In Vitro Cellular & Developmental Biology. Animal最新文献

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PstS1-loaded exosomes promote Mycobacterium tuberculosis infection via miR-122-mediated PI3K/AKT/mTOR activation and autophagy suppression. 负载psts1的外泌体通过mir -122介导的PI3K/AKT/mTOR激活和自噬抑制促进结核分枝杆菌感染。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-05-12 DOI: 10.1007/s11626-026-01189-5
JiPing Yang, Wei Qiu, MeiZhen Xu, JianSheng Chen, XiaoMei Liu, Xiaohui Feng
{"title":"PstS1-loaded exosomes promote Mycobacterium tuberculosis infection via miR-122-mediated PI3K/AKT/mTOR activation and autophagy suppression.","authors":"JiPing Yang, Wei Qiu, MeiZhen Xu, JianSheng Chen, XiaoMei Liu, Xiaohui Feng","doi":"10.1007/s11626-026-01189-5","DOIUrl":"10.1007/s11626-026-01189-5","url":null,"abstract":"<p><p>Tuberculosis (TB), caused by Mycobacterium tuberculosis (MTB), is a chronic respiratory infectious disease. With the continuous increase in new cases, TB has become the second leading infectious disease worldwide, posing a significant challenge to public health. Previous studies have shown that exosomes play a crucial role in MTB infection, and microRNA-122 (miR-122) is highly expressed in MTB-infected cells. Exosomes secreted under the induction of phosphate-specific transport system substrate-binding protein 1 (PstS1) were characterized using transmission electron microscopy (TEM) and Western blot. Given that miR-122 expression increases upon MTB infection, quantitative real-time polymerase chain reaction (RT-qPCR) was performed to measure miR-122 levels in exosome-treated cells. Western blot, immunofluorescence (IF), and colony-forming unit assays were conducted to assess MTB survival and the expression of phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) signaling pathway components and autophagy-related proteins after transfection with miR-122 inhibitor or mimic. A mouse model was established to further validate the role of exosomes in MTB infection. Enzyme-linked immunosorbent assay (ELISA) measured serum cytokine levels, and flow cytometry was used to sort immune cells. Hematoxylin and eosin (H&E) staining evaluated lung tissue pathology, while Western blot and IF analyzed signaling pathway and autophagy-related protein expression in lung tissues. A PI3K-specific inhibitor (LY294002) was used to confirm miR-122-mediated regulation of the pathway. TEM revealed the characteristic bilayer vesicle morphology of exosomes, and Western blot confirmed exosomal markers (cluster of differentiation 63, cluster of differentiation 9, tumor susceptibility gene 101) and PstS1 in PstS1-induced exosomes. RT-qPCR showed significantly elevated miR-122 levels in exosome-treated cells. Both in vitro and in vivo experiments demonstrated that miR-122 overexpression upregulated phosphorylated PI3K, AKT, and mTOR while downregulating autophagy-related proteins microtubule-associated protein 1A/1B-light chain 3-phosphatidylethanolamine conjugate and Beclin1. ELISA and flow cytometry analyses indicated that miR-122 promoted cytokine secretion and increased immune cell numbers. H&E staining confirmed that miR-122 upregulation exacerbated MTB-induced lung damage. Furthermore, LY294002 treatment confirmed that exosome-derived miR-122 activates the PI3K/AKT/mTOR pathway, suppresses autophagy, and facilitates MTB infection. PstS1-loaded exosomes upregulate miR-122, activating the PI3K/AKT/mTOR pathway to inhibit autophagy and promote MTB infection.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1143-1154"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Optimized conditions for the long-term growth of primary cell cultures derived from the southern green stink bug, Nezara viridula. 优化了南方绿臭虫原代细胞培养长期生长的条件。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-28 DOI: 10.1007/s11626-026-01243-2
Ke Wu, Bryony C Bonning
