In Vitro Cellular & Developmental Biology. Animal最新文献_第4页

Enhancement of 5-fluorouracil efficacy in colorectal cancer cells through thymidylate synthase inhibition by sodium propionate. 丙酸钠抑制胸苷酸合成酶增强5-氟尿嘧啶在结直肠癌细胞中的作用。

IF 1.7 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-08-01 Epub Date: 2025-06-06 DOI: 10.1007/s11626-025-01058-7

Nayeon Kim, Yeoreum Lee, Taerim Kim, Jiyun Kim, Changwon Yang

{"title":"Enhancement of 5-fluorouracil efficacy in colorectal cancer cells through thymidylate synthase inhibition by sodium propionate.","authors":"Nayeon Kim, Yeoreum Lee, Taerim Kim, Jiyun Kim, Changwon Yang","doi":"10.1007/s11626-025-01058-7","DOIUrl":"10.1007/s11626-025-01058-7","url":null,"abstract":"5-Fluorouracil (5-FU) is a cornerstone chemotherapeutic agent commonly employed in colorectal cancer (CRC) treatment. Prolonged use of 5-FU can trigger drug resistance, primarily through the upregulation of thymidylate synthase (TS). Consequently, strategies targeting TS suppression could enhance 5-FU's therapeutic potential in resistant CRC cases. Short-chain fatty acids (SCFAs), derived from the fermentation of dietary fibers by gut microbiota, are implicated in various disease mechanisms, including cancer. Among SCFAs, sodium butyrate (NaB) is known to inhibit TS expression, reduce CRC cell viability, and promote apoptosis. However, the potential of sodium propionate (NaP), another SCFA, to exhibit similar effects remains under investigation. This study reveals that NaP, when combined with 5-FU, synergistically decreases CRC cell survival and enhances apoptosis. Furthermore, NaP counteracts the 5-FU-induced upregulation of TS, amplifying its inhibitory effects on drug-resistant CRC cells. These results suggest that NaP may serve as an effective adjunct in improving the therapeutic outcomes of 5-FU-based CRC treatments.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"838-847"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234000","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 Rb1 inhibits M1 macrophages-induced IGFBP2-mediated endothelial-mesenchymal transition to alleviate myocardial fibrosis in mice with chronic heart failure. 人参皂苷Rb1抑制M1巨噬细胞诱导的igfbp2介导的内皮-间质转化，减轻慢性心力衰竭小鼠心肌纤维化。

IF 1.7 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-08-01 Epub Date: 2025-07-02 DOI: 10.1007/s11626-025-01060-z

Yang Jiang, Qi Zhao, Ting Zhang, Songbo Lan, Xu Yan, Qi Chen

{"title":"Ginsenoside Rb1 inhibits M1 macrophages-induced IGFBP2-mediated endothelial-mesenchymal transition to alleviate myocardial fibrosis in mice with chronic heart failure.","authors":"Yang Jiang, Qi Zhao, Ting Zhang, Songbo Lan, Xu Yan, Qi Chen","doi":"10.1007/s11626-025-01060-z","DOIUrl":"10.1007/s11626-025-01060-z","url":null,"abstract":"Ginsenoside Rb1 ameliorates renal fibrosis, yet its effects on myocardial fibrosis (MF) remain unclear. In this study, we aimed to explore the role of ginsenoside Rb1 in chronic heart failure (CHF) and MF. To explore the correlation between endothelial-mesenchymal transition (EndMT) in endothelial cells and IGFBP2 expression in M1 macrophages, M1 macrophages were polarized and co-cultured with myocardial microvascular endothelial cells (MMVECs). IGFBP2 levels in the macrophages and levels of endothelial-specific markers and EndMT-related indexes in MMVECs were measured. Additionally, we treated the macrophages with ginsenoside Rb1. The CHF mice model was established using transverse aortic constriction (TAC) and then treated with ginsenoside Rb1. The effects of Rb1 on cardiac function, MF, and cardiomyocyte hypertrophy in CHF mice were assessed. We observed the successful differentiation of M1 macrophages using in vitro experiments. M1 macrophages co-cultured with MMVECs demonstrated the ability to enhance the EndMT effect in MMVECs, as evidenced by elevated levels of IGFBP2 in the macrophages and a reduction in the viability of MMVECs. This decrease in cell viability was mitigated following the knockdown of IGFBP2. Rb1 treatment significantly suppressed the expression of IGFBP2 and inhibited the occurrence of the EndMT in MMVECs. The in vivo experiment findings showed that ginsenoside Rb1 notably enhanced cardiac function, attenuated cardiomyocyte hypertrophy, and alleviated MF in CHF mice. Furthermore, ginsenoside Rb1 inhibited M1 macrophage polarization, reduced IGFBP2 expression in the myocardium, and suppressed the EndMT effect of MMVECs in mice. Ginsenoside Rb1 alleviated MF in mice with CHF by inhibiting M1 macrophage IGFBP2-mediated EndMT.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"848-861"},"PeriodicalIF":1.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553399","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

