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        <title>Experimental Biology and Medicine | Biochemistry and Molecular Biology section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/biochemistry-and-molecular-biology</link>
        <description>RSS Feed for Biochemistry and Molecular Biology section in the Experimental Biology and Medicine journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-04-10T23:34:12.451+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10845</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10845</link>
        <title><![CDATA[Functional roles of Keratin 6A in disease pathogenesis across cancer and skin disorders]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yanyan Su</author><author>Shudong Su</author><author>Min Li</author><author>Zhixia Zhang</author><author>Shiyi Zhang</author><author>Caixia Fan</author><author>Wei Luo</author><author>Shuming Guo</author>
        <description><![CDATA[Keratin 6A (KRT6A) is an epithelial-specific type II keratin localized within cytoskeletal intermediate filaments and functions in cooperation with KRT16/17 to maintain epidermal homeostasis and tissue repair. Accumulating evidence highlights its multifaceted roles in cancer. Aberrant KRT6A expression promotes cell cycle progression, epithelial–mesenchymal transition, migration, and invasion, thereby driving tumor initiation and metastasis, although tumor-suppressive effects have been observed in specific contexts. Mechanistically, KRT6A regulates adhesion, cytoskeletal remodeling, and critical signaling pathways, thereby reshaping tumor immunity and metabolism to facilitate immune evasion and metabolic dysregulation. Elevated KRT6A expression is strongly associated with resistance to chemotherapy, targeted therapy, and radiotherapy. Therapeutic approaches targeting KRT6A include nucleic acid-based interventions, protein degradation strategies, inhibition of upstream regulatory pathways, and combinatorial regimens to overcome drug resistance. Clinically, KRT6A has emerged as both a diagnostic and prognostic biomarker, supporting treatment monitoring and enhancing predictive models for risk stratification and individualized outcome evaluation. Beyond oncology, mutations in KRT6A underlie pachyonychia congenita, and its dysregulation contributes to epidermal hyperproliferative disorders such as psoriasis. Overall, systematic elucidation of the structure–function–pathway–clinical axis of KRT6A offers new opportunities for precision medicine and supports its potential as a therapeutic target in cancer management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10766</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10766</link>
        <title><![CDATA[LncRNA HOTAIR promotes LPS-induced inflammatory responses by activating the NF-κB pathway]]></title>
        <pubdate>2026-01-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Fengqing Zhu</author><author>Zexun Mo</author><author>Wuzhou Lin</author><author>Cheng Sun</author><author>Xiaomei Huang</author><author>Meifeng Ye</author><author>Hua He</author><author>Yujun Li</author><author>Kangwei Wang</author><author>Juan Zhu</author><author>Chuwen Lin</author><author>Shuquan Wei</author><author>Zhike Liang</author>
        <description><![CDATA[Acute lung injury (ALI) is a disease with an excessive inflammatory response triggered by activating the NF-κB signaling pathway. Our study aims to investigate the role of the long non-coding RNA HOTAIR in ALI-associated hyperinflammation, providing evidence for HOTAIR as a potential therapeutic target for ALI. Here, we examined the contribution of HOTAIR to LPS-induced lung injury using both A549 cell and murine models. LPS stimulation markedly increased HOTAIR expression in A549 cells, accompanied by reduced cell viability and elevated secretion of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α. Overexpression of HOTAIR further amplified NF-κB signaling, as indicated by increased phosphorylation of IκBα and p65 and enhanced nuclear translocation of p65, whereas silencing HOTAIR effectively reversed these effects. In vivo, knockdown of HOTAIR significantly mitigated LPS-induced lung injury, reduced inflammatory cytokine production, and suppressed NF-κB activation in mice. Our findings reveal the contribution of HOTAIR to NF-κB–driven inflammatory injury in ALI, offering insight into its regulatory role and informing future exploration of targeted therapeutic approaches.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10527</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10527</link>
