 1, serine palmitoyltransferase, caspase, p38 MAPK and casein kinase 1α. Altogether, these findings underscore the differential mechanisms by which NRL modulates divergent erythrocyte injury pathways and collectively advance the current knowledge of the extent of its cellular effects.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 4","pages":"180-191"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dysregulated BARD1 Contributes to Paclitaxel Resistance in Ovarian Cancer via Up-regulating CYP2C8. BARD1失调通过上调CYP2C8参与卵巢癌紫杉醇耐药

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071030109

Li Zhang, Zixuan Pan, Liqin Zhang, Hua Liu, Zonglan Li, Shuo Feng

{"title":"Dysregulated BARD1 Contributes to Paclitaxel Resistance in Ovarian Cancer via Up-regulating CYP2C8.","authors":"Li Zhang, Zixuan Pan, Liqin Zhang, Hua Liu, Zonglan Li, Shuo Feng","doi":"10.14712/fb2025071030109","DOIUrl":"https://doi.org/10.14712/fb2025071030109","url":null,"abstract":"Ovarian cancer remains one of the most lethal gynaecological malignancies, with paclitaxel resistance being a major therapeutic challenge that limits treatment efficacy and patient survival. We found that although the BARD1 level was not signi-ficantly altered in patients with ovarian cancer (OC), patients with higher BARD1 levels had increased survival time, suggesting that the down-regulation of BARD1 may be related to the paclitaxel sensitivity. Through examining the expression of BARD1 in tumour samples from paclitaxel responders and non-responders, we observed that the BARD1 level was significantly reduced in non-responders. CYP2C8 was up-regulated in non-responders. Also, the BARD1 level was negatively correlated with the level of CYP2C8. BARD1 over-expression in OC cells could repress the CYP2C8 expression, while knockdown of BARD1 could up-regulate CYP2C8 expression, which could be rescued by H2A-Ub. Results from gain and loss of functional experiments indicated that BARD1 functions as a tumour suppressor during paclitaxel treatment, and BARD1 down-regulation increased the IC50 of paclitaxel from 2.46 nM to 5.33 nM in SK-OV-3 cells and from 3.11 nM to 7.51 nM in CaoV-3 cells. We are the first to demonstrate that the down-regulation of BARD1 contributes to paclitaxel resistance via up-regulating CYP2C8 in patients with OC, which provides a potent target for clinical OC treatment.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 3","pages":"109-117"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145400270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Potential Inflammatory Role of IL-6 Signalling in Perturbing the Energy Metabolism Function by Stimulating the Akt-mTOR Pathway in Jurkat T Cells. IL-6信号在Jurkat T细胞中通过刺激Akt-mTOR通路干扰能量代谢功能的潜在炎症作用

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071010008

Abdullah Alghamdi, Mohammed Alissa

{"title":"The Potential Inflammatory Role of IL-6 Signalling in Perturbing the Energy Metabolism Function by Stimulating the Akt-mTOR Pathway in Jurkat T Cells.","authors":"Abdullah Alghamdi, Mohammed Alissa","doi":"10.14712/fb2025071010008","DOIUrl":"https://doi.org/10.14712/fb2025071010008","url":null,"abstract":"Numerous studies have reported that increased interleukin 6 (IL-6) and soluble IL-6 receptor (sIL-6) levels induce inflammatory conditions. However, the exact mechanisms by which IL-6 drives inflammatory conditions remain unclear. Therefore, we investigated the potential role of IL-6/sIL-6R in inducing energy metabolism, including glycolysis, oxidative phosphorylation, lactate secretion and Akt/mTOR phosphorylation, in Jurkat cells, and whether IL-6 would increase the risk of developing inflammatory conditions due to the high metabolic profile of the T cells. Jurkat CD4 T-cell lines were stimulated with IL-6/sIL-6R for 24 h prior to 48-h stimulation with anti-CD3/CD28. Lactate secretion, glycolysis and oxidative phosphorylation levels were characterized using the Seahorse XF analyser. The Akt and mTOR phosphorylation status was detected using Western blotting. IL-6/sIL-6R significantly induced glycolysis and oxidative phosphorylation and their related parameters, including glycolytic capacity and maximal respiration, followed by significantly increased lactate secretion. Akt and mTOR phosphorylation were increased, which could have resulted from energy metabolism. Here we show that IL-6 enhanced the metabolic profile of Jurkat cells. This effect could have consequences for the metabolism-related signalling pathways, including Akt and mTOR, suggesting that IL-6 might promote T-cell energy metabolism, where T-cell hyperactivity might increase the inflammatory disease risk. The findings should be validated using studies on primary cells isolated from humans.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 1","pages":"8-17"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical Value and Regulatory Mechanism of miR-767-5p in Colorectal Cancer. miR-767-5p在结直肠癌中的临床价值及调控机制

