{"title":"The effects of omentin on estradiol and progesterone release in human granulosa cell culture.","authors":"Pınar Tarıkahya, Burcu Baba, Leyla Özer, Tolga Ecemiş, Çağla Zübeyde Köprü","doi":"10.1007/s11626-026-01187-7","DOIUrl":"10.1007/s11626-026-01187-7","url":null,"abstract":"<p><p>Adipokines serve as a link between energy metabolism and reproduction, helping to explain infertility related to polycystic ovary syndrome (PCOS). Granulosa cells are known to produce adipokines such as omentin; however, research on the potential effects of omentin on hormone levels in PCOS patients is lacking. Thus, the aim of our study was to evaluate the effect of different concentrations of omentin, FSH, and FSH + omentin on estradiol and progesterone secretion from human granulosa cells of PCOS patients. Granulosa cells were obtained from follicular fluid of 12 women undergoing IVF/ICSI treatment. Then they were treated with different doses of omentin (1 and 10 ng/ml), FSH (10 and 100 ng/ml), and with combinations of omentin and FSH for 48 h. The levels of estradiol and progesterone secreted by granulosa cells into the culture supernatants were measured by ELISA. Progesterone levels were increased when 10 ng/ml omentin was administered together with high-dose FSH (100 ng/ml), and were also increased at 1 and 10 ng/ml omentin doses compared to the control. Estradiol levels increased with 1 and 10 ng/ml omentin, and this effect was enhanced when combined with high-dose FSH; however, the combination of 1 ng/ml omentin with high-dose FSH resulted in reduced estradiol secretion. These findings demonstrated that omentin treated with different doses changed the secretion of estradiol and progesterone in granulosa cells in a dose-dependent manner.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"839-845"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837561","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}
Mengyuan Wu, Fanlong Meng, Meiqi Xu, Feng Pei, Yakun Luo
{"title":"ALKBH4 confers ferroptosis resistance and drives tumorigenesis via dysregulation of GPX4 in breast cancer cells.","authors":"Mengyuan Wu, Fanlong Meng, Meiqi Xu, Feng Pei, Yakun Luo","doi":"10.1007/s11626-026-01184-w","DOIUrl":"10.1007/s11626-026-01184-w","url":null,"abstract":"<p><p>Breast cancer (BC) remains a predominant source of cancer-related fatalities among women globally. While the AlkB homolog family member ALKBH4 has been implicated in cancer, its role and mechanism in BC are unknown. Its role within BC and its correlation with ferroptosis-a type of iron-mediated regulated cell death, were examined in this work. Data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and immunohistochemistry (IHC) analyses indicate ALKBH4 overexpression in BC, further associating its high expression levels with unfavorable clinical outcomes. Functional experiments in BC cells demonstrated that ALKBH4 knockdown exerted inhibitory effects on proliferation, migration, and invasion. Concurrently, it promoted apoptosis. Transcriptomic and biochemical investigations revealed that knocking down ALKBH4 sets off a ferroptotic cascade, with telltale signs including heightened levels of malondialdehyde (MDA) and ferrous iron (Fe<sup>2+</sup>), a serious drain on reduced glutathione (GSH) reserves, and a buildup of reactive oxygen species (ROS). Fortunately, this ferroptotic cell death was prevented by the ferroptosis inhibitor Ferrostatin-1 (Fer-1) and enhanced by the inducer Erastin. Mechanistically, we demonstrated that ALKBH4 maintains GPX4 protein levels in a demethylase activity-dependent manner, and GPX4 overexpression reversed the ferroptosis and growth defects caused by ALKBH4 loss. Combined application of ALKBH4 knockdown and GPX4 overexpression resulted in enhanced anti-tumor effects both in cellular and animal models. In conclusion, our findings establish that ALKBH4 is a novel driver of BC progression, which confers ferroptosis resistance to cancer cells by governing GPX4 levels in an enzyme activity-dependent way. Therefore, targeting ALKBH4 to disrupt its regulatory effect on GPX4 may offer a new therapeutic strategy for BC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"768-788"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041841","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}
{"title":"Establishment and characterization of air-liquid interface cultures of human small airway epithelial cells from two commercial sources.","authors":"Kyoung Jin Nho","doi":"10.1007/s11626-026-01180-0","DOIUrl":"10.1007/s11626-026-01180-0","url":null,"abstract":"","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"733-737"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770171","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}
Zuzana Kiššová, Klaudia Jaszcza, Veronika Vinclérová, Rege Anna Márton, Máté Mackei, Gábor Mátis, Viera Karaffová