        <title><![CDATA[Mechanisms of AGE-induced VSMC phenotypic switching and macrophage modulation in human abdominal aortic aneurysms]]></title>
        <pubdate>2025-08-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaoying Ma</author><author>Jinfang Xu</author><author>Huiying Sun</author><author>Jiajun Liu</author><author>Shibo Xia</author><author>Hao Zhang</author><author>Chaoyi Cui</author><author>Chao Song</author>
        <description><![CDATA[Advanced glycation end products (AGEs) have been associated with vascular pathologies including abdominal aortic aneurysms (AAAs), although their causal role remains unclear. In this study, we observed significant accumulation of AGEs in human AAAs, particularly in cases associated with intraluminal thrombus (ILT). In vitro, AGE exposure induced vascular smooth muscle cell (VSMC) migration and suppressed contractility, accompanied by reduced expression of contractile markers (α-SMA and MYH11) and elevated MMP-2. This phenotypic transformation was linked to the activation of the NLRP3 inflammasome and RAGE/RhoA/ROCK signaling, and was reversible upon inhibition of RAGE, RhoA, or ROCK. In macrophages, AGE pretreatment had minimal effects on basal cytokine secretion but attenuated LPS-induced IL-6 and IL-1β release and NF-κB activation. Co-culture experiments further revealed that AGE-pretreated macrophages reduced LPS-driven pro-migratory effects on VSMCs. Spatial transcriptomics demonstrated enriched AGE-RAGE signaling in αSMA+ VSMCs and CD68+αSMA+ macrophage-like VSMCs in ILT-containing AAAs. Overall, these associative findings implicate AGE-RAGE signaling in AAA pathogenesis and warrant further investigation to establish causality.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10456</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10456</link>
        <title><![CDATA[Vitamin D3 affects liver expression of pro-/anti-inflammatory cytokines and nitric oxide synthases in type 2 diabetes]]></title>
        <pubdate>2025-07-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ihor Shymanskyi</author><author>Olha Lisakovska</author><author>Mykola Veliky</author><author>Olha Mezhenska</author><author>Vasyl Bilous</author><author>Andrii Siromolot</author><author>Anna Khomenko</author><author>Dmytro Labudzynskyi</author><author>Tetyana Horid’ko</author><author>Elvira Pasichna</author>
        <description><![CDATA[Our objective was to study the effect of vitamin D3 (VD) on hepatocellular oxidative-nitrosative stress and pro/anti-inflammatory cytokines in relation to nitric oxide (NO) formation and NO synthase (NOS) levels in type 2 diabetes mellitus (T2DM). After T2DM induction by high-fat diet and a single streptozotocin injection (25 mg/kg b. w.), male Wistar rats were treated with/without VD (1,000 IU/kg b. w., 30 days). Oxidative stress/inflammation and NOS/NO were assessed by flow cytometry, RT-qPCR, western blotting, and ELISA. A 3.3-fold decrease in serum 25(OH)D3 was established in diabetic rats, suggesting their VD deficient status. T2DM was associated with excess reactive oxygen species (ROS; 2.4-fold) and NO (2.5-fold) production in hepatocytes paralleled by elevated levels of myeloperoxidase (1.7-fold), carbonylated (2.8-fold) and nitrotyrosylated (1.7-fold) proteins in liver tissue vs. control, indicative of oxidative-nitrosative stress. Low-grade inflammation in diabetic liver was confirmed by increased NF-κB transcriptional activity (1.24-fold) and mRNA expression of proinflammatory cytokines TNF-α (3.5-fold) and IL-1β (2.2-fold) with alleviating mRNAs of anti-inflammatory cytokines IL-4 (1.7-fold) and IL-10 (2.6-fold), while TGF-β1 expression raised 1.4-fold vs. control. Higher iNOS and eNOS mRNAs (2.7- and 3.3-fold, respectively) and protein (2.1- and 3.2-fold, respectively) levels, as well as NOS activity (1.6-fold) were found in diabetic liver. VD supplementation restored 25(OH)D3, partially normalized NF-κB transcriptional activity and pro/anti-inflammatory cytokines, lowered hepatocellular ROS/NO, and oxidative protein modifications. However, VD had no effect on eNOS, IL-10 and TGF-β1 mRNAs. It also led to a further increase in myeloperoxidase, eNOS and iNOS proteins and NOS activity compared to diabetes. In conclusion, abnormal oxidative metabolism in T2DM is associated with enhanced NF-κB/NOS/NO response, which can be partially attenuated by VD treatment via normalization of pro-oxidative/pro-inflammatory processes. The paradoxical sustained increase in NOS expression in the presence of VD antioxidant activity likely improves hepatocellular NO bioavailability, ultimately reducing T2DM-associated liver injury.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10523</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10523</link>
