Preprints.orgPub Date : 2025-07-28DOI: 10.20944/preprints202507.2219.v1
M.A. Akinci, Filiz Yıldırım
{"title":"Mining-Induced Environmental Degradation and Displacement in the Context of Ecosocial Work: A Qualitative Study in Rural Areas","authors":"M.A. Akinci, Filiz Yıldırım","doi":"10.20944/preprints202507.2219.v1","DOIUrl":"https://doi.org/10.20944/preprints202507.2219.v1","url":null,"abstract":"The increasing demand to leverage mining for economic development poses severe risks to rural communities, especially in developing countries that are particularly vulnerable to its negative impacts. This study assesses the processes of mining-induced environmental degradation and displacement through the lens of two villages in Turkey and highlights the need for ecosocial work within these contexts. A qualitative case study design was adopted involving 18 individuals from both villages who were recruited through snowball sampling. The data, collected through in-depth interviews and participant observation, were analyzed using reflexive thematic analysis with the help of MAXQDA 24 software. The findings reveal that mining-related environmental degradation has adversely affected not only the ecosystems of the villages but also their social and economic structures. Moreover, the study identifies the need to address multiple and overlapping challenges experienced by villagers in relation to displacement, including both material and psychosocial difficulties. This research is the first attempt to provide an empirical foundation for ecosocial work interventions at the micro, mezzo, and macro levels in the context of rural, mining-affected communities in Turkey. As such, it offers valuable insights into how ecosocial work can engage with these levels of intervention in rural settings.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/170c29ec83169ebadc5c40716602b030/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147913815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Preprints.orgPub Date : 2025-07-22DOI: 10.20944/preprints202507.1850.v1
Maher M. Akl, Amr Ahmed
{"title":"Sulfur-Dependent Misfolding of Insulin as a Root Cause of Type 2 Diabetes: A Hypothesis Centered on Disulfide Bond Disruption at A6–A11, A7–B7, and A20–B19 in the Etiology of Insulin Resistance","authors":"Maher M. Akl, Amr Ahmed","doi":"10.20944/preprints202507.1850.v1","DOIUrl":"https://doi.org/10.20944/preprints202507.1850.v1","url":null,"abstract":"Type 2 diabetes mellitus (T2DM), projected to affect over 700 million people by 2045, necessitates a transformative etiological perspective. The Sulfur Insulin Deformation Hypothesis redefines T2DM as a sulfur metabolism disorder driven by insulin misfolding due to organic sulfur deficiency, originating from mitochondrial dysfunction in intestinal epithelial cells. Evidence demonstrates 30–73.8% reductions in cysteine and glutathione levels in T2DM patients (RBC glutathione: 1.78 ± 0.28 vs. 6.75 ± 0.47 µmol/g Hb, P < 0.001), driven by impaired transsulfuration pathways (cystathionine β-synthase, γ-lyase) and elevated oxidative stress (increased ROS, lipid peroxides). This redox imbalance inhibits protein disulfide isomerase (PDI), an endoplasmic reticulum enzyme critical for forming and isomerizing insulin’s disulfide bonds: A6–A11 (intra-A-chain, stabilizing α-helical core), A7–B7 (interchain, anchoring A- and B-chains), and A20–B19 (interchain, enabling receptor-binding conformation). Disruption of the A6–A11 hinge bond reduces insulin receptor affinity by 50–70% (r = -0.65, P < 0.05 for HOMA-IR), impairing PI3K-Akt signaling, GLUT2/GLUT4 translocation, and promoting gluconeogenesis, sustaining hyperglycemia. Cysteine deficiency activates NF-κB and JNK, elevating pro-inflammatory cytokines (TNF-α, IL-6), exacerbating insulin resistance via serine phosphorylation. Impaired mucin synthesis weakens the gut barrier, triggering TLR4-mediated endotoxemia and SOCS-driven inflammation. Interventions like N-acetylcysteine (NAC) and GlyNAC restore glutathione by 20–40% (P < 0.01), improve insulin sensitivity by 31% (P < 0.05), and enhance mitochondrial fatty acid oxidation. This model explains hyperinsulinemia alongside hyperglycemia, as misfolded insulin accumulates but fails to signal, while exogenous insulin restores function. This hypothesis proposes that insulin resistance and T2DM stem from insulin’s structural deformation due to disrupted disulfide bonds (A6–A11, A7–B7, A20–B19), mediated by impaired PDI function.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147886431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Preprints.orgPub Date : 2025-07-15DOI: 10.20944/preprints202507.1174.v1