{"title":"Optimized conditions for the long-term growth of primary cell cultures derived from the southern green stink bug, Nezara viridula.","authors":"Ke Wu, Bryony C Bonning","doi":"10.1007/s11626-026-01243-2","DOIUrl":"https://doi.org/10.1007/s11626-026-01243-2","url":null,"abstract":"<p><p>The southern green stink bug, Nezara viridula L., is a highly polyphagous global pest that causes substantial economic losses on a broad range of crops. Current management strategies rely heavily on chemical insecticides, which can promote resistance development and negatively affect non-target beneficial organisms. The lack of a tractable in vitro cell culture system has limited the development of more targeted and sustainable control approaches for this species. In this study, we identified the optimal egg age for culture initiation and evaluated seven insect cell culture media or medium combinations, as well as several supplements, for their ability to support embryo-derived N. viridula primary cultures. A total of 200 primary cultures were initiated using ~ 6,000 dissected N. viridula eggs over 16 months. Of the media tested, GS medium, a combination of CLG#2 and Shields and Sang medium, supplemented with 9% heat-inactivated fetal bovine serum produced, on average, 40% more attached cell clusters than CLG#2, the next best medium, although this difference was not statistically significant. GS medium also supported the long-term survival and growth of N. viridula primary cells for more than 22 months. Several chemical additives previously reported to enhance insect cell proliferation did not improve N. viridula primary cell growth or survival. The optimized culture conditions described here provide a foundation for the establishment of continuous N. viridula cell lines and support future studies of host-pathogen interactions, insect physiology, and the development of novel pest management strategies.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148850477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Selective oncolytic activity of newcastle disease virus in equine sarcoid primary cells: a preclinical investigation. 新城疫病毒在马肉瘤原代细胞中的选择性溶瘤活性:临床前研究。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-26 DOI: 10.1007/s11626-026-01231-6
Daniele Fernanda Rosim, Arina Lázaro Rochetti, Pedro Luiz Porfírio Xavier, Talal Jamil Qazi, Eduarda Costa Câmara Pimentel, Amanda da Matta Santos, Ricardo Francisco Strefezzi, Cristina Oliveira Massoco, Renata Gebara Sampaio Dória, Heidge Fukumasu
{"title":"Selective oncolytic activity of newcastle disease virus in equine sarcoid primary cells: a preclinical investigation.","authors":"Daniele Fernanda Rosim, Arina Lázaro Rochetti, Pedro Luiz Porfírio Xavier, Talal Jamil Qazi, Eduarda Costa Câmara Pimentel, Amanda da Matta Santos, Ricardo Francisco Strefezzi, Cristina Oliveira Massoco, Renata Gebara Sampaio Dória, Heidge Fukumasu","doi":"10.1007/s11626-026-01231-6","DOIUrl":"https://doi.org/10.1007/s11626-026-01231-6","url":null,"abstract":"<p><p>Equine sarcoids are the most common skin tumors in horses and are characterized by local invasiveness, high recurrence rates, and inconsistent responses to current therapies. Oncolytic virotherapy represents a promising alternative approach that exploits defects in antiviral signaling pathways in tumor cells. Newcastle disease virus (NDV), an avian paramyxovirus that is nonpathogenic in mammals, has demonstrated tumor-selective activity in several species; however, its effects on equine sarcoids have not been previously investigated. In this study, primary cell cultures derived from equine sarcoid tumors were established to evaluate the selective cytotoxicity of NDV. Sarcoid tissues from six horses generated thirteen primary sarcoid cultures, while three primary equine fibroblast cultures served as non-tumor controls. Bovine papillomavirus (BPV) DNA was assessed by quantitative polymerase chain reaction. Cells were infected with a green fluorescent protein-expressing Newcastle disease virus (NDV-GFP), and cell viability was measured after seventy-two hours using a metabolic viability assay. Sarcoid cultures exhibited significantly greater sensitivity to viral infection than normal fibroblasts, with substantially lower half-maximal inhibitory concentrations. Viral infectivity, quantified by fluorescence intensity, correlated with increased susceptibility to virus-induced cytotoxicity. Notably, the oncolytic activity of Newcastle disease virus was observed in both bovine papillomavirus-positive and bovine papillomavirus-negative sarcoid cultures. These findings demonstrate that NDV-GFP induces stronger cytotoxic effects in equine sarcoid cells than in normal fibroblasts, supporting its potential as a novel therapeutic strategy in equine oncology.