Cytotechnology最新文献

{"title":"Adipose-derived mesenchymal stem cell-derived extracellular vesicles carry microRNA-214-3p to target GSTZ1 to curb ferroptosis in lung epithelial cells during sepsis.","authors":"Minggen Li, Jian Zhong, Xiaoying Li","doi":"10.1007/s10616-025-00793-9","DOIUrl":"10.1007/s10616-025-00793-9","url":null,"abstract":"<p><p>Ferroptosis pitches in sepsis-caused pulmonary diseases. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) pitches in ferroptosis. This study explored the mechanism of adipose-derived MSC-EVs (ADMSC-EVs) protecting against ferroptosis in lung epithelial cells during sepsis. ADMSC-EVs were extracted using ultracentrifugation, followed by ADMSC and EV characterization. MLE-12 cells received 24-h lipopolysaccharide (LPS) treatment to mimic sepsis-induced ferroptosis, and treatment with EVs, a ferroptosis inhibitor (Fer-1), or the glutathione S-transferase zeta 1 overexpression plasmid. Cell viability, and levels of glutathione (GSH), malondialdehyde (MDA), Fe²⁺, reactive oxygen species (ROS), lipid peroxidation (LPO), ferroptosis-related proteins (glutathione peroxidase 4 [GPX4], solute carrier family 7 member 11 [SLC7A11]), miR-214-3p, and GSTZ1 were assessed. A mouse model of sepsis-induced acute lung injury was established by cecal ligation and puncture, and mice were intratracheally injected with EVs, followed by evaluation of resting ventilation per minute, inspiratory resistance, dynamic lung compliance, lung wet-to-dry weight ratio, and lung tissue cell morphology. The miR-214-3p-GSTZ1 targeted relationship was analyzed by Starbase database and dual-luciferase assay. LPS treatment reduced MLE12 cell viability, decreased GSH, GPX4 and SLC7A11 levels, and elevated Fe²⁺ and MDA contents and ROS and LPO levels, while ADMSC-EVs reversed these effects. miR-214-3p was down-regulated in the in vitro model. ADMSC-EVs carried miR-214-3p to target GSTZ1. GSTZ1 overexpression partly counteracted ADMSC-EV-inhibited lung epithelial cell ferroptosis during sepsis. In vivo, ADMSC-EVs inhibited ferroptosis through miR-214-3p/GSTZ1, thus improving sepsis-induced lung injury in mice. ADMSC-EVs carrying miR-214-3p attenuated ferroptosis in lung epithelial cells by targeting GSTZ1, thereby ameliorating sepsis-induced lung injury.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"132"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12214176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Osthole attenuates airway inflammation in asthma by inhibiting the HMGB1-RAGE/TLR4-NF-κB signaling pathway.","authors":"Yanli Li, Yushan Zhou, Dailing Yan, Yunfeng Yang, Yi Xiao","doi":"10.1007/s10616-025-00812-9","DOIUrl":"https://doi.org/10.1007/s10616-025-00812-9","url":null,"abstract":"<p><p>Osthole (OS), an active component of traditional Chinese herbal medicine, has demonstrated a wide range of pharmacological effects and potential therapeutic value. This study aimed to explore the role of OS in alleviating airway inflammation in asthma. Ovalbumin (OVA) was used to induce a C57BL/6 J mouse asthma model. The mice were injected intraperitoneally with 15 mg/kg or 40 mg/kg OS. Serum IgE levels and lung inflammation were assessed; the inflammatory cell count in the BALF was determined using Wright‒Giemsa staining, and protein levels were measured by ELISA and Western blotting. Histopathological analysis of lung tissue was conducted using HE and PAS staining. OS effectively lowered IgE levels in mouse serum, reduced lung damage, and inhibited the infiltration of inflammatory cells and the proliferation of goblet cells in the lungs. Furthermore, OS reduced the number of inflammatory cells, eosinophils, and leukocytes in the BALF. With respect to cytokines, OS inhibited the levels of Th2 cytokines (IL-4, IL-5, and IL-13) and increased the levels of Th1 cytokines (IFN-γ and IL-2). Mechanistically, OS treatment inhibited activation of the HMGB1-RAGE/TLR4-NF-κB signaling pathway, thereby alleviating airway inflammation in asthma. These data suggest that OS may be a promising drug for alleviating airway inflammation in mice with bronchial asthma and provide potential molecular targets for the action of OS.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00812-9.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 4","pages":"147"},"PeriodicalIF":2.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12260148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Neurotrophomodulatory effect of TNF-α through NF-κB in rat cortical astrocytes.","authors":"Jaldeep Langhnoja, Lipi Buch, Prakash Pillai","doi":"10.1007/s10616-025-00743-5","DOIUrl":"10.1007/s10616-025-00743-5","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1007/s10616-024-00698-z.].