In Vitro Cellular & Developmental Biology. Animal最新文献_第2页

Serotype-specific effects of adenovirus 5 and 52 E4ORF1 proteins on endothelial cell-mediated regulation of hematopoietic stem cell expansion and lineage differentiation. 腺病毒5和52 E4ORF1蛋白在内皮细胞介导的造血干细胞扩增和谱系分化中的血清型特异性作用

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-06-04 DOI: 10.1007/s11626-026-01192-w

Hanluo Li, Qifa Jin, Yuqing Peng, Yuansheng Wang, Xiaoke Shang, Peipei Guo

{"title":"Serotype-specific effects of adenovirus 5 and 52 E4ORF1 proteins on endothelial cell-mediated regulation of hematopoietic stem cell expansion and lineage differentiation.","authors":"Hanluo Li, Qifa Jin, Yuqing Peng, Yuansheng Wang, Xiaoke Shang, Peipei Guo","doi":"10.1007/s11626-026-01192-w","DOIUrl":"10.1007/s11626-026-01192-w","url":null,"abstract":"Umbilical cord blood HSCs transplantation is limited by low cell numbers and engraftment efficiency. The bone marrow endothelial cell (EC) niche is vital for HSCs. Adenoviral E4ORF1 protein enables ECs (e.g., HUVECs) to support HSCs expansion, but functional differences between E4ORF1 from distinct serotypes (respiratory Ad5 vs. enteric Ad52) are unknown. This study compared Ad5- and Ad52-E4ORF1 effects on engineered HUVECs and their support of hematopoietic stem/progenitor cells (HSPCs). Transcriptome analysis confirmed relevant receptor/metabolism gene expression in HUVECs. Sequence alignment revealed no significant nucleotide/amino acid homology between Ad5- and Ad52-E4ORF1. Engineered HUVECs expressing Ad5- or Ad52-E4ORF1 were co-cultured with mouse HSPCs. Outcomes were assessed via in vitro expansion, flow cytometry phenotyping, and competitive transplantation into irradiated mice evaluating engraftment and multilineage reconstitution. In vitro, Ad5-E4ORF1 promoted greater total hematopoietic cell expansion, while Ad52-E4ORF1 better maintained stemness, yielding a significantly higher proportion of ST-HSCs. Competitive transplantation revealed Ad5-E4ORF1 co-cultured HSPCs achieved higher early engraftment and superior initial myeloid reconstitution. Conversely, Ad52-E4ORF1 supported HSPCs exhibited significantly enhanced and sustained late-phase T-cell production, though B-cell levels declined after 12 weeks. Ad5 and Ad52 E4ORF1 exert serotype-specific regulation on HUVECs, differentially impacting HSPC fate: Ad5-E4ORF1 favors expansion and early myeloid engraftment, while Ad52-E4ORF1 preserves ST-HSCs and enhances short-term T-lymphopoiesis. These differences correlate with high E4ORF1 sequence divergence and are crucial for optimizing HSCs transplantation strategies.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1041-1051"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148156038","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

The influence of specific groups of osteogenic supplements on the differentiation of MC3T3-E1 cells over time. 特定组的成骨补充剂对MC3T3-E1细胞随时间分化的影响

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-07-20 DOI: 10.1007/s11626-026-01194-8

Erik Betzold, Monika Bubel, Norbert Pütz, Matthias Hannig, Emmanouil Liodakis, Tim Pohlemann, Wolfgang Metzger

{"title":"The influence of specific groups of osteogenic supplements on the differentiation of MC3T3-E1 cells over time.","authors":"Erik Betzold, Monika Bubel, Norbert Pütz, Matthias Hannig, Emmanouil Liodakis, Tim Pohlemann, Wolfgang Metzger","doi":"10.1007/s11626-026-01194-8","DOIUrl":"10.1007/s11626-026-01194-8","url":null,"abstract":"The setup of experimental designs in basic bone research begins with selecting appropriate osteogenic supplements to induce differentiation. Many studies describe the use of the supplements ascorbic acid, dexamethasone, and β-glycerophosphate in varying combinations and concentrations. To clarify their individual and combined effects on MC3T3-E1 cells, we conducted a detailed study focusing on cell morphology, mineralization, and gene expression of key osteogenic markers at four time points. Cell morphology was analyzed using light and scanning electron microscopy. Mineralization was assessed via Alizarin Red staining for calcium and von Kossa staining for phosphate. Additionally, energy-dispersive X-ray analysis was used to detect calcium and phosphorus in the cell layer. Sirius Red staining was applied to characterize the fiber formation observed under electron microscopy. To evaluate the influence of the supplements on gene expression, real-time quantitative PCR was performed for the osteogenic markers alkaline phosphatase, bone sialoprotein, bone morphogenetic protein 2, collagen 1a2, osteocalcin, osterix, and runt-related transcription factor 2. Osteogenic differentiation of MC3T3-E1 cells could be induced by application of ascorbic acid and β-glycerophosphate leading to upregulation of osteogenic markers, changes in cellular morphology, and mineralizing activity. Nevertheless, this effect could be further increased by additional use of dexamethasone. While most osteogenic marker genes were already upregulated on day 7, we did not see the first signs of mineralization until day 14. We recommend using ascorbic acid, β-glycerophosphate, and dexamethasone in order to get an osteogenic phenotype of MC3T3-E1 on day 14 at the earliest.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1112-1130"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520267","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}