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148828017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A phlorotannin-rich seaweed extract activates AMPK/PGC-1α signaling and antioxidant defences in skeletal muscle cells. 富含褐藻素的海藻提取物可激活骨骼肌细胞中的AMPK/PGC-1α信号传导和抗氧化防御。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-19 DOI: 10.1007/s11626-026-01230-7
Anaïs Marandeau, Morgane Pengam, Solène Connan, Valérie Stiger-Pouvreau, Laurence Meslet-Cladière, Marie-Dominique Jezequel, Hélène Talarmin, Aline Amérand
{"title":"A phlorotannin-rich seaweed extract activates AMPK/PGC-1α signaling and antioxidant defences in skeletal muscle cells.","authors":"Anaïs Marandeau, Morgane Pengam, Solène Connan, Valérie Stiger-Pouvreau, Laurence Meslet-Cladière, Marie-Dominique Jezequel, Hélène Talarmin, Aline Amérand","doi":"10.1007/s11626-026-01230-7","DOIUrl":"https://doi.org/10.1007/s11626-026-01230-7","url":null,"abstract":"<p><p>Sedentary behaviour, ageing and chronic diseases represent major public health burdens associated with impaired skeletal muscle function and increased oxidative stress. Identifying bioactive compounds capable of mimicking the molecular adaptations induced by physical exercise therefore constitutes a relevant pharmacological strategy. Phlorotannins, polyphenolic compounds exclusively biosynthesised by brown macroalgae, are promising candidates owing to their antioxidant and metabolic properties. This study aimed to characterise a phlorotannin-enriched ethyl acetate extract from Halidrys siliquosa (HS extract) and assess its pharmacological properties in L6 rat myoblasts, a well-established skeletal muscle cell model. Chemical profiling by LC-MS and NMR identified carmalol- and fuhalol-type derivatives, two subclasses of phlorotannins, as predominant constituents, with strong radical scavenging activity in the DPPH assay. HS extract was non-cytotoxic at 1 and 10 µg/mL and did not alter basal ROS levels after 24-h treatment. At the molecular level, HS extract significantly increased the P-AMPK/AMPK ratio and PGC-1α transcript levels, two key mediators of exercise-induced metabolic adaptation, and enhanced glutathione peroxidase (GPx) enzymatic activity, indicating reinforced antioxidant defences. In a preventive setting, HS extract pretreatment markedly reduced H₂O₂-induced cell death and ROS overproduction. Collectively, these findings demonstrate that HS extract activates exercise-associated metabolic signaling pathways in rat skeletal muscle cells. These results suggest that HS extract may represent a promising source of bioactive compounds capable of modulating exercise-related molecular responses, warranting further investigation in differentiated muscle models and in vivo studies.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Establishment of a stable three-dimensional fibrotic cell culture model for reproducible baseline and experimental applications. 建立稳定的三维纤维化细胞培养模型,用于可重复的基线和实验应用。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-18 DOI: 10.1007/s11626-026-01233-4
Ayse Kocak-Sezgin, Elif Aydin, Meliha Koldemir-Gündüz, Güllü Kaymak
{"title":"Establishment of a stable three-dimensional fibrotic cell culture model for reproducible baseline and experimental applications.","authors":"Ayse Kocak-Sezgin, Elif Aydin, Meliha Koldemir-Gündüz, Güllü Kaymak","doi":"10.1007/s11626-026-01233-4","DOIUrl":"https://doi.org/10.1007/s11626-026-01233-4","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is characterized by progressive fibrosis and complex alterations in extracellular matrix dynamics; however, experimental modeling of fibrotic processes remains limited by poor control of baseline signaling and spontaneous phenotypic drift in vitro. Such variability complicates the interpretation of perturbation-driven responses and