        <title><![CDATA[Potential supplementary tumor markers for liquid biopsy in non-small cell lung cancer]]></title>
        <pubdate>2025-05-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jin Xiang</author><author>Junyan Peng</author><author>Zhifang Xing</author><author>Guoqiang Ren</author><author>Huating Zhang</author><author>Xiaodong Song</author><author>Bo Zhang</author><author>Ming Guan</author><author>Guojun Cao</author>
        <description><![CDATA[The identification of epidermal growth factor receptor (EGFR) tyrosine kinase (TK) domain mutations in non-small cell lung cancer (NSCLC) patients is crucial for therapeutic decision-making and monitoring EGFR-tyrosine kinase inhibitor (TKI) resistance. Liquid biopsy has emerged as a promising alternative for patients ineligible for invasive tissue sampling. This study investigated the clinical utility of a novel chip-based digital PCR (dPCR) platform for detecting two important EGFR mutations - exon 19 deletions (19del) and threonine-methionine amino acid substitution at position 790 (T790M) - in serum samples, while exploring potential serum biomarkers for mutation prediction. The collection of 350 serum samples were conducted on patients diagnosed with NSCLC at Huashan Hospital between August 2023 and February 2024. Cell-free deoxyribonucleic acid (cfDNA) was extracted from serum and was analyzed for EGFR mutations using dPCR. The serum tumor marker levels were quantified. The dPCR assay demonstrated positive predictive values of 73.33% for 19del and 28.57% for T790M. Biomarker analysis revealed a carbohydrate antigen (CA) 199 cutoff of 11.75 U/mL (AUC = 0.707, 95% CI: 0.573–0.841, P = 0.005) for 19del detection, while progastrin-releasing peptide (ProGRP) showed a cutoff of 45.15 pg/mL (AUC = 0.628, 95% CI: 0.521–0.735, P = 0.028) for T790M identification. Variant rate exhibited significant positive correlations with biomarker concentrations: 19del variant rates significantly associated with CA125 levels (r = 0.624, P = 0.010), while T790M correlated with both carcinoembryonic antigen (CEA) (r = 0.531, P = 0.004) and ProGRP (r = 0.395, P = 0.041) in mutation-positive cohorts. These findings indicate that serum-based dPCR liquid biopsy demonstrates potential clinical utility as a supplementary approach to tissue biopsy for NSCLC genotyping. Notably, elevated serum tumor marker levels correlate with enhanced mutation detection rates in liquid biopsy, implying their potential supplementary value in prioritizing patients for molecular profiling.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10387</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10387</link>
        <title><![CDATA[Detection of respiratory syncytial virus based on RT-RPA and CRISPR-Cas12a]]></title>
        <pubdate>2025-05-01T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Ariya Khamwut</author><author>Juthamas Nimnual</author><author>Nantinee Chomta</author><author>Pattaraporn Nimsamer</author><author>Oraphan Mayuramart</author><author>Pornchai Kaewsapsak</author><author>Siripat Pasittungkul</author><author>Yong Poovorawan</author><author>Sunchai Payungporn</author>
        <description><![CDATA[Human respiratory syncytial virus (hRSV) is one of the most prevalent viruses infecting children globally. In this study, we employed the RT-RPA with CRISPR/Cas12a detection methodology to detect and differentiate RSV-A and RSV-B, particularly in resource-limited settings. The detection limit for RSV-A and RSV-B was approximately 102 and 103 copies/reaction, respectively. The assay revealed 100% specificity in detecting both RSV-A and RSV-B. Diagnostic accuracy was 90.32 and 93.55% for RSV-A and RSV-B, respectively, compared to RT-qPCR. These data indicate a proficient strategy for RSV screening, demonstrating promise for prospective applications in detecting diverse viral infections.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10537</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10537</link>
        <title><![CDATA[Critical role of alpha spectrin in DNA repair: the importance of μ-calpain and Fanconi anemia proteins]]></title>