引用次数: 0

Liposome-iRGD loaded with astragaloside IV alleviates the functional damage of endothelial progenitor cells via the Hippo-YAP/TAZ signaling pathway. 载黄芪甲苷的脂质体- irgd通过希波- yap /TAZ信号通路减轻内皮祖细胞的功能损伤。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-07-24 DOI: 10.1007/s11626-026-01201-y

Churuo Zeng, Qinxia Li, Dongwei Guo, Wu Xiong, Xiaoling Zou, Wei Li, Jie Bin, Xiuping Wang, Zihao Zhang, Bingqian Xue, Ruowei Hu, Xi Zhang

{"title":"Liposome-iRGD loaded with astragaloside IV alleviates the functional damage of endothelial progenitor cells via the Hippo-YAP/TAZ signaling pathway.","authors":"Churuo Zeng, Qinxia Li, Dongwei Guo, Wu Xiong, Xiaoling Zou, Wei Li, Jie Bin, Xiuping Wang, Zihao Zhang, Bingqian Xue, Ruowei Hu, Xi Zhang","doi":"10.1007/s11626-026-01201-y","DOIUrl":"10.1007/s11626-026-01201-y","url":null,"abstract":"The characteristics of diabetic vascular complications are impaired angiogenesis, which leads to hindlimb ischemia. Although astragaloside IV (AS-IV) can promote angiogenesis, its poor targeting to endothelial progenitor cells (EPCs) limits its therapeutic effect. Here, we developed liposomes modified with iRGD to load AS-IV (Lp-iRGD@AS-IV) to enhance its delivery and explored its mechanism. Lp-iRGD@AS-IV and fluorescently labeled liposomes were prepared, and their phenotypic characteristics were detected. The study results showed that the uptake efficiency of Lp-iRGD@AS-IV by EPCs was higher than that of Lp@AS-IV. In a diabetic mouse hindlimb ischemia model induced by streptozotocin, Lp@AS-IV and Lp-iRGD@AS-IV improved cell damage, increased capillary density, and reduced reactive oxygen species accumulation. However, the therapeutic effect of Lp-iRGD@AS-IV was more significant than that of Lp@AS-IV. Lp-iRGD@AS-IV attenuated high glucose-induced inhibitory effect on cell viability, migration, and invasion capability of EPCs. Additionally, we analyzed the regulatory effects of the Hippo-YAP/TAZ signaling pathway in diabetic vascular complications. AS-IV increased the expression of vascular growth factors (VEGFa, VEGFb, VEGFc, FGF, and Ang-1), eNOS, and osteopontin, and enhanced glucose-lipid metabolism, via activating the upstream Hippo signaling pathway while inactivating the downstream YAP/TAZ activity. In conclusion, Lp-iRGD@AS-IV significantly enhanced the delivery of AS-IV to EPCs and improved hindlimb ischemia in diabetic mice. AS-IV can restore diabetes-associated impaired angiogenesis through the Hippo-YAP/TAZ pathway. Lp-iRGD@AS-IV may be a targeted therapy for diabetic vascular complications.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1075-1092"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148584281","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

RMI2 knockdown suppresses ovarian cancer cell growth by impairing DNA damage repair via the ATR/CHK1 signaling pathway. RMI2敲低通过ATR/CHK1信号通路损害DNA损伤修复来抑制卵巢癌细胞生长。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-07-10 DOI: 10.1007/s11626-026-01196-6