reduces the reliability of antifibrotic and toxicological studies. In this study, we developed and characterized a three-dimensional (3D) fibrotic in vitro platform designed to maintain a stable and controlled baseline state across distinct microenvironmental conditions. Primary dermal fibroblasts derived from a bleomycin-induced scleroderma model and human idiopathic pulmonary fibrosis fibroblasts (CCL-191) were embedded in collagen-fibrinogen-based bioinks (Matrigel and Cellink Skin) and fabricated using extrusion-based 3D bioprinting. Across all conditions, the 3D constructs preserved structural integrity, sustained cell viability, and maintained consistent myofibroblast features, including α-SMA expression, fibrotic gene transcription (TGF-β, IL-6, IL-1, collagen I), and canonical signaling activity (pSmad2/3). Importantly, no evidence of spontaneous overactivation or loss of fibrotic signaling was observed, indicating tight regulation of baseline pathway activity independent of bioink composition. These findings demonstrate that fibrotic signaling can be stabilized within a controlled 3D microenvironment, minimizing baseline drift and enabling reproducible molecular and biochemical readouts. By establishing a non-fluctuating fibrotic baseline, this platform provides a robust framework for future perturbation-based studies and enhances the interpretability of antifibrotic and toxicological screening approaches.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
E3 ubiquitin ligase SYVN1 promotes the malignant phenotype of A549 cells by upregulating GATA3 expression via NRP1. E3泛素连接酶SYVN1通过NRP1上调GATA3表达,促进A549细胞的恶性表型。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-18 DOI: 10.1007/s11626-026-01235-2
Shan Wang, Suli Lu, Zhen Wang, Guiping Xuan, Jianhua Tan
{"title":"E3 ubiquitin ligase SYVN1 promotes the malignant phenotype of A549 cells by upregulating GATA3 expression via NRP1.","authors":"Shan Wang, Suli Lu, Zhen Wang, Guiping Xuan, Jianhua Tan","doi":"10.1007/s11626-026-01235-2","DOIUrl":"https://doi.org/10.1007/s11626-026-01235-2","url":null,"abstract":"<p><p>Lung cancer remains one of the most lethal and prevalent malignancies worldwide. Although E3 ubiquitin ligase SYVN1 is frequently amplified in lung cancer, its functional role has not been fully elucidated. This study investigates the mechanistic involvement of SYVN1 in regulating the GATA3/NRP1 axis in A549 cells to provide novel insights into potential therapeutic strategies for lung cancer. Expression levels of SYVN1 were assessed in BEAS-2B, A549, NCI-H647, NCI-H2170, and NCI-H520, NCI-H69 cells. Functional assays were conducted after overexpressing or silencing SYVN1, GATA3, and/or NRP1 in A549 cells to examine their interdependent roles. The cells' proliferation, wound healing, invasion and migration abilities were evaluated through CCK-8, scratch assay and Transwell assays, respectively. The results indicated that SYVN1 was upregulated in A549 cells and significantly promoted cell proliferation, invasion, and migration. Mechanistically, SYVN1 interacted with GATA3 and regulated its ubiquitination. Knockdown of SYVN1 suppressed A549 cell proliferation, wound healing, invasion, and migration, and these effects could be reversed by overexpressing GATA3. Similarly, silencing GATA3 reduced these malignant characteristics, but these effects could be restored by overexpressing NRP1, and the knockdown of NRP1 could abrogate the tumor-promoting effects of SYVN1 overexpression. SYVN1 overexpression counteracted the inhibitory effects of NRP1 silencing on A549 tumor progression. Taken together, all these findings prove that SYVN1 could promote the malignant characteristics of A549 cells by modulating the GATA3/NRP1 axis. Thus, targeting SYVN1 could represent a promising therapeutic approach for treating lung cancer.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
FTO suppresses PRTN3 translation via m⁶A demethylation to block the CXCL9/CXCR3 axis and attenuate atherosclerosis. FTO通过m 26 A去甲基化抑制PRTN3翻译,阻断CXCL9/CXCR3轴,减轻动脉粥样硬化。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-11 DOI: 10.1007/s11626-026-01211-w