H. Cao, Yao Tan, Xuemei Yuan, Jieping Song, Xi Wu, Wuxiang Guan, Quanfu Ma
{"title":"RBM24 Interacts with RPL3 and Regulates RPL3-eIF6 Interaction","authors":"H. Cao, Yao Tan, Xuemei Yuan, Jieping Song, Xi Wu, Wuxiang Guan, Quanfu Ma","doi":"10.20944/preprints202507.1174.v1","DOIUrl":"https://doi.org/10.20944/preprints202507.1174.v1","url":null,"abstract":"RBM24 is a critical post-translational regulator involved in the regulation of RNA stability, RNA splicing, cap-dependent and cap-independent translation. Previously, we demonstrated that RBM24 prevents 80S ribosome assembly. However, the detailed mechanisms remain unknown. Here, we identified RPL3, a ribosomal 60S subunit protein, as an interaction partner of RBM24. Pulldown assays with truncated RPL3 indicated that RBM24 binds both exposed and 28S-embeded region of RPL3. Ribosome affinity capture assay revealed that RBM24 enhances the interaction between RPL3 and eIF6, a translation initiation factor that prevents the association of the 40S and 60S ribosomal subunits. Further analysis revealed that RBM24 did not interact with eIF6. Moreover, RBM24 blocked the binding of eIF6 to 28S-embeded region of RPL3, but did not affect the binding of eIF6 to reported eIF6-contacting region of RPL3 in 60S subunit. Peptide competitor derived from eIF6-contacting region of RPL3 rescue RBM24 mediated translation inhibition in vitro. In conclusion, the present study demonstrated that RBM24 binds RPL3 and facilitates eIF6-RPL3 interaction, and elucidated a probably explanation to the inhibition of 80S ribosome assembly by RBM24 observed in previous studies.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/d08553adf62148b51cd15518ac4d23e0/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Preprints.orgPub Date : 2025-06-30DOI: 10.20944/preprints202506.2376.v1
Wenhong Zhi, H. Y. Yao, Donghe Chen, Zaili Li, Zhiguang Liu
{"title":"Edaravone Modulates Neuron Cuproptosis in Ischemic Stroke by Targeting NF-kB Signaling Pathway","authors":"Wenhong Zhi, H. Y. Yao, Donghe Chen, Zaili Li, Zhiguang Liu","doi":"10.20944/preprints202506.2376.v1","DOIUrl":"https://doi.org/10.20944/preprints202506.2376.v1","url":null,"abstract":"Background: Edaravone (EDA) is a neuroprotective and antioxidant drug that widely used for improving the symptoms of patients with ischemic stroke. Cuproptosis is a recently identified cell death form that caused by intracellular copper accumulation and regulated by FDX1. Increasing number of studies indicated that cuproptosis is involved in the progression of ischemic stroke. This study aimed to investigate the effects of EDA on cuproptosis during ischemic stroke. Methods: PC12 neurons were induced with OGD-R model to mimic the ischemic stroke in vitro. Mouse middle cerebral artery occlusion (MCAO) model was established and treated with EDA. Brain damage was measured by TCC staining. The in vitro cell viability was measured by cell counting kit-8 (CCK-8). Cuproptosis was measured by the intracellular levels of copper (Cu), pyruvic acid (PA) and α-ketoglutarate (α-KG), as well as the protein expression of FDX1 and lipoylation of DLST and DLAT. The NF-κB activation was measured by western blot assay. Results: Treatment with EDA improved the proliferation, suppressed the accumulation of Cu, elevated the levels of PA and α-KG, and downregulated the expression of FDX1, lipid-DLAT, and lipid-DLST, indicating the alleviated cuproptosis. Besides, EDA treatment suppressed the activation of NF-κB signaling pathway. Treatment with NF-κB activator reversed the effects of EDA on PC12 cell viability and cuproptosis. EDA treatment alleviated the infarct size and improved neurological function, which were reversed by the cuproptosis inducer elesclomol. Conclusion: EDA improved the brain function and recovered neuron viability through targeting the NF-κB signaling pathway in ischemic stroke.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/3f1c9a8983ab6b05aaf21bf63c110795/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147894140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Preprints.orgPub Date : 2025-06-30DOI: 10.20944/preprints202506.2315.v1
Xinjin Chen, Yaqi Huang, Yilin Wu, Lin Sheng, Hongchen Yan, Fanghui Chen, Fengwei Li, Hirpha Ketema, Yafei Cai