Kean Zhu, Zhao Li, Yingying Wei, Ying Lin

{"title":"RMI2 knockdown suppresses ovarian cancer cell growth by impairing DNA damage repair via the ATR/CHK1 signaling pathway.","authors":"Kean Zhu, Zhao Li, Yingying Wei, Ying Lin","doi":"10.1007/s11626-026-01196-6","DOIUrl":"10.1007/s11626-026-01196-6","url":null,"abstract":"RecQ-mediated genome instability protein 2 (RMI2), a component of the RecQ helicase complex, has been shown to be highly expressed in various cancers and is often associated with poorer patient survival. However, its specific role in ovarian cancer (OC) remains unclear. This study investigates whether RMI2 contributes to OC progression via the ATR/CHK1 pathway. Bioinformatics analysis and experimental validation revealed that RMI2 was highly expressed in OC tissues and cell lines compared with normal controls. Functional assays demonstrated that knockdown of RMI2 inhibited OC cell proliferation and colony formation, induced G2/M phase arrest, and promoted apoptosis. Furthermore, the knockdown of RMI2 led to increased DNA damage (manifested as the accumulation of γH2AX) and downregulated homologous recombination repair proteins (BRCA1, NBS1, RAD51). Under DNA damage stress induced by Olaparib, a Poly (ADP-ribose) Polymerase (PARP) inhibitor, RMI2 knockdown synergistically enhanced DNA damage and apoptosis. Mechanistically, RMI2 directly interacted with ATR, and its knockdown reduced ATR phosphorylation and the expression of its downstream effector CHK1. Additionally, overexpression of ATR partially rescued the inhibitory effects of RMI2 knockdown on OC cell growth and DNA damage. In conclusion, RMI2 may promote OC development by activating the ATR/CHK1 pathway to sustain genomic stability, highlighting its potential as a prognostic biomarker and therapeutic target in OC.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1052-1064"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420830","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

The miR-335-5p/DKK1/autophagy axis regulates TNF-α-mediated dysfunction of dental pulp stem cells. miR-335-5p/DKK1/自噬轴调控TNF-α-介导的牙髓干细胞功能障碍。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-07-24 DOI: 10.1007/s11626-026-01199-3

Guijuan Feng, Lan Huang, Xiaofeng Sun, Fanting Sun, Han Su, Haoting Shi, Ke Zheng, Shiyu Shi

{"title":"The miR-335-5p/DKK1/autophagy axis regulates TNF-α-mediated dysfunction of dental pulp stem cells.","authors":"Guijuan Feng, Lan Huang, Xiaofeng Sun, Fanting Sun, Han Su, Haoting Shi, Ke Zheng, Shiyu Shi","doi":"10.1007/s11626-026-01199-3","DOIUrl":"10.1007/s11626-026-01199-3","url":null,"abstract":"Dental pulp stem cells (DPSCs) play a critical role in maintaining dental pulp homeostasis and supporting dentin-pulp complex regeneration, while tumor necrosis factor-α (TNF-α)-mediated inflammation severely impairs their biological functions. This study explored the role of the miR-335-5p/DKK1/autophagy axis in TNF-α-induced DPSCs dysfunction. Human DPSCs were stimulated with 20 ng/mL TNF-α; miR-335-5p overexpression and DKK1 silencing were achieved via transfection. qRT-PCR, Western blot, SA-β-gal staining, immunofluorescence, transmission electron microscopy, ALP/ARS staining, and dual-luciferase assay were used to detect related indicators. Results showed TNF-α downregulated miR-335-5p, upregulated DKK1, inhibited autophagy, induced senescence, disrupted cytoskeleton, and suppressed osteogenesis; miR-335-5p directly targeted DKK1's 3'-UTR. Overexpressing miR-335-5p or silencing DKK1 restored DPSCs' autophagic flux, alleviated senescence, and rescued osteogenic potential. In conclusion, the miR-335-5p/DKK1/autophagy axis mediates TNF-α-induced DPSCs dysfunction, and targeting this axis may improve stem cell-based dental pulp and bone reconstruction under inflammation.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1065-1074"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578536","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

Distinct adhesion energy and extracellular matrix profiles of healthy and osteoarthritic human chondrocytes. 健康和患骨关节炎的人软骨细胞的不同粘附能量和细胞外基质谱。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-06-11 DOI: 10.1007/s11626-026-01193-9