Gulizibaer Mamuti, Buajieerguli Nasier, Aliye Ainiwa, Qian Wang, Mayila Mutailipu, Miernisha Saimaiti, Aihemaiti Abudukadier, YuPing Feng
{"title":"FTO suppresses PRTN3 translation via m⁶A demethylation to block the CXCL9/CXCR3 axis and attenuate atherosclerosis.","authors":"Gulizibaer Mamuti, Buajieerguli Nasier, Aliye Ainiwa, Qian Wang, Mayila Mutailipu, Miernisha Saimaiti, Aihemaiti Abudukadier, YuPing Feng","doi":"10.1007/s11626-026-01211-w","DOIUrl":"https://doi.org/10.1007/s11626-026-01211-w","url":null,"abstract":"<p><p>Coronary artery disease (CAD) involves intricate immune-related pathways; however, the contribution of epigenetic mechanisms remains inadequately defined. The fat mass and obesity-associated protein (FTO), which functions as an N⁶-methyladenosine (m⁶A) demethylase, has been implicated in the progression of atherosclerotic conditions. This study sought to elucidate how FTO downregulates proteinase 3 (PRTN3) through m⁶A demethylation and inhibits neutrophil activation via the C-X-C motif chemokine ligand 9/C-X-C motif chemokine receptor 3 (CXCL9/CXCR3) signaling pathway in the context of CAD. RNA sequencing was carried out on peripheral blood mononuclear cells (PBMCs) obtained from CAD patients and healthy individuals to detect gene expression differences. Functional enrichment analyses, including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, were performed along with experimental validation in endothelial progenitor cells (EPCs). The regulatory relationship between FTO and PRTN3 was examined via luciferase reporter assays, RNA immunoprecipitation, and methylated RNA immunoprecipitation quantitative polymerase chain reaction. Neutrophil activation was evaluated by measuring CXCL9/CXCR3 expression, tracking cell migration, and assessing reactive oxygen species (ROS) generation in HL-60 cells. For in vivo validation, apolipoprotein E-deficient (ApoE⁻/⁻) mice were maintained on a high-fat diet and treated with the AAV9 vector carrying FTO via tail vein injection to evaluate effects on atherosclerotic development. Findings indicated that PRTN3 is significantly upregulated in CAD patients, which was corroborated in EPCs. FTO was shown to directly bind to PRTN3 and decrease its expression by reducing m⁶A methylation. Overexpression of FTO enhanced proliferation and migration of EPCs and reduced apoptosis, whereas FTO silencing produced opposing outcomes. Furthermore, PRTN3 was found to stimulate the CXCL9/CXCR3 axis, leading to increased neutrophil migration and ROS production. In vivo, FTO inhibits the activation of neutrophils by down-regulating the expression of PRTN3, reduces the inflammatory response, and protects the occurrence and development of atherosclerosis in mice. These results uncover a novel regulatory pathway involving FTO, m⁶A, PRTN3, and CXCL9/CXCR3 in CAD pathogenesis, highlighting FTO as a promising target for therapeutic intervention.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148712267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Enhancing adipogenic differentiation efficiency and gene expression in yak stromal vascular cells through 3D spheroid culture. 三维球体培养提高牦牛间质血管细胞成脂分化效率及基因表达。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-07 DOI: 10.1007/s11626-026-01206-7
Yannan Ma, Lei Zheng, Pengjia He, Chanchan Pan, Bo Wang, Shuzhen Song, Mingjie Hou, Wen Chen, Xiaoyan Ma, Zhaomin Lei
{"title":"Enhancing adipogenic differentiation efficiency and gene expression in yak stromal vascular cells through 3D spheroid culture.","authors":"Yannan Ma, Lei Zheng, Pengjia He, Chanchan Pan, Bo Wang, Shuzhen Song, Mingjie Hou, Wen Chen, Xiaoyan Ma, Zhaomin Lei","doi":"10.1007/s11626-026-01206-7","DOIUrl":"https://doi.org/10.1007/s11626-026-01206-7","url":null,"abstract":"<p><p>Intramuscular fat deposition is a key determinant of meat quality in livestock species; however, yak (Bos grunniens) stromal vascular cells (SVCs) exhibit relatively low adipogenic differentiation efficiency under conventional in vitro conditions. In this study, we established a three-dimensional (3D) spheroid culture system to improve adipogenic differentiation of yak SVCs and