{"title":"CDK5RAP3 Deficiency Exacerbates Hepatic Inflammation via NLRP3 Inflammasome-Mediated Pyroptosis and Apoptotic Crosstalk","authors":"Xinjin Chen, Yaqi Huang, Yilin Wu, Lin Sheng, Hongchen Yan, Fanghui Chen, Fengwei Li, Hirpha Ketema, Yafei Cai","doi":"10.20944/preprints202506.2315.v1","DOIUrl":"https://doi.org/10.20944/preprints202506.2315.v1","url":null,"abstract":"Background/Objectives: CDK5RAP3 (CDK5 regulatory subunit associated protein 3), is a ubiquitously expressed protein in mammalian tissues, with emerging evidence indicating its critical involvement in hepatic inflammation. Although its precise mechanistic roles remain elusive. Methods: To delineate the pathological link between CDK5RAP3 deficiency and liver inflammation, we established liver-specific CDK5RAP3 knockout murine models and mouse embryonic fibroblasts (MEFs) from conditional knockout mice. Results: CDK5RAP3 deficiency induces hepatic injury and inflammatory responses in mice accompanied by NLRP3 inflammasome activation. This activation was mechanistically characterized by ASC oligomerization, Caspase-1 recruitment, and subsequent Gasdermin D (GSDMD) cleavage, which collectively triggered pyroptosis. Notably, CDK5RAP3-deficient MEFs exhibit compromised proliferative capacity and elevated apoptotic rates. Conclusions: Our findings demonstrate that CDK5RAP3 is indispensable for maintaining hepatic homeostasis. Its deficiency can induce liver damage and inflammatory cell death in mice. Therefore, CDK5RAP3 can be a potential therapeutic target for treating inflammatory liver pathologies.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/618bf32f0591c3e41eeae21e39be996a/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Factors Influencing Speciation Changes of Hexavalent Chromium and Distribution Correlations between Chromium and Other Elements in Chromium Slag Field Soil in North China","authors":"Shuai Zhu, Junru Chen, Yuntian Zhu, B.-P. Zhang, Jing Jia, Meng Pan, Zhipeng Yang, Yating Shen","doi":"10.20944/preprints202506.2257.v1","DOIUrl":"https://doi.org/10.20944/preprints202506.2257.v1","url":null,"abstract":"This study investigated the main factors involved in the speciation transformation of Cr(VI) and linkages between elements of soil from chromium slag field using chro-mium contaminated soil from North China. The study utilized macro condition ex-periments and in-situ micro-XRF fluorescence spectroscopy (μ-XRF) to com-prehen-sively elucidate the transformation mechanisms and elemental interrelationships. The findings indicated that under acidic conditions (pH< 7), there is a notable increase in reduction efficiency due to the conversion of Cr (VI) from CrO₄²⁻ to HCrO₄⁻/Cr₂O₇²⁻. The hierarchy of reducing agent efficiency follows the order of FeSO₄ > citric acid > fulvic acid. Temperature variations (-20℃ to 30℃) had minimal impact on Cr (VI) transformation, while reducing humidity indirectly reduced Cr(VI) levels by promoting the diffusion of the reducing agent and microbial metabolism, albeit to a lesser extent compared to chemical interventions. Variations in soil mechanical composition led to uneven distribution of Cr (VI). Larger particles (>0.2 mm) in BC-35 and BC-36-4 served as the main reservoirs of Cr (VI) by accumulating Fe and Mn oxides. In contrast, the Cr (VI) content in smaller particles (< 0.074 mm) of BC-36-3 increased as particle size decreased, contrary to the typical expectation of higher Cr (VI) content in finer particles. Micro-X-ray fluorescence (μ-XRF) and Pearson correlation analysis revealed a strong positive correlation between chromium (Cr) and calcium (Ca), iron (Fe), manganese (Mn), and nickel (Ni) (Pearson coefficient >0.7, p < 0.01). Conversely, chromium showed a weak correlation with magnesium (Mg), aluminum (Al), silicon (Si), and potassium (K). This suggests a dual mechanism involving oxidation-reduction coupling through coordinated adsorption and electron transfer on the surface of iron and manganese oxides. Through a combined "macro-micro" analytical approach, the study elucidated the complex factors in-fluencing the presence of hexavalent chromium (Cr (VI)) in soil at chromium slag dis-posal sites. These findings provide valuable insights to guide remediation strategies for chromium-contaminated soil.