Robert Stannert, Lindsey Attebery, Abraham Rodriguez

{"title":"Distinct adhesion energy and extracellular matrix profiles of healthy and osteoarthritic human chondrocytes.","authors":"Robert Stannert, Lindsey Attebery, Abraham Rodriguez","doi":"10.1007/s11626-026-01193-9","DOIUrl":"10.1007/s11626-026-01193-9","url":null,"abstract":"Osteoarthritis (OA) is a common degenerative joint disease characterized by the progressive degeneration of articular cartilage (AC), resulting in pain, stiffness, and reduced joint function. Despite its widespread prevalence, effective treatments for OA remain elusive, partly due to challenges in accurately modeling the disease. In the present study, adhesion energy, collagen (COL), and total glycosaminoglycans (GAG), the main extracellular matrix (ECM) components of AC, and their potential correlations were evaluated in human chondrocytes derived from both healthy and OA male donors. A model surface of silicon nitride was used to investigate adhesion energy using atomic force microscopy (AFM), while colorimetric assays were applied to quantify COL and GAG at five different time points during monoculture (days 0, 1, 7, 14, and 21). Our results indicate significant heterogeneity in adhesion energies at both donor and phenotype levels. Chondrocytes isolated from healthy donors consistently display higher adhesion energies, along with greater heterogeneity, compared to those derived from OA donors. These differences in adhesion energy and heterogeneity can be attributed to greater diversity and density of cellular surface molecules in cells from healthy donors. In contrast, total GAG and COL levels were significantly elevated in OA chondrocytes compared to those in healthy chondrocytes. Moreover, the study found a positive correlation between adhesion energy and GAG production in OA-derived chondrocytes, but no significant correlations with DNA or COL levels. No correlation was observed between adhesion energy and GAG, DNA, or COL levels in healthy cells. In conclusion, these findings highlight the importance of considering individual donor characteristics when developing OA disease models, therapeutics, or engineered tissues.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1104-1111"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148217584","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}

引用次数: 0

Apigenin in TMG inhibits colorectal tumorigenesis by targeting GSK3β/APC/β-catenin signaling pathway. TMG中的芹菜素通过靶向GSK3β/APC/β-catenin信号通路抑制结直肠癌的发生。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-08-03 DOI: 10.1007/s11626-026-01198-4

Mei Li, Wei Wang, Renjing Lin, Fan Hu, Chongsi Xu, Biao Xie

{"title":"Apigenin in TMG inhibits colorectal tumorigenesis by targeting GSK3β/APC/β-catenin signaling pathway.","authors":"Mei Li, Wei Wang, Renjing Lin, Fan Hu, Chongsi Xu, Biao Xie","doi":"10.1007/s11626-026-01198-4","DOIUrl":"10.1007/s11626-026-01198-4","url":null,"abstract":"Colorectal cancer (CRC) is a malignant tumor with a high global incidence. Tianma granule (TMG) is a traditional Chinese medicine compound. However, its pharmacodynamic material basis and mechanism of action against CRC remained unclear. This study systematically analyzed the anti-CRC mechanism of TMG by integrating metabolomics, network pharmacology, and experimental validation. HPLC-MS identified the main active components of TMG. Core targets and pathways were predicted by network pharmacology. The binding affinity between components and targets was evaluated by molecular docking. In vitro experiments utilized the HCT116 and HCT-8 cells model, where the effects of TMG and its key component Apigenin on cell activity. Apigenin was identified as a key flavonoid component in TMG by metabolomics. Network pharmacology analysis indicated that TMG intervened in CRC through multi-target actions, with the Wnt/β-catenin pathway being the core regulatory pathway. In vitro experiments demonstrated that both TMG and Apigenin inhibited HCT116 and HCT-8 cell proliferation, promoted apoptosis, and weakened invasion and migration capabilities. Apigenin promotes β-catenin degradation and suppresses its nuclear translocation by upregulating GSK3β and APC expression. The ablation or mutation of GSK3β or APC abolishes this effect, whereas β-catenin knockdown alone recapitulates the anti-cancer effects of TMG and Apigenin, demonstrating that their actions are strictly dependent on β-catenin. Apigenin, as the core active ingredient of TMG, was demonstrated to target GSK3β/APC to promote β-catenin degradation and inhibit the activation of the Wnt/β-catenin pathway, thereby exerting anti-CRC effects.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1182-1197"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669608","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

Correction: PRRX1 upregulates PD-L1 in human mesenchymal stem cells. 更正：PRRX1上调人间充质干细胞中的PD-L1。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 DOI: 10.1007/s11626-026-01202-x

Taro Osawa, Daisuke Yamada, Tomoka Takao, Lu Ming, Takeshi Takarada

引用次数: 0

Paclitaxel-induced cytoskeletal and focal adhesion reorganisation alters connexin43 and α-smooth muscle actin in cardiac cells. 紫杉醇诱导的细胞骨架和局灶黏附重组改变心肌细胞中的连接蛋白43和α-平滑肌肌动蛋白。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 Epub Date: 2026-07-30 DOI: 10.1007/s11626-026-01203-w