compared it with traditional two-dimensional (2D) monolayer culture. Yak SVCs were isolated from longissimus dorsi muscle and characterized prior to differentiation. Cells were subjected to adipogenic induction under both 2D and 3D conditions. Adipogenic differentiation was evaluated by morphological observation, Oil Red O staining and quantification, and quantitative real-time PCR (RT-qPCR) analysis of adipogenic marker genes. Additionally, Western blot analysis of key adipogenic proteins was performed specifically on yak SVCs. To validate the induction system, murine C3H10T1/2 cells were included as a parallel control group and evaluated using the aforementioned non-protein assays. The results showed that 3D culture significantly enhanced lipid accumulation and increased the expression of adipogenic marker genes compared with 2D culture in yak SVCs. Consistently, protein levels of PPAR γ were significantly elevated in the 3D group of yak SVCs, while FABP4 showed an upward trend. Furthermore, the C3H10T1/2 control group exhibited successful adipogenic differentiation with similarly enhanced lipid accumulation and gene expression under 3D conditions, confirming the reliability of our system. In conclusion, 3D spheroid culture improves adipogenic differentiation of yak SVCs and provides a useful in vitro model for studying adipose development in yak. This system may facilitate future studies on the regulation of intramuscular fat deposition in livestock species.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Quercetin, an ingredient of Jiedu Xiaozheng Yin, alleviates hepatocellular carcinoma progression by regulating CYP1A2/PTEN/PI3K/Akt axis. 解毒消正饮成分槲皮素通过调节CYP1A2/PTEN/PI3K/Akt轴调控肝癌进展。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-07 DOI: 10.1007/s11626-026-01212-9
Zhenhua Zhou, Zhenliang Xiao, Wu Wen, Yongkang Zhu
{"title":"Quercetin, an ingredient of Jiedu Xiaozheng Yin, alleviates hepatocellular carcinoma progression by regulating CYP1A2/PTEN/PI3K/Akt axis.","authors":"Zhenhua Zhou, Zhenliang Xiao, Wu Wen, Yongkang Zhu","doi":"10.1007/s11626-026-01212-9","DOIUrl":"https://doi.org/10.1007/s11626-026-01212-9","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) has a poor prognosis and limited treatment options. This study investigated the role and mechanism of Jiedu Xiaozheng Yin (JXY) in HCC using network pharmacology and in vivo/in vitro experiments. Active components of JXY and their potential therapeutic targets for HCC were identified via network pharmacology. A protein-protein interaction (PPI) network was constructed to identify core targets, and bioinformatics analysis confirmed their association with HCC. LC-MS/MS was used to isolate major components, which were then subjected to molecular docking with core targets. The effects of JXY on HCC were further validated through in vivo and in vitro experiments. Analysis of 171 core target genes was performed using PPI network screening and enrichment analysis. Quercetin was identified as the primary active component of JXY. Molecular docking confirmed its interaction with CYP1A2, which is overexpressed in HCC tissues. In vivo, JXY and quercetin significantly increased CYP1A2 and PTEN expression, while decreasing p-PI3K and p-Akt levels in HCC-bearing mice, thereby suppressing tumor growth and lung metastasis and promoting apoptosis. In vitro, both JXY and quercetin inhibited HCC cell proliferation and migration. CYP1A2 knockdown partially reversed, while its overexpression enhanced, these inhibitory effects. Quercetin, the main active component of JXY, upregulates CYP1A2 to promote PTEN expression, thereby inhibiting the PI3K/Akt signaling pathway and suppressing HCC progression.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148689188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cycloheximide, a specific inhibitor of eukaryotic protein synthesis, enhances infection of mosquito cells with Wolbachia. 环己亚胺是一种真核蛋白合成的特异性抑制剂,可增强蚊子细胞对沃尔巴克氏体的感染。
IF 2 4区 生物学
In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-08-06 DOI: 10.1007/s11626-026-01237-0
Ann M Fallon
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