</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"85"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11968621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional changes in β-lactoglobulin by conjugation with carboxymethyl cellulose.","authors":"Tatsuya Arai, Moeko Ono, Maiko Yoneda, Marika Sugamura, Tadashi Yoshida, Makoto Hattori","doi":"10.1007/s10616-025-00741-7","DOIUrl":"10.1007/s10616-025-00741-7","url":null,"abstract":"<p><p>β-lactoglobulin (BLG) and carboxymethylcellulose (CMC) were conjugated by using 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC). The BLG-CMC conjugates with different CMC content and molecular weights were prepared. Confirmation of conjugation was carried out by SDS-PAGE. CD spectra revealed that the secondary structure of BLG had maintained in the conjugates. Fluorescence studies indicated that the conformation around Trp had not changed in the conjugates. Retinol-binding activity indicated that the retinol-binding site of BLG changed by the conjugation. Equilibrium constants (K_AS) of anti-BLG monoclonal antibodies (mAbs) to BLG after conjugating with CMC by competitive ELISA indicated that the structure around ¹⁵Val-²⁹Ile and ⁸Lys-¹⁹Trp maintained their native structure, and the structure around ¹²⁵Thr-¹³⁵Lys changed by conjugation. By conjugation with CMC, emulsifying property of BLG in the acidic pH region and in the presence of NaCl were much improved. Because acidic pH and salt are frequently used in food, the BLG-CMC conjugates are considered to be useful for food applications. Immunogenicity of BLG in BALB/c mice was reduced by this conjugation. In particular, there was a marked improvement in both emulsifying property and reduced immunogenicity in the BLG-high molecular weight (HMW) CMC conjugate. Therefore, conjugation with CMC is an effective way to improve BLG's function, and CMC with a high molecular weight is preferable.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"79"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRELP regulated by GAS5/miR-3127-5p suppresses cisplatin resistance in oral squamous cell carcinoma.","authors":"Xiaoni Sun, Yang Liu, Luyi Chai, Jianbo Zhou","doi":"10.1007/s10616-025-00749-z","DOIUrl":"10.1007/s10616-025-00749-z","url":null,"abstract":"<p><p>Our previous study has identified that PRELP inhibits the progression of oral squamous cell carcinoma (OSCC). This study aimed to investigate the influence of PRELP on cisplatin (DDP) resistance in OSCC cells and to elucidate the underlying mechanism. The levels of PRELP, miR-3127-5p, and GAS5 in established DDP-resistant OSCC cell lines (CAL27/DDP and SCC-15/DDP) and parental cells were detected. Following transfection with PRELP overexpressing or silencing plasmids in DDP-resistant OSCC cells, DDP resistance was evaluated by the IC50 values, proliferation, apoptosis and ABCB1 expression. Bioinformatic analysis, dual-luciferase reporter assays, and rescue experiments were employed to explore the upstream miRNA and lncRNA of PRELP. Our results demonstrated that in both DDP-resistant cells, PRELP and GAS5 levels were decreased, while miR-3127-5p expression was increased compared with parental cells. PRELP overexpression reduced the IC50 of DDP and EdU-positive cell number, enhanced cell apoptosis, and suppressed ABCB1 expression in resistant cells. Conversely, PRELP silencing caused opposite effects. In the TCGA database, miR-3127-5p was highly expressed in HNSC, and patients with higher miR-3127-5p expression had shorter overall survival. A negative correlation was observed between miR-3127-5p and PRELP in HNSC. miR-3127-5p promoted DDP resistance in OSCC by targeting PRELP. GAS5 positively modulated PRELP expression by sponging miR-3127-5p. The alleviation of DDP resistance by GAS5 was attenuated by miR-3127-5p mimic and PRELP downregulation. In conclusion, PRELP, which is regulated by lncRNA GAS5/miR-3127-5p axis, suppresses DDP resistance in OSCC through decreasing ABCB1 expression. Targeting the GAS5/miR-3127-5p/PRELP axis may offer a promising strategy to overcome DDP resistance in OSCC.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00749-z.