{"title":"Dynamics of viability and apoptotic regulation in chicken ileal explant culture.","authors":"Zuzana Kiššová, Klaudia Jaszcza, Veronika Vinclérová, Rege Anna Márton, Máté Mackei, Gábor Mátis, Viera Karaffová","doi":"10.1007/s11626-026-01173-z","DOIUrl":"10.1007/s11626-026-01173-z","url":null,"abstract":"<p><p>The development of a reliable ex vivo intestinal model is essential for studying gut physiology and host-microbe interactions under controlled conditions. This study evaluated the temporal dynamics of viability, morphology, and apoptotic regulation in chicken ileal explants cultured ex vivo. Ileal tissues from 21-d-old broiler chickens were incubated for 0, 4, and 8 h and analyzed using metabolic assays (MTS, CCK-8), histological staining (hematoxylin and eosin (H&E), Periodic Acid-Schiff (PAS)), and quantitative PCR for apoptosis-related genes (BCL2L11, cytochrome c, caspase-3, caspase-8, and caspase-9). After 4 h, explants retained structural integrity with well-developed villi and active mucus secretion. Metabolic assays confirmed preserved cell viability, while transcriptional analysis revealed moderate upregulation of cytochrome c and downregulation of BCL2L11, suggesting transient adaptation to culture stress. After 8 h, villi appeared shortened with epithelial exfoliation and reduced PAS reactivity, indicating progressive tissue deterioration. Correspondingly, BCL2L11 and cytochrome c were significantly upregulated together with caspase-8, reflecting activation of intrinsic and extrinsic apoptotic pathways. Metabolic activity declined markedly, confirming reduced tissue vitality. These findings demonstrate that chicken ileal explants with a diameter of 4 mm remain viable and functionally stable up to approximately 4 h of ex vivo culture, after which apoptotic processes intensify, compromising tissue integrity. The results define the practical viability window for short-term intestinal explant studies and provide methodological guidance for future investigations on host-pathogen or probiotic interactions in poultry gut models.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"727-732"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147456905","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}
{"title":"Establishment and characterization of a cell line (OS-MM) originating from a human malignant melanoma of the oral mucosa.","authors":"Tomoaki Shintani, Atsuko Hamada, Sachiko Yamasaki, Yukari Jono, Koichi Koizumi, Ryouji Tani, Akihiko Sakamoto, Yasusei Kudo, Mikihito Kajiya, Souichi Yanamoto, Tetsuji Okamoto","doi":"10.1007/s11626-026-01162-2","DOIUrl":"10.1007/s11626-026-01162-2","url":null,"abstract":"<p><p>The prognosis for patients diagnosed with oral mucosal melanoma is poor, and the etiology of this disease remains to be elucidated. The underlying reason for this is that no malignant melanoma (MM) cell line derived from oral mucosal tissue has been successfully established to date. The establishment of a human MM cell line designated OS-MM from a tissue sample of a patient diagnosed with palatal mucosal melanoma was undertaken. For a period exceeding three decades, tumor cells have undergone uninterrupted proliferation, exhibiting a spindle-like morphology. Chromosomes exhibit a low-triploid pattern with an observed mode of 47. Heterotransplantation of the cells into SCID mice has resulted in the formation of tumor masses. The cells expressed vascular endothelial growth factor (VEGF) and its receptors. The addition of exogenous recombinant VEGF<sub>165</sub> did not alter proliferation but enhanced motility. A genetic analysis of OS-MM cells revealed the absence of BRAF and NRAS mutations; however, a GNAS mutation was identified. The OS-MM cell line should contribute to advances in personalized therapy for malignant oral mucosal melanoma.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"673-684"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13246917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146776322","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":"Direct reprogramming of Müller glia into photoreceptors via multiple transcription factors and small molecules: molecular mechanisms and transcriptomic analysis.","authors":"Yuka Endo, Eriko Sugano, Yuko Seko, Tomokazu Fukuda, Kitako Tabata, Taira Kakizaki, Shu Maruoka, Takanori Yokoyama, Hanaho Mori, Taku Ozaki, Lanlan Bai, Hiroshi Tomita","doi":"10.1007/s11626-026-01164-0","DOIUrl":"10.1007/s11626-026-01164-0","url":null,"abstract":"<p><p>Direct reprogramming, involving overexpression of transcription factors in combination with specific small-molecule treatments to induce cell fate conversion, represents a promising strategy for regenerative medicine and disease modeling. Monocistronic expression of four transcription factors (CRX, NEUROD, RAX, and OTX2) has been demonstrated to induce the expression of phototransduction-associated genes and confer light responsiveness in fibroblasts. In contrast, polycistronic expression of the same four factors resulted in the upregulation of only two cone-specific genes, indicating that optimization of reprogramming conditions is required to achieve complete photoreceptor differentiation. In this study, we focused on Müller glial cells, which exhibit regenerative potential in the retina of lower vertebrates, and explored their reprogramming into photoreceptor-like cells. We thus combined polycistronic expression of the aforementioned transcription factors and a pharmacological reprogramming approach utilizing a defined cocktail of small molecules. Transcriptomic analysis revealed that transcription factor introduction alone led to the upregulation of the genes related to neuronal identity and extracellular matrix components. Notably, the combination of transcription factor expression and chemical treatment induced photoreceptor-specific gene expression. However, no genes associated with phototransduction were detected, suggesting that further refinement is required to promote full differentiation into functionally mature light-responsive photoreceptors. Overall, our findings demonstrate that immortalized Müller glia can partially activate neuronal and photoreceptor genes through reprogramming, suggesting their potential for scalable drug screening and disease modeling. Clinical trial number: not applicable.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"685-703"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13246565/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283782","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}