        <pubdate>2025-05-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Muriel W. Lambert</author>
        <description><![CDATA[Nonerythroid spectrins are proteins important in maintaining the structural integrity and flexibility of the cell and nuclear membranes and are essential for a number of functionally important cellular processes. One of these proteins, nonerythroid α spectrin (αSpII), plays a critical role in DNA repair, specifically repair of DNA interstrand crosslinks (ICLs), where it acts as a scaffold, recruiting repair proteins to sites of damage. Loss or breakdown of αSpII is an important factor in a number of disorders. One of these is Fanconi anemia (FA), a genetic disorder characterized by bone marrow failure, chromosome instability, cancer predisposition, congenital abnormalities and a defect in DNA ICL repair. Significantly, breakdown of αSpII occurs in cells from a number of FA complementation groups, due to excessive cleavage by the protease, μ-calpain, leading to defective repair of DNA ICLs in telomeric and non-telomeric DNA. Knockdown of μ-calpain in FA cells by μ-calpain siRNA results in restoration of αSpII levels to normal and repair of DNA ICLs in telomeric and non-telomeric DNA, demonstrating the importance of αSpII stability in the repair process. It is hypothesized that there is a mechanistic link between excessive cleavage of αSpII by μ-calpain and defective DNA ICL repair in FA and that FA proteins, which are deficient in FA, play a key role in maintaining the stability of αSpII and preventing its cleavage by μ-calpain. All of these events are proposed to be important key factors involved in the pathophysiology of FA and suggest new avenues for potential therapeutic intervention.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10170</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10170</link>
        <title><![CDATA[Dysregulated transfer RNA-derived small RNAs as potential gastric cancer biomarkers]]></title>
        <pubdate>2024-12-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jie Yuan</author><author>Wenchao Gu</author><author>Tianxin Xu</author><author>Yan Zhang</author><author>Lei Shen</author><author>Jianliang Yan</author><author>Xi Guan</author><author>Haidan Chu</author><author>Ruoyu Yuan</author><author>Shaoqing Ju</author>
        <description><![CDATA[Gastric cancer (GC) is the kind of carcinoma that has the highest rates of morbidity and death worldwide. In the early stages of GC, there is currently an absence of sensitive and specific biomarkers. The newly-discovered class of non-coding RNAs (ncRNAs) known as transfer RNA-derived small RNAs (tsRNAs) is highly expressed in bodily fluids and neoplastic cells. High-throughput sequencing was initially employed to identify differentially expressed tsRNAs in early GC patients, followed by validation in patient serum, GC tissues, and cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). We identified dysregulated tsRNAs (the up-regulated tsRNAs included tRF-31-PNR8YP9LON4VD, tRF-30-MIF91SS2P4FI, and tRF-30-IK9NJ4S2I7L7, whereas the down-regulated tsRNAs included tRF-38-W6RM7KYUPRENRHD2, tRF-37-LBRY73W0K5KKOV2, tRF-36-JB59V3WD8YQ84VD, tRF-25-MBQ4NKKQBR, and tRF-36-0KFMNKYUHRF867D) in GC, and we verified that the serum of patients, GC cells and tissues both consistently expressed these tsRNAs. Additionally, GC patients’ serum had considerably greater expression levels of the three up-regulated tsRNAs than did healthy controls. Receiver operating characteristic (ROC) curve analysis demonstrated that the sensitivity and specificity of the three up-regulated tsRNAs were superior to those of CEA, CA199, and CA724 in the process of diagnosing GC, particularly in its early stages. This suggests that tsRNAs have great diagnostic efficacy and potential as new “liquid biopsy” biomarkers for the diagnosis of GC. Using bioinformatics software, we predicted that dysregulation of tsRNAs may be a potential regulatory mechanism for the development of GC.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10303</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10303</link>
        <title><![CDATA[Association of immunity-related gene SNPs with Alzheimer’s disease]]></title>
        <pubdate>2024-11-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nisrine Bissar</author><author>Rayan Kassir</author><author>Ali Salami</author><author>Said El Shamieh</author>