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"92"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12037964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLGA microspheres loaded with si-circETS1 as a therapeutic strategy to delay intervertebral disc degeneration.","authors":"Wenlei Nie, Rong Zhang, Pingfeng Xie, Min Yang, Jiaming Wu","doi":"10.1007/s10616-025-00768-w","DOIUrl":"10.1007/s10616-025-00768-w","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) is one of the leading causes of chronic low back pain and functional impairment, severely affecting the quality of life of patients. In recent years, circular RNA (circRNA), has gained attention for its critical role in cellular function regulation, especially its potential therapeutic effects in IDD. This study aims to elucidate the function of circETS1 in nucleus pulposus cells (NPCs) and develop a novel targeted therapeutic strategy. CircETS1, which was abnormally highly expressed in degenerated nucleus pulposus tissue, was identified through circRNA sequencing (circRNA-seq). The circular nature of circETS1 was confirmed by Sanger sequencing, RNase R digestion, and fluorescence in situ hybridization (FISH). Primary human NPCs were cultured, and the effects of regulating circETS1 on cell proliferation, apoptosis, and extracellular matrix metabolism were studied using reverse transcription quantitative polymerase chain reaction (RT-qPCR), Western blotting, flow cytometry, and immunofluorescence. Polylactic-<i>co</i>-glycolic acid (PLGA) microspheres (MS) loaded with si-circETS1 were prepared, and their therapeutic effects were evaluated. PLGA MS loaded with si-circETS1 effectively delivered si-circETS1 to nucleus pulposus tissue in both in vitro and in vivo experiments, significantly downregulating circETS1 expression, reducing inflammation, promoting extracellular matrix synthesis and repair, and ultimately delaying the progression of IDD. Consequently, PLGA MS loaded with si-circETS1 present an innovative and promising therapeutic strategy for IDD, demonstrating strong potential for clinical application.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"99"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12075713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TUBB4A relieves high glucose-induced cardiomyocyte hypertrophy and apoptosis through the regulation of ubiquitination and activation of the NOTCH signaling pathway.","authors":"Jiarui Zhang, Wenwei Bai, Xiaoyong Liu, Jingjing Huang, Zhenxia Feng, Hu Li","doi":"10.1007/s10616-025-00763-1","DOIUrl":"10.1007/s10616-025-00763-1","url":null,"abstract":"<p><p>Diabetic cardiomyopathy (DCM), a cardiac condition resulting from diabetes, is linked to significant morbidity and mortality rates. TUBB4A, a variant of tubulin, is highly expressed in heart-related illnesses, yet its function in DCM remains unclear. In this study, 60 mg/kg streptozotocin (STZ) was intraperitoneally injected into mice to induce a diabetic model, and 30 mM glucose was added to H9C2 cell medium for 48 h to induce a high glucose (HG) cell model. In this study, TUBB4A expression was decreased in STZ- or HG-induced animal or cellular DCM models. The overexpression of TUBB4A diminished the effects of STZ or HG, enhanced the growth of myocardial cells, and prevented their hypertrophy and apoptosis. Moreover, it inhibited the expression of ROS, Bax and C-Caspase-3; promoted the expression of Bcl-2 and also alleviated DCM in vivo. Mechanistically, TUBB4A interacts with MYH9 and promotes NOTCH1 expression through MYH9-mediated deubiquitination, thereby inhibiting HG-induced cardiomyocyte hypertrophy and apoptosis and alleviating the development of DCM. Our study suggests that increasing TUBB4A expression may be a potential strategy for the treatment of DCM.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"100"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA OIP5-AS1 promotes immune evasion in abdominal aortic aneurysm cells by recruiting MDSCs and inhibiting CD8 + T cells through STK24 upregulation.","authors":"Baoping Deng, Qili Liu, Qingqing Xiao, Minjie Yang, Xiaoyong Ge, Jiacong Weng, Hongmei Zheng, Weiping Deng","doi":"10.1007/s10616-025-00767-x","DOIUrl":"10.1007/s10616-025-00767-x","url":null,"abstract":"<p><p>This study aims to investigate the expression and immune function of long non-coding RNA OIP5-AS1 (OIP5-AS1) and Serine/Threonine Kinase 24 (STK24) in abdominal aortic aneurysm (AAA). An animal model of AAA was established, along with cell models for overexpression and underexpression of OIP5-AS1 and STK24. Histological staining, qPCR, enzyme-linked immunosorbent assay (ELISA), Cell Counting Kit-8 assay, western blotting, RNA immunoprecipitation (RIP) analysis, and flow cytometry were employed to assess their effects on inflammation, cell proliferation, and apoptosis. In this study, Immunohistochemistry and qPCR analyses revealed significant upregulation of OIP5-AS1 and STK24 in both AAA tissue samples as well as cell models. ELISA demonstrated that elevated levels of OIP5-AS1 and STK24 significantly enhanced the secretion of inflammatory cytokines (IL-1β, IL-6, TNF-α, and IFN-γ), promoted cell proliferation while inhibiting