Nuclear protein 1 protects against neonatal hypoxic-ischemic encephalopathy by inhibiting neuronal ferroptosis by improving iron storage. 核蛋白1通过改善铁储存抑制神经元铁下垂来预防新生儿缺氧缺血性脑病。

IF 1.7 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-07-31 DOI: 10.1007/s11626-025-01088-1

Xining He, Simeng Wei, Yunsheng Fu, Hongxia Li, Jie Zhang, Li Liu

{"title":"Nuclear protein 1 protects against neonatal hypoxic-ischemic encephalopathy by inhibiting neuronal ferroptosis by improving iron storage.","authors":"Xining He, Simeng Wei, Yunsheng Fu, Hongxia Li, Jie Zhang, Li Liu","doi":"10.1007/s11626-025-01088-1","DOIUrl":"https://doi.org/10.1007/s11626-025-01088-1","url":null,"abstract":"Recent studies have highlighted the role of ferroptosis in neuronal damage during neonatal hypoxic-ischemic encephalopathy (HIE). Nuclear protein 1 (NUPR1), a newly identified crucial modulator of ferroptosis, remains unexplored in the context of HIE. This study aimed to investigate whether NUPR1 modulates ferroptosis and influences hypoxic-ischemic brain injury through specific molecular mechanisms. NUPR1-knockdown neurons presented increased sensitivity to Erastin-induced neuronal ferroptosis, whereas NUPR1 overexpression conferred resistance. Notably, silencing NUPR1 exacerbated OGD/R-induced neuronal damage and ferroptosis, as evidenced by increased lipid peroxidation, malondialdehyde (MDA) levels, and iron concentrations, as well as decreased glutathione (GSH) levels and altered expression of ferroptosis-related proteins (elevated PTGS2 and reduced GPX4). Conversely, NUPR1 overexpression alleviated OGD/R-induced neuronal damage and ferroptosis. HIE animal model experiments demonstrated that NUPR1 overexpression mitigated brain damage, reduced infarct size, and decreased brain edema, which were correlated with diminished ferroptosis markers. Furthermore, NUPR1 knockdown reduced ferritin heavy chain 1 (FTH1) expression, whereas NUPR1 overexpression increased FTH1 levels, indicating a regulatory role in iron metabolism. Silencing FTH1 reversed the inhibitory effect of NUPR1 on neuronal ferroptosis. Collectively, our findings indicate that NUPR1 protects against ferroptosis in HIE, making it a potential therapeutic target for reducing neuronal injury associated with this condition. NUPR1 suppresses neuronal ferroptosis by increasing FTH1 expression and improving iron storage, enhancing our understanding of the mechanisms involved in ferroptosis in neonatal HIE.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759992","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 method to evaluate the dynamics of highly chemotactic THP-1 cells during differentiation into monocyte-M1 macrophage-like cells. 建立一种评价高趋化THP-1细胞向单核- m1巨噬细胞样细胞分化过程动力学的方法。

IF 1.7 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-07-30 DOI: 10.1007/s11626-025-01074-7

Shuichiro Okamoto, Kei Miyano, Yasumitsu Nishimura, Nahoko Tomonobu, Rie Kinoshita, Masakiyo Sakaguchi, Einosuke Ikeshita, Ayasa Kamezaki, Aya Morihara, Futoshi Kuribayashi, Akira Yamauchi