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071010018

Ping Lin, Xiuju Qin, Caiyun Yi, Man Jiang, Lili Yi, Yuemian Liang

{"title":"Clinical Value and Regulatory Mechanism of miR-767-5p in Colorectal Cancer.","authors":"Ping Lin, Xiuju Qin, Caiyun Yi, Man Jiang, Lili Yi, Yuemian Liang","doi":"10.14712/fb2025071010018","DOIUrl":"https://doi.org/10.14712/fb2025071010018","url":null,"abstract":"The poor prognosis of colorectal cancer (CRC) contributes to a yearly increase in CRC mortality, while microRNAs (miRNAs) were found to play a regulatory function in diversiform cancers, including CRC. The objective of this research was to evaluate the clinical value and possible regulatory mechanisms of miR-767-5p in CRC. The expression level of miR-767-5p in CRC tissues and cells was examined. The Kaplan-Meier curve was utilized to analyse the function of miR-767-5p in CRC prognosis. The independent prognostic factors in CRC were assessed by a multivariate COX regression analysis. Additionally, the regulatory mechanism of miR-767-5p in CRC was determined through an in vitro cell experiment. The miR-767-5p expression was down-regulated in CRC tumour tissues and CRC cells. Indicators such as tumour differentiation, TNM, LNM and miR-767-5p were identified as independent prognostic factors for a poor CRC prognosis. The regulatory relationship between miR-767-5p and nuclear factor I A (NFIA) was verified by the dual-luciferase reporter assay, and the NFIA expression level was significantly suppressed by over-expressed miR-767-5p. The proliferation, migration and invasion of CRC cells were inhibited by over-expressing miR-767-5p, while the inhibition effect could be reversed by over-expressing NFIA. The over-expressed miR-767-5p could serve as a tumour suppressor to inhibit the progression of CRC by suppressing the expression level of NFIA.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 1","pages":"18-28"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144001705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comprehensive Analysis of Hub Telomere-Related Genes and Synovial Immune Characteristics in Osteoarthritis. 骨关节炎中心端粒相关基因与滑膜免疫特征的综合分析。

IF 0.6 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071030123

Chunxiao Du, Weidan Xu

{"title":"Comprehensive Analysis of Hub Telomere-Related Genes and Synovial Immune Characteristics in Osteoarthritis.","authors":"Chunxiao Du, Weidan Xu","doi":"10.14712/fb2025071030123","DOIUrl":"https://doi.org/10.14712/fb2025071030123","url":null,"abstract":"Osteoarthritis (OA) is a degenerative arthritis associated with aging. It is recognized that telomere attrition is a hallmark of aging. However, the transcriptional dynamics of synovial telomere-related genes (TRGs) in OA has not yet been elucidated. OA synovium microarray profiles were sourced from GEO and TRGs from TelNet. GO, KEGG, DO and GSVA enrichment analyses were employed to explore the underlying mechanisms. WGCNA and machine learning methods were utilized to screen hub differentially expressed TRGs (TRDEGs) that highly correlated with OA traits (hub OA-TRDEGs). Nomograms and receiver operating characteristic (ROC) curves were used to evaluate the diagnostic performance of hub OA-TRDEGs. An RNA-binding protein (RBP) network was developed to predict potential RBP target genes. The CIBERSORT analysis was performed to assess associations between hub OA-TRDEGs and immune infiltration. We identified 77 TRDEGs in normal and OA synovium samples. Functional enrichment analysis implicated these ge-nes primarily in metabolism regulation, DNA repair and inflammatory response. LTA4H, HNMT, ANKMY2, UFSP2, HLTF and RPA3 were established as hub OA-TRDEGs, demonstrating strong diagnostic performance for OA. Wilcox testing confirmed significant up-regulation of all hub OA-TRDEGs in OA synovium - a finding validated through independent datasets and qRT-PCR assays. Immune infiltration analysis further indicated that resting mast cells, CD4+ memory resting T cells and activated mast cells are implicated in OA pathogenesis and exhibit significant correlations with hub OA-TRDEGs. These results nominate hub OA-TRDEGs as potential dia-gnostic biomarkers and underscore immune cell infiltration as a critical driver of OA progression.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 3","pages":"123-139"},"PeriodicalIF":0.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145400308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-296-3p Controls Osteogenic Proliferation and Differentiation by Targeting ICAT and Is Involved in Fracture Healing. miR-296-3p通过靶向ICAT调控成骨增殖和分化并参与骨折愈合。

IF 1.1 4区医学

Folia Biologica Pub Date : 2025-01-01 DOI: 10.14712/fb2025071020064

Feng Xu, Kun Huang, Wenjun Ji, Miao Huang, Jincheng Sima, Jin Li, Hao Song, Wei Xiong, Zhong Tian

{"title":"miR-296-3p Controls Osteogenic Proliferation and Differentiation by Targeting ICAT and Is Involved in Fracture Healing.","authors":"Feng Xu, Kun Huang, Wenjun Ji, Miao Huang, Jincheng Sima, Jin Li, Hao Song, Wei Xiong, Zhong Tian","doi":"10.14712/fb2025071020064","DOIUrl":"https://doi.org/10.14712/fb2025071020064","url":null,"abstract":"Fragility fractures have been a cause for concern because of their high incidence. For the prevention and treatment of osteoporotic fractures, it is important to understand how to promote bone formation and increase bone mass. This study investigated miR-296-3p expression and function in fragility fracture. The study enrolled 98 patients with hip fractures, 90 patients with wrist fractures and 35 healthy controls. RT-qPCR was used to detect the miR-296-3p level changes before and after surgery in fracture patients and during the differentiation of human bone mesenchymal stem cells (BMSCs). The starBase bioinformatics database was used for prediction of the miR-296-3p target gene, and dual luciferase report was used for verification of the target relationship. Our results demonstrated that miR-296-3p levels are up-regulated in fracture patients, while they gradually decrease during human BMSC differentiation. The up-regulation of miR-296-3p inhibited the proliferation and differentiation ability of human BMSCs, while inhibition of its expression had the opposite effects. miR-296-3p negatively regulates osteogenic differentiation, and over-expression of inhibitor of β-catenin and TCF (ICAT) could counteract the negative regulatory effect. miR-296-3p targets ICAT and affects the expression of key proteins in the Wnt/β-catenin signalling pathway. In conclusion, miR-296-3p can regulate the division and differentiation of osteoblasts by affecting the expression of ICAT and participate in fracture healing.","PeriodicalId":12281,"journal":{"name":"Folia Biologica","volume":"71 2","pages":"64-72"},"PeriodicalIF":1.1,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0