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/03207f9562834162a645352c7ac82ea8/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Increased Oxygen Treatment in the Fermentation Process Im-proves the Taste and Liquor Color Qualities of Black Tea","authors":"Xinfeng Jiang, Xin Jian Lei, Chen Li, Lixian Wang, Xiaoling Wang, Heyuan Jiang","doi":"10.20944/preprints202506.2117.v1","DOIUrl":"https://doi.org/10.20944/preprints202506.2117.v1","url":null,"abstract":"Black tea is a globally popular beverage, whose unique flavor and color are attributed to the fer-mentation process, during which polyphenols undergo enzymatic oxidation to form key pigments such as theaflavins (TFs), thearubigins (TRs), and theabrownins (TBs). This study investigated the effects of increased oxygen treatment during fermentation on the sensory and chemical qualities of Congou black tea. Fresh tea leaves (variety "Fuyun 6") were subjected to four oxygen treatments: 0 h (CK), 1 h (TY-1h), 2 h (TY-2h), and 3 h (TY-3h), with oxygen supplied at 8.0 L/min. Sensory evaluation revealed that oxygen-treated samples exhibited tighter and darker appearances, redder liquor, thicker taste, and sweeter aroma compared to CK. Chromatic analysis showed significant increases in redness (a*) and luminance (L*), alongside reduced yellowness (b*), indicating en-hanced liquor color. Chemical analyses demonstrated elevated levels of TFs, TRs, and TBs in oxygen treatments, with TRs showing the most pronounced increase. Non-targeted metabolomics identified 2318 non-volatile and 761 volatile metabolites, highlighting upregulated flavonoids, phenolic acids, and lipids, and downregulated catechins and tannins, which collectively contributed to improved taste and aroma. Optimal results were achieved with 2–3 h of oxygen treatment, balancing pigment formation and sensory quality. These findings can provide a scientific basis for optimizing oxygen conditions in black tea fermentation to improve product quality.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/7900a8127da2f54fe7773bdb66f774f5/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148394134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Preprints.orgPub Date : 2025-06-25DOI: 10.20944/preprints202506.1950.v1
Jianan Zhang, Meiyin Zou
{"title":"GCDH Mediates Histone Crotonylation to Regulate GLS1 Expression and Promote Reprogramming of Glutamine Metabolism in Breast Cancer","authors":"Jianan Zhang, Meiyin Zou","doi":"10.20944/preprints202506.1950.v1","DOIUrl":"https://doi.org/10.20944/preprints202506.1950.v1","url":null,"abstract":"Background: Metabolic remodeling plays critical role in cancer development and targeting the glutamine metabolism is a promising strategy for cancer therapy. Histone crotonylation is a novel histone modification that has been confirmed to play roles in multiple physiological and pathological processes, making it a hot topic and frontier area of research. In this study, we aimed to investigate the potential effects and regulatory mechanisms of glutaryl-CoA dehydrogenase (GCDH), a reported crotonylation regulator, during breast cancer growth. Methods: Breast cancer cells were depleted of GCDH, then in vitro cell growth was detected by cell counting kit-8 (CCK-8) and EdU assay, and in vivo cell growth was measured by a xenograft tumor model. The intracellular glutamine, glutamate acid, ATP and α-Ketoglutaric acid (α-KG) levels were detected to analyze glutamine metabolism. The protein expression and histone crotonylation level were detected using western blot assay. The enrichment of crotonylation at histone was detected using chromatin immunoprecipitation (ChIP) assay. The promoter activity of GLS1 was measured by luciferase reporter gene assay. Results: GCDH depletion suppressed the in vitro and in vivo growth of breast cancer cells. Knockdown of GCDH reduced glutamine metabolism and ATP production in breast cancer cells. The enrichment of H3K27 crotonylation on GLS1 promoter region was notably reduced under depletion of GCDH. The promoter activity of GLS1 was significantly suppressed by siGCDH. The overexpression of GLS1 in breast cancer cells could recover the protein expression of GLS1 that suppressed by siGCDH. Depletion of GLS1 repressed the proliferation and glutamine metabolism of breast cancer cells, whereas overexpression of GCDH abolished these effects. Conclusion: GCDH modulates the histone crotonylation and expression of GLS1 to mediate the growth and glutamine metabolism of breast cancer cells.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/4ecc40217576abd99c698821d035bf91/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Preprints.orgPub Date : 2025-06-25DOI: 10.20944/preprints202506.1984.v1
James Henderson, Logan Blair