{"title":"Establishment of a method to evaluate the dynamics of highly chemotactic THP-1 cells during differentiation into monocyte-M1 macrophage-like cells.","authors":"Shuichiro Okamoto, Kei Miyano, Yasumitsu Nishimura, Nahoko Tomonobu, Rie Kinoshita, Masakiyo Sakaguchi, Einosuke Ikeshita, Ayasa Kamezaki, Aya Morihara, Futoshi Kuribayashi, Akira Yamauchi","doi":"10.1007/s11626-025-01074-7","DOIUrl":"https://doi.org/10.1007/s11626-025-01074-7","url":null,"abstract":"Differentiation of the human monocytic leukemia cell line THP-1 is widely used to analyze the function of monocyte/macrophage-like cells in vitro. Although chemotaxis, a critical function of monocytes/macrophages enabling tissue accumulation, has been extensively studied, methods to evaluate sustained, long-distance chemotaxis remain underexplored. Therefore, we aimed to evaluate macrophage-like cells in vitro by differentiating THP-1 cells into monocyte/macrophage-like cells exhibiting sustained, strong chemotaxis over long distances (up to 260 μm). Using various reagents, we identified the combination of vitamin D, panobinostat, and granulocyte-macrophage-colony-stimulating factor as optimal for achieving high directionality and velocity in cell migration, as analyzed using the TAXIScan cell dynamics assay device. The differentiated cells matured into M1 macrophage-like cells and displayed reduced migratory capacity post-maturation, along with enhanced phagocytosis and reactive oxygen species production. Collectively, our differentiation and analysis methods provide a reliable platform for basic research into cellular maturation processes and drug development targeting the regulation of monocyte/macrophage dynamics.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753233","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

Exploring the effects of roscovitine, serum starvation, and contact inhibition at G₀/G₁ arrest in northern tiger cat dermal fibroblasts. 探讨罗斯维汀、血清饥饿和接触抑制对北虎猫表皮成纤维细胞G0/G1阻滞的影响。

IF 1.7 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-07-30 DOI: 10.1007/s11626-025-01073-8

João Vitor da Silva Viana, Brenna de Sousa Barbosa, Luanna Lorenna Vieira Rodrigues, Antonia Beatriz Mendonça Pereira, Patrícia Vasconcelos Alves, Herlon Victor Rodrigues Silva, Sarah Sant'Anna Maranhão, Carlos Roberto Koscky Paier, Maria Claudia Dos Santos Luciano, Cláudia Pessoa, Alexsandra Fernandes Pereira

{"title":"Exploring the effects of roscovitine, serum starvation, and contact inhibition at G0/G1 arrest in northern tiger cat dermal fibroblasts.","authors":"João Vitor da Silva Viana, Brenna de Sousa Barbosa, Luanna Lorenna Vieira Rodrigues, Antonia Beatriz Mendonça Pereira, Patrícia Vasconcelos Alves, Herlon Victor Rodrigues Silva, Sarah Sant'Anna Maranhão, Carlos Roberto Koscky Paier, Maria Claudia Dos Santos Luciano, Cláudia Pessoa, Alexsandra Fernandes Pereira","doi":"10.1007/s11626-025-01073-8","DOIUrl":"https://doi.org/10.1007/s11626-025-01073-8","url":null,"abstract":"Nuclear reprogramming studies are important tools in conserving wild felids, with efficacy depending on efficient G0/G1 cell cycle arrest methodologies. This study evaluated different culture conditions at G0/G1 arrest and the quality of northern tiger cat fibroblasts. Cells from four animals were assigned to groups: 7.5 and 15 µM roscovitine (RSV) for 24 and 48 h; serum starvation (SS) for 24, 48, 72, and 96 h; and contact inhibition (CI) for 24, 48, and 72 h. Cells with 50-60% confluence were used as control. The cell quality parameters included morphology, and viability and apoptotic levels were assessed through microscopic analysis, while cell cycle phases were evaluated using flow cytometry. RSV affected the cell viable percentage and morphology with the increase of concentration and exposure time. Moreover, RSV did not improve the cells at G0/G1. CI did not significantly affect cell quality or increase the proportion of cells in G0/G1 phase. Interestingly, SS for 24 h increased the cells at G0/G1. However, SS affected the apoptosis levels. The SS for 24 h is the most efficient method of G0/G1 arrest for northern tiger cat fibroblasts. However, adjustments are still necessary to optimize cell arrest for northern tiger cat fibroblasts.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753234","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

Role of PDGFRα-mediated signalling in anoikis resistance in glioblastoma: in vitro study. pdgfr α-介导的信号在胶质母细胞瘤耐药中的作用：体外研究。

IF 1.5 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-07-21 DOI: 10.1007/s11626-025-01075-6