apoptosis. RIP analysis combined with RNA pull-down assays indicated that OIP5-AS1 binds to the promoter region of STK24 by recruiting Zinc Finger Protein 93 (ZNF93) transcription factor leading to increased transcriptional expression of STK24. Furthermore, it was found that the functional role played by OIP5-AS1/STK24 axis operates through the AKT pathway. Increased expression levels of either OIP5-SAI or STK24 facilitated myeloid- derived suppressor cells (MDSCs) migration while suppressing CD8 + T-cell activity. The findings from this study highlight the critical involvement of the OIP5-SAI/STK24 axis in AAA progression by promoting MDSCs migration while inhibiting CD8 + T-cell activity. These insights provide novel perspectives into understanding the molecular pathology underlying AAA development while identifying potential therapeutic targets.</p><p><strong>Supplementary information: </strong>The online version contains supplementary material available at 10.1007/s10616-025-00767-x.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"102"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of miR-29a-3p on renal interstitial fibrosis in diabetic kidney disease through FOXP1-mediated TGF-β1/Smad3 signaling pathway.","authors":"Juntai Zhang, Yan Qin, Jie Liu, Jie Ding, Mengying Xu, Li Yang, Yuanxin Zheng, Chin Kai Ling, Xi Zhang","doi":"10.1007/s10616-025-00779-7","DOIUrl":"10.1007/s10616-025-00779-7","url":null,"abstract":"<p><p>Renal interstitial fibrosis (RIF) is a major manifestation of diabetic kidney disease (DKD). This study aimed to elucidate the specific mechanism by which miR-29a-3p affects RIF in DKD through Forkhead box protein 1 (FOXP1)-mediated TGF-β1/Smad3 and to provide novel ideas and therapeutic targets for RIF. Cell and animal models were constructed, and CCK-8, flow cytometry, Western blotting, immunofluorescence, RT‒qPCR, Masson's trichrome staining, hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining, Sirius red staining, and immunohistochemistry were used to detect the related indicators of RIF in DKD. The interaction between miR-29a-3p and FOXP1 was confirmed using a dual-luciferase assay. These findings suggested that miR-29a-3p can act on renal interstitial fibrosis cells in DKD through the TGF-β1/Smad3 signaling pathway mediated by FOXP1. The overexpression of miR-29a-3p inhibited the expression of fibrin-associated proteins in renal tissue, contracted the mesangial matrix and decreased the accumulation of renal fibrils to ultimately alleviate RIF in DKD. This study is the first to propose the specific molecular mechanism of miR-29a-3p in renal interstitial cells in DKD, which provides novel targets and strategies for the clinical treatment of RIF-related DKD.</p><p><strong>Graphical abstract: </strong></p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"120"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12146237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomes derived from human umbilical cord blood mesenchymal stem cells protect against blue light-induced damage to retinal pigment epithelial cells by inhibiting FGF2 expression.","authors":"Guang-Ming Liu, Yan Liu","doi":"10.1007/s10616-025-00752-4","DOIUrl":"10.1007/s10616-025-00752-4","url":null,"abstract":"<p><p>Age-related macular degeneration (AMD) is a debilitating retinal disorder that may lead to progressive vision loss. One contributing factor to AMD pathogenesis is excessive blue light (BL) exposure. In this study, we investigated the therapeutic potential of exosomes derived from human umbilical cord blood mesenchymal stem cells (hUCMSC-EXs) in addressing BL-induced damage to ARPE-19 human retinal pigment epithelial (RPE) cells and explored the underlying mechanisms. Our findings revealed that BL exposure induced morphological alterations in ARPE-19 cells, accompanied by a time-dependent decline in cell viability, increased apoptosis, heightened oxidative stress, and inflammatory responses; however, hUCMSC-EXs dose-dependently mitigated BL-induced ARPE-19 cell damage. Interestingly, hUCMSC-EXs were found to suppress the upregulation of fibroblast growth factor 2 (FGF2) in BL-exposed ARPE-19 cells. Furthermore, FGF2 overexpression partially counteracted the inhibitory effects of hUCMSC-EXs on FGF2 expression and compromised the protective benefits of hUCMSC-EXs against BL-induced ARPE-19 cell damage. In conclusion, our results suggest that hUCMSC-EXs shield ARPE-19 cells from BL-induced harm by inhibiting FGF2 expression.</p>","PeriodicalId":10890,"journal":{"name":"Cytotechnology","volume":"77 3","pages":"88"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11982010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}