        <description><![CDATA[Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder characterized by progressive cognitive decline. Genetic factors have been implicated in disease susceptibility as its etiology remains multifactorial. The CD33 and the HLA-DRB1 genes, involved in immune responses, have emerged as potential candidates influencing AD risk. In this study, 644 Lebanese individuals, including 127 AD patients and 250 controls, were genotyped, by KASP assay, for six SNPs selected from the largest GWAS study in 2021. Logistic regression analysis assessed the association between SNP genotypes and AD risk, adjusting for potential confounders. Among the six SNPs analyzed, rs1846190G>A in HLA-DRB1 and rs1354106T>G in CD33 showed significant associations with AD risk in the Lebanese population (p < 0.05). Carriers of the AG and AA genotypes of rs1846190 in HLA-DRB1 exhibited a protective effect against AD (AG: OR = 0.042, p = 0.026; AA: OR = 0.052, p = 0.031). The GT genotype of rs1354106T>G in CD33 was also associated with reduced risk (OR = 0.173, p = 0.005). Following Bonferroni correction, a significant correlation of rs1354106T > G with AD risk was established. Our results might highlight the complex interplay between genetic and immunological factors contributing to the development of the disease.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10200</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10200</link>
        <title><![CDATA[Fructose metabolism is unregulated in cancers and placentae]]></title>
        <pubdate>2024-10-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fuller W. Bazer</author><author>Guoyao Wu</author><author>Gregory A. Johnson</author>
        <description><![CDATA[Fructose and lactate are present in high concentrations in uterine luminal fluid, fetal fluids and fetal blood of ungulates and cetaceans, but their roles have been ignored and they have been considered waste products of pregnancy. This review provides evidence for key roles of both fructose and lactate in support of key metabolic pathways required for growth and development of fetal-placental tissues, implantation and placentation. The uterus and placenta of ungulates convert glucose to fructose via the polyol pathway. Fructose is sequestered within the uterus and cannot be transported back into the maternal circulation. Fructose is phosphorylated by ketohexokinase to fructose-1-PO4 (F1P) by that is metabolized via the fructolysis pathway to yield dihydoxyacetone phosphate and glyceraldehyde-3-PO4 that are downstream of phosphofructokinase. Thus, there is no inhibition of the fructolysis pathway by low pH, citrate or ATP which allows F1P to continuously generate substrates for the pentose cycle, hexosamine biosynthesis pathway, one-carbon metabolism and tricarboxylic acid cycle, as well as lactate. Lactate sustains the activity of hypoxia-inducible factor alpha and its downstream targets such as vascular endothelial growth factor to increase utero-placental blood flow critical to growth and development of the fetal-placental tissues and a successful outcome of pregnancy. Pregnancy has been referred to as a controlled cancer and this review addresses similarities regarding metabolic aspects of tumors and the placenta.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10084</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10084</link>
        <title><![CDATA[Exosomal circPTPRK promotes angiogenesis after radiofrequency ablation in hepatocellular carcinoma]]></title>
        <pubdate>2024-10-14T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yufeng Zhu</author><author>Qianru He</author><author>Ming Qi</author>
        <description><![CDATA[Radiofrequency ablation (RFA) is an effective treatment for hepatocellular carcinoma (HCC), but the recurrence rate remains high due to angiogenesis in residual cancer cells. We used thermal stimulation to simulate the post-RFA microenvironment. The expression profile of circRNAs between normal control HCC cell-derived exosomes and exosomes after heat stimulation were analyzed by RNA sequencing. Quantitative real-time PCR was applied to evaluate the expression of circPTPRK in exosomes and human umbilical vein endothelial cells (HUVECs). Then, the functions of heat-stimulated HCC cell-derived exosomes and exosomal circPTPRK on HUVECs were unveiled. Transcriptome sequencing was utilized to determine targeted genes of circPTPRK. Heat-stimulated HCC cell-derived exosomes augmented cell proliferation, migration, and angiogenesis of HUVECs. In total, 229 differentially