Sneha Raut, Meet Makwana, Prakash Pillai

{"title":"Role of PDGFRα-mediated signalling in anoikis resistance in glioblastoma: in vitro study.","authors":"Sneha Raut, Meet Makwana, Prakash Pillai","doi":"10.1007/s11626-025-01075-6","DOIUrl":"https://doi.org/10.1007/s11626-025-01075-6","url":null,"abstract":"Anoikis resistance, the evasion of programmed cell death when cells detach from the extracellular matrix (ECM), is a critical feature of glioblastoma (GBM) malignancy, contributing to tumor survival, spread, and resistance to therapy. We focused on the role of growth factor receptors, particularly platelet-derived growth factor receptor-α (PDGFRα), and integrin expression patterns in mediating this resistance. We first cultured cells under non-adherent conditions using polyHEMA-treated plates to induce anoikis resistance. We performed assays like cell survival, migration, and sphere formation. To delineate the role of PDGFRα signalling in anoikis resistance, we further employed pharmacological inhibitors of key signalling molecules such as AG1295 (PDGFRα blocker), HS173 (PI3K inhibitor), U0126 (ERK inhibitor), and AG490 (JAK-STAT inhibitor) which led to a decrease in cell survival, proliferation, and migration. These findings highlight the critical role of PDGFRα and associated signalling pathways in mediating anoikis resistance in GBM, offering potential therapeutic targets for intervention.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682557","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

Adhesion extracellular matrix proteins improve in vitro cellular and functional properties of enriched caprine adult dermal fibroblast. 黏附细胞外基质蛋白改善富集的绵羊成皮成纤维细胞的体外细胞和功能特性。

IF 1.5 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-07-21 DOI: 10.1007/s11626-025-01065-8

Juhi Pathak, Shiva Pratap Singh, Manisha Pathak, Vishal Khandelwal, Yogesh Kumar Soni, Manoj Kumar Singh

引用次数: 0

Functions of ectodysplasin A2 receptor (EDA2R) in inducing capacitation of sperm in mice. 外胞浆异常蛋白A2受体（EDA2R）在小鼠精子获能中的作用。

IF 1.5 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-07-21 DOI: 10.1007/s11626-025-01084-5

Oluwakemi I Anjorin, Takahiro Yamanaka, Masayuki Shimada

{"title":"Functions of ectodysplasin A2 receptor (EDA2R) in inducing capacitation of sperm in mice.","authors":"Oluwakemi I Anjorin, Takahiro Yamanaka, Masayuki Shimada","doi":"10.1007/s11626-025-01084-5","DOIUrl":"https://doi.org/10.1007/s11626-025-01084-5","url":null,"abstract":"Sperm capacitation, a prerequisite for fertilization, is regulated not only by intrinsic signaling but also by paracrine factors within the female tract. Analysis of previously published RNA-seq datasets identified the ectodysplasin-A2 receptor (EDA2R), an X-linked member of the TNF-receptor superfamily, as a candidate regulator of this process. This study was conducted to test the hypothesis that the EDA-A2/EDA2R axis is a regulator that directly regulates sperm capacitation during fertilization process. Western blotting and immunofluorescence showed that EDA2R was localized in late spermatogenic cells and in the midpiece of epididymal sperm. Incubation of mouse sperm in HTF medium containing the corresponding ligand EDA-A2 (0-1 µg/mL) resulted in a dose-dependent improvement in the amplitude of lateral head displacement and curvilinear velocities. Ligand exposure promoted the appearance of capacitation hallmarks: tyrosine phosphorylation level was elevated within 30 min and the proportion of FITC-PNA positive, acrosome-reacted cells increased at 30 and 60 min (p < 0.05). The EDA-A2 treated sperm yielded a higher cleavage rate (78.5% vs. 48.3%) and a higher blastocyst formation rate (97.6% vs. 88.4%) after in vitro fertilization. qPCR in hormonally synchronized females revealed transient ovarian and prolonged oviductal Eda-a2 upregulation surrounding ovulation, suggesting that the ligand is present at the site of sperm-oocytes fertilization. These results clarify that EDA-A2/EDA2R is a rapid physiological driver of sperm capacitation. This provides a tractable cytokine axis for optimizing assisted reproduction.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682556","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

Bone marrow-derived mesenchymal stem cells and their extracellular vesicles suppress splenocyte activation and ameliorate experimental autoimmune encephalomyelitis. 骨髓源性间充质干细胞及其细胞外囊泡抑制脾细胞活化并改善实验性自身免疫性脑脊髓炎。