{"title":"Developing a Dataset and Benchmark for Poetry Generation in Low-Resource Languages","authors":"James Henderson, Logan Blair","doi":"10.20944/preprints202506.1984.v1","DOIUrl":"https://doi.org/10.20944/preprints202506.1984.v1","url":null,"abstract":"This study presents the development of a comprehensive dataset and benchmark for poetry generation in low-resource languages, addressing a critical gap in the field of natural language processing (NLP) and creative AI. As transformer-based models have demonstrated remarkable capabilities in generating text, their application to low-resource languages remains underexplored. This research aims to curate a diverse corpus of poetic texts across various forms and themes, encompassing cultural nuances and linguistic features unique to these languages. We outline the methodologies employed in dataset collection, including the selection of representative poetic forms and the involvement of native speakers to ensure authenticity and richness. Additionally, we establish a set of evaluation metrics tailored to assess the quality of generated poetry, focusing on thematic coherence, stylistic diversity, and adherence to poetic structures. Preliminary experiments with transformer architectures reveal both the potential and challenges of generating poetry in low-resource contexts, highlighting the importance of dataset quality in influencing model performance. The findings underscore the necessity for further research in this domain, advocating for the development of inclusive and representative datasets that can enhance the creative capabilities of AI in diverse linguistic landscapes. This work not only contributes to the advancement of NLP but also fosters cultural preservation and appreciation through the lens of generative poetry.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/b299cf07b982cc00624d6ca4e236e9a5/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147916614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Preprints.orgPub Date : 2025-06-24DOI: 10.20944/preprints202506.1887.v1
A-Qiong Chen, A-Xiao Pan, Dan-Qiong Zhang, Jiayuan Chen, Weili Liu, Juan Liu
{"title":"The Impact and Mechanisms of LncRNA TCONS_00483150 on the Function of Self-Reactive B Cells in Systemic Lupus Erythematosus","authors":"A-Qiong Chen, A-Xiao Pan, Dan-Qiong Zhang, Jiayuan Chen, Weili Liu, Juan Liu","doi":"10.20944/preprints202506.1887.v1","DOIUrl":"https://doi.org/10.20944/preprints202506.1887.v1","url":null,"abstract":"Background: Excessive proliferation and activation of B cells, resulting in the production of various autoantibodies, is a crucial link and significant feature of the pathogenesis of systemic lupus erythematosus (SLE). Accumulating evidence indicated that long non-coding RNAs (lncRNAs) play a significant role in SLE. TCONS_00483150 is reported as a novel diagnostic biomarker that recently reported as a potential for SLE. However, the detailed functions and mechanisms are unclear. This study aimed to investigate the effects of TCONS_00483150 on B cell function and SLE progression. Methods: B cells were administrated with TCONS_00483150 overexpression and JAK activator. The activation of B cells was measured by flow cytometry. The production of IgG and IgM antibodies was measured by ELISA assay. The protein expression was assessed by western blot. Cell viability, cell cycle, and apoptosis were measured by cell counting kit-8 (CCK-8) and flow cytometry. Results: Overexpression of TCONS_00483150 led to deceased portion of CD19+CD138+ B cells and suppressed the expression of BAFF and APRIL. The production of IgG and IgM was significantly suppressed by TCONS_00483150 overexpression. TCONS_00483150 suppressed the viability and cell portion in S phase, as well as promoted the apoptosis of B cells. Overexpression of TCONS_00483150 suppressed the phosphorylation of the JAK and STAT3 protein. Treatment with STAT3 activator notably increased the viability of B cells and suppressed cell apoptosis, whereas overexpression of TCONS_00483150 repressed these effects. Conclusion: TCONS_00483150 overexpression could suppress the proliferation and activation of B cells, potentially via suppressing the activation of JAK/STAT3.","PeriodicalId":521283,"journal":{"name":"Preprints.org","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.preprints.org/frontend/manuscript/9e917b8f695fa9f84aee93df605df398/download_pub","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147915500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}