Neethu Mohan, Sruthi Radhakrishnan, Dhakshmi Sasankan, Renu Mohan

{"title":"Paclitaxel-induced cytoskeletal and focal adhesion reorganisation alters connexin43 and α-smooth muscle actin in cardiac cells.","authors":"Neethu Mohan, Sruthi Radhakrishnan, Dhakshmi Sasankan, Renu Mohan","doi":"10.1007/s11626-026-01203-w","DOIUrl":"10.1007/s11626-026-01203-w","url":null,"abstract":"Paclitaxel, a microtubule-stabilising anticancer drug, exhibits cardiotoxicity; however, the impact of microtubule stabilisation on cytoskeletal and focal adhesion proteins and their consequences on key proteins in cardiac cells remains inconclusive. A 10-100 nmol of paclitaxel treatment for 24 h stabilised microtubules in H9c2 cells and rat cardiac fibroblasts. In H9c2 cells, a significant increase in the mean fluorescence intensity of bundled microtubules and a decrease in microtubule spreading area were observed. Actin was reorganised into more parallelly aligned stress filaments, with vinculin at the actin filament ends significantly decreased, and appeared localised at the centre in all treated groups. In cardiac fibroblasts, the changes in mean fluorescent intensity of bundled microtubules and spreading area were evident only at higher paclitaxel concentrations. Actin stress fibres were disrupted to punctate actin, peripherally localised vinculin appeared filamentous or punctate, and dose-dependent changes were observed in actin and vinculin. The results indicate that the rearrangements in cytoskeletal and focal adhesion proteins were specific in each cell type. Further, proteins specific to H9c2 and cardiac fibroblasts were probed. Connexin 43 (Cx43) in H9c2 cells showed altered localisation with a significant decrease in mean intensity, number, and plaque size at the periphery or apposition membranes, indicating compromised cell-cell communications. Additionally, in cardiac fibroblasts, the cage-like network of vimentin and the prominent α-SMA stress fibres were disrupted into smaller aggregates. Disrupted α-SMA stress fibres increased with paclitaxel concentration. Collectively, these changes reduced cell migration in cardiac fibroblasts, which may affect the repair and remodelling process following cardiac injury.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"1155-1167"},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620050","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

Ginsenoside Rc exerts protective effects against cerebral ischemia‒reperfusion injury by boosting the Nrf2 pathway through targeted activation of Sirt1. 人参皂苷Rc通过靶向激活Sirt1促进Nrf2通路，对脑缺血再灌注损伤具有保护作用。

IF 2 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2026-09-01 DOI: 10.1007/s11626-026-01242-3

Fang Yang, Qiufang Lian, Xin Zhang, Feng Sun, Baogui Liu

{"title":"Ginsenoside Rc exerts protective effects against cerebral ischemia‒reperfusion injury by boosting the Nrf2 pathway through targeted activation of Sirt1.","authors":"Fang Yang, Qiufang Lian, Xin Zhang, Feng Sun, Baogui Liu","doi":"10.1007/s11626-026-01242-3","DOIUrl":"https://doi.org/10.1007/s11626-026-01242-3","url":null,"abstract":"Ginsenoside Rc (G-Rc), a major active ingredient of Panax ginseng, has protective effects against various pathological alterations associated with diseases. Nonetheless, the potential benefits of G-Rc in treating cerebral ischemia-reperfusion (CIR) injury remain inadequately explored. In the present study, we evaluated the potential effects of G-Rc on CIR injury via cellular and animal models and explored the underlying mechanisms. Oxygen-glucose deprivation and reoxygenation (OGD/R)-induced neurons treated with G-Rc exhibited a marked reduction in apoptosis, oxidative stress, and inflammation. Rats treated with G-Rc presented significant reductions in neurological deficits, cerebral infarction, and pathological alterations resulting from CIR injury. Moreover, neuronal death, oxidative stress damage, and the inflammatory response in the brains of rats with CIR injury were markedly ameliorated by G-Rc treatment. Molecular docking, molecular dynamics simulations, and relevant experiments validated Sirtuin 1 (Sirt1) as a target of G-Rc. G-Rc increased Sirt1 expression and augmented its enzymatic activity. Notably, G-Rc promoted the activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) by targeting Sirt1. G-Rc failed to induce Nrf2 activation in Sirt1-silenced neurons. Furthermore, the benefits of G-Rc in defending against OGD/R damage were strongly negated by pharmacologically suppressing Nrf2. These observations indicate that G-Rc offers considerable benefits in treating CIR injury in experimental models. These beneficial effects are achieved by enhancing Nrf2 activation via the targeting of Sirt1. This study emphasizes the potential utilization of G-Rc as a pharmaceutical candidate for treating CIR damage.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874148","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