IF 1.5 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-07-16 DOI: 10.1007/s11626-025-01077-4

Sina Vakili, Majid Reza Farrokhi, Mahsa Motamed, Morteza Jafarinia, Shima Shapoori

{"title":"Bone marrow-derived mesenchymal stem cells and their extracellular vesicles suppress splenocyte activation and ameliorate experimental autoimmune encephalomyelitis.","authors":"Sina Vakili, Majid Reza Farrokhi, Mahsa Motamed, Morteza Jafarinia, Shima Shapoori","doi":"10.1007/s11626-025-01077-4","DOIUrl":"https://doi.org/10.1007/s11626-025-01077-4","url":null,"abstract":"Multiple sclerosis (MS) is a neurodegenerative and autoimmune disease affecting the central nervous system (CNS). Recently, mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) have been extensively studied as a potential treatment for MS. In this study, we examined the impact of therapy using EVs derived from murine bone marrow MSCs (BMSC-EVs) on the proliferation of splenocytes, frequency of regulatory T cells (Tregs), and cytokine secretion in mice induced with experimental autoimmune encephalomyelitis (EAE), comparing the effects with those of their parent cells. After inducing EAE in 30 mice, the animals were divided into three groups and treated with PBS, BMSCs, or BMSC-EVs. The mice were sacrificed on day 30 post-immunization, and their splenocytes were isolated for further analysis. The proliferation of splenocytes was assessed by measuring the fluorescent intensity of CFSE dye using a FACSCalibur flow cytometer, the frequency of Treg cells was determined by flow cytometry, and cytokine levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, IL-10, and transforming growth factor-beta (TGF-β) were measured using enzyme-linked immunosorbent assay (ELISA). The results showed that treatment with BMSC and BMSC-EV both significantly reduced splenocyte proliferation, increased Treg cell frequency, and shifted cytokine profiles toward reduced pro-inflammatory (TNF-α, IL-1β, IL-6) and increased anti-inflammatory (IL-10, TGF-β) cytokines compared to untreated EAE controls, with comparable efficacy between BMSCs and BMSC-EVs. These findings emphasize the capability of BMSC-EVs to serve as a cell-free therapy for immune response modulation in EAE.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649312","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

Grb2/Sos1 signaling regulates the number of reserve cells in C2C12 cell culture. Grb2/Sos1信号调控C2C12细胞培养中储备细胞的数量。

IF 1.5 4区生物学

In Vitro Cellular & Developmental Biology. Animal Pub Date : 2025-06-30 DOI: 10.1007/s11626-025-01071-w

Yosuke Nagata, Hiroto Iitsuka, Tomoharu Hagiwara

{"title":"Grb2/Sos1 signaling regulates the number of reserve cells in C2C12 cell culture.","authors":"Yosuke Nagata, Hiroto Iitsuka, Tomoharu Hagiwara","doi":"10.1007/s11626-025-01071-w","DOIUrl":"https://doi.org/10.1007/s11626-025-01071-w","url":null,"abstract":"Skeletal muscle regeneration depends on satellite cells that maintain tissue homeostasis through self-renewal and the production of myoblasts that differentiate into mature myofibers. Dysregulation of these processes can lead to muscle degeneration, highlighting the need to elucidate their molecular mechanisms. In this study, we investigated the role of the Grb2/Sos1 signaling pathway in regulating satellite cell self-renewal and differentiation using C2C12 cells. Knockdown of either Grb2 or Sos1 significantly reduced the formation of Bcl-2-positive reserve cells and increased the proportion of differentiated myotubes. Conversely, forced expression of Grb2 increased the number of reserve cells, whereas the Grb2 P49L mutant, which disrupts its interaction with Sos1, decreased reserve cell formation and resulted in thinner myotubes. Although forced expression of Sos1 alone did not significantly increase reserve cell numbers, the chimeric protein cSos-SH2, which combines elements of Grb2 and Sos1, produced a pronounced increase of reserve cells. These results demonstrate that a precise balance between Grb2 and Sos1, along with their coordinated subcellular localization, is critical for controlling reserve cell populations. Activated by growth factor receptor tyrosine kinases and extracellular matrix/integrin interactions, the Grb2/Sos1 signaling pathway is critical for maintaining the muscle satellite cell pool, thereby playing an essential role in muscle regeneration.","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144527751","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