expressed circRNAs were obtained, including 211 upregulated circRNAs and 18 downregulated circRNAs in heat-stimulated HCC cell-derived exosomes. The expression of circPTPRK was remarkably increased in heat-stimulated HCC cell-derived exosomes and the HUVECs incubated with them. Heat-stimulated HCC cell-derived exosomes with circPTPRK knockdown significantly inhibited cell proliferation, migration, and angiogenesis of HUVECs. Mechanistic studies indicated that PLA2G4E is a downstream target of circPTPRK, and PLA2G4E overexpression reversed the inhibitory effect of circPTPRK knockdown on HUVEC angiogenesis. Our results indicated that exosomal circPTPRK activated HUVEC angiogenesis by upregulating PLA2G4E expression.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10070</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10070</link>
        <title><![CDATA[The molecular mechanism responsible for HbSC retinopathy may depend on the action of the angiogenesis-related genes ROBO1 and SLC38A5]]></title>
        <pubdate>2024-07-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sueli Matilde da Silva Costa</author><author>Mirta Tomie Ito</author><author>Pedro Rodrigues Sousa da Cruz</author><author>Bruno Batista De Souza</author><author>Vinicius Mandolesi Rios</author><author>Victor de Haidar e Bertozzo</author><author>Ana Carolina Lima Camargo</author><author>Marina Gonçalves Monteiro Viturino</author><author>Carolina Lanaro</author><author>Dulcinéia Martins de Albuquerque</author><author>Amanda Morato do Canto</author><author>Sara Teresinha Olalla Saad</author><author>Stephanie Ospina-Prieto</author><author>Margareth Castro Ozelo</author><author>Fernando Ferreira Costa</author><author>Mônica Barbosa de Melo</author>
        <description><![CDATA[HbSC disease, a less severe form of sickle cell disease, affects the retina more frequently and patients have higher rates of proliferative retinopathy that can progress to vision loss. This study aimed to identify differences in the expression of endothelial cell-derived molecules associated with the pathophysiology of proliferative sickle cell retinopathy (PSCR). RNAseq was used to compare the gene expression profile of circulating endothelial colony-forming cells from patients with SC hemoglobinopathy and proliferative retinopathy (n = 5), versus SC patients without retinopathy (n = 3). Real-time polymerase chain reaction (qRT-PCR) was used to validate the RNAseq results. A total of 134 differentially expressed genes (DEGs) were found. DEGs were mainly associated with vasodilatation, type I interferon signaling, innate immunity and angiogenesis. Among the DEGs identified, we highlight the most up-regulated genes ROBO1 (log2FoldChange = 4.32, FDR = 1.35E-11) and SLC38A5 (log2FoldChange = 3.36 FDR = 1.59E-07). ROBO1, an axon-guided receptor, promotes endothelial cell migration and contributes to the development of retinal angiogenesis and pathological ocular neovascularization. Endothelial SLC38A5, an amino acid (AA) transporter, regulates developmental and pathological retinal angiogenesis by controlling the uptake of AA nutrient, which may serve as metabolic fuel for the proliferation of endothelial cells (ECs) and consequent promotion of angiogenesis. Our data provide an important step towards elucidating the molecular pathophysiology of PSCR that may explain the differences in ocular manifestations between individuals with hemoglobinopathies and afford insights for new alternative strategies to inhibit pathological angiogenesis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10275</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10275</link>
        <title><![CDATA[Retraction: MicroRNA-34a alleviates steroid-induced avascular necrosis of femoral head by targeting Tgif2 through OPG/RANK/RANKL signaling pathway]]></title>
        <pubdate>2024-06-25T00:00:00Z</pubdate>
        <category>Retraction</category>
        <author>EBM Editorial Office </author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10243</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10243</link>
        <title><![CDATA[Retraction: TRIM29 promotes the progression of colorectal cancer by suppressing EZH2 degradation]]></title>
        <pubdate>2024-06-10T00:00:00Z</pubdate>
        <category>Retraction</category>
        <author>EBM Editorial Office </author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10122</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10122</link>
        <title><![CDATA[TLR3 signaling-induced interferon-stimulated gene 56 plays a role in the pathogenesis of rheumatoid arthritis]]></title>
        <pubdate>2024-05-31T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hikaru Kristi Ishibashi</author><author>Yuzuru Nakamura</author><author>Tatsuro Saruga</author><author>Tadaatsu Imaizumi</author><author>Akira Kurose</author><author>Shogo Kawaguchi</author><author>Kazuhiko Seya</author><author>Eiji Sasaki</author><author>Yasuyuki Ishibashi</author>
        <description><![CDATA[Rheumatoid fibroblast-like synoviocytes (RFLS) have an important role in the inflammatory pathogenesis of rheumatoid arthritis (RA). Toll-like receptor 3 (TLR3) is upregulated in RFLS; its activation leads to the production of interferon-β (IFN-β), a type I IFN. IFN-stimulated gene 56 (ISG56) is induced by IFN and is involved in innate immune responses; however, its role in RA remains unknown. Therefore, the purpose of this study was to investigate the role of TLR3-induced ISG56 in human RFLS. RFLS were treated with polyinosinic-polycytidylic acid (poly I:C), which served as a TLR3 ligand. ISG56, melanoma differentiation-associated gene 5 (MDA5), and C-X-C motif chemokine ligand 10 (CXCL10) expression were measured using quantitative reverse transcription-polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay. Using immunohistochemistry, we found that ISG56 was expressed in synovial tissues of patients with RA and osteoarthritis. Under poly I:C treatment, ISG56 was upregulated in RFLS. In addition, we found that the type I IFN-neutralizing antibody mixture suppressed ISG56 expression. ISG56 knockdown decreased CXCL10 expression and MDA5 knockdown decreased ISG56 expression. In addition, we found that ISG56 was strongly expressed in the synovial cells of patients with RA. TLR3 signaling induced ISG56 expression in RFLS and type I IFN was involved in ISG56 expression. ISG56 was also found to be associated with CXCL10 expression, suggesting that ISG56 may be involved in TLR3/type I IFN/CXCL10 axis, and play a role in RA synovial inflammation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10111</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10111</link>
        <title><![CDATA[miR-539-5p targets BMP2 to regulate Treg activation in B-cell acute lymphoblastic leukemia through TGF-β/Smads/MAPK]]></title>
        <pubdate>2024-02-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Qingkai Dai</author><author>Rui Shi</author><author>Ge Zhang</author><author>Yuefang Wang</author><author>Lei Ye</author><author>Luyun Peng</author><author>Siqi Guo</author><author>Jiajing He</author><author>Hao Yang</author><author>Yongmei Jiang</author>
        <description><![CDATA[MicroRNAs (mRNAs) were believed to play an important role in cancers, and this study aimed to explore the mechanism of miRNA regulating Treg in B-cell acute lymphoblastic leukemia (B-ALL). Firstly, the differentially expressed miRNAs and target genes significantly associated with Tregs were screened out by high-throughput sequencing, and their enrichment pathways were analyzed. The binding relationship between miRNA and target genes was further verified, and the effects of miRNA on the proliferation and apoptosis of B-ALL Nalm-6 cells and Treg activation were analyzed. Results showed that differentially expressed miR-539-5p was significantly under-expressed, and its target gene BMP2 was significantly over-expressed in B-ALL, and significantly enriched in the TGF-β1 pathway. In addition, both miR-539-5p and BMP2 were significantly correlated with Treg activity in B-ALL. In vitro experiments further confirmed that miR-539-5p could directly target BMP2. The low expression of miR-539-5p in B-ALL significantly promoted BMP2 expression to promote the proliferation and inhibit apoptosis of Nalm-6 cells. Furthermore, the high expression of BMP2 in B-ALL could cooperate with TGF-β1 to promote the activation of human CD4+CD25-T cells to Treg, and significantly activate the TGF-β/Smads/MAPK pathway. In vivo experiments also confirmed that overexpression of miR-539-5p significantly inhibited BMP2 to suppress Treg activation and Smad1 and Smad2 phosphorylation, and finally inhibit the B-ALL process. In conclusion, miR-539-5p was significantly under-expressed in B-ALL and could target BMP2 to promote its expression, and the overexpressed BMP2 further promoted Treg activation in B-ALL by regulating TGF-β/Smads/MAPK pathway.]]></description>
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