Yiming Chen, Li Zhang, Jie Zhang, Xuezhen Peng, Ying Chen, Jing Xie
{"title":"miR-3614-5p prevents endothelial differentiation and angiogenesis in human exfoliated deciduous teeth by targeting lysophosphatidic acid receptor 2.","authors":"Yiming Chen, Li Zhang, Jie Zhang, Xuezhen Peng, Ying Chen, Jing Xie","doi":"10.1007/s11626-026-01171-1","DOIUrl":"10.1007/s11626-026-01171-1","url":null,"abstract":"<p><p>The contribution of microRNAs (miRNAs) to the endothelial differentiation of stem cells from human exfoliated deciduous teeth (SHED) remains largely unclear. This study sought to uncover novel miRNAs implicated in this process. SHED were obtained from deciduous teeth and verified via flow cytometric profiling of CD34, CD90, and CD105. Cells were induced toward endothelial lineage and subjected to miRNA sequencing at 0, 7, and 14 d. Differentially expressed miRNAs were validated by quantitative Polymerase Chain Reaction (qPCR). The influence of miR-3614-5p on endothelial differentiation was examined using qPCR, Western blotting, immunofluorescence, and angiogenesis assays. Direct targeting of lysophosphatidic acid receptor 2 (LPAR2) was tested through luciferase reporter assays, and rescue experiments were performed by LPAR2 overexpression. Results showed that SHED expressed CD34 (19.5%), CD90 (99.1%), and CD105 (92.5%), confirming effective isolation. Sequencing identified 9 consistently downregulated and 11 consistently upregulated miRNAs at both days 7 and 14, with miR-3614-5p denoting stable upregulation and qPCR confirmation. Functionally, miR-3614-5p exerted opposing effects: its overexpression suppressed von Willebrand factor and CD31 expression and impaired tube formation, whereas its inhibition enhanced marker expression and angiogenesis. Mechanistically, LPAR2 was validated as a direct target of miR-3614-5p. Importantly, LPAR2 overexpression reversed the inhibitory effects of miR-3614-5p on endothelial differentiation and angiogenesis. Together, these findings indicated that miR-3614-5p negatively regulates SHED endothelial differentiation and angiogenesis by directly targeting LPAR2, highlighting its potential role as a molecular regulator in this process.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"602-613"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581254","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}
Tongbin Liu, Qi Tang, Min Liu, Fangping Ren, Rubing Liu
{"title":"Mechanism of LPS-activated gingival fibroblasts promote the migration of gastric cancer cells via CXCL12/CXCR4-Snail2-EMT axis.","authors":"Tongbin Liu, Qi Tang, Min Liu, Fangping Ren, Rubing Liu","doi":"10.1007/s11626-026-01168-w","DOIUrl":"10.1007/s11626-026-01168-w","url":null,"abstract":"<p><p>The objective of this article is to explore the influence and process by which periodontitis affects the metastasis of gastric cancer cells. Human gingival fibroblasts (HGFs) underwent stimulation with lipopolysaccharide (LPS), and ELISA was used to detect inflammatory factor expression. Using cell co-culture technology, the effect of HGFs on the migration of gastric cancer cells was observed. CCK8, qPCR, Western blot, RNAi, Cell scratch and transwell were used to analyze the relationship between CXCL12/CXCR4, Snail2 and EMT, and their effects on cancer cell migration. The results showed that CXCL12 levels rise in periodontitis and gastric cancer. HGFs can promote the migration of gastric cancer cells. CXCL12 also boosts Snail2 expression in gastric cancer cells. AMD3100 and si-CXCR4 can significantly inhibit the expression of Snail2. Moreover, CXCL12 can promote EMT, while si-Snail2 and si-CXCR4 significantly reduced the upregulation trend of N-cadherin and Vimentin expression, and reverses the downregulation trend of E-cadherin expression. CXCL12 can promote the migration of gastric cancer cells, while the migration rates of gastric cancer cells are notably reduced after AMD3100, si-CXCR4 or si-Snail2 intervention. In summary, the CXCL12/CXCR4-Salil2-EMT signaling pathway is involved in the migration of gastric cancer cells promoted by periodontitis. This will uncover new insights into the mechanisms that might play a role in the development of gastric cancer and strategies for targeted therapy.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"589-601"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520872","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}
Bo Jiang, Fenyu Fu, Shiqiang Yu, Yinbo Wang, Lei Chen, Zhilong Xiu
{"title":"Influence of puerarin upon mouse hippocampal neurons involved in corticosterone-induced dysfunction.","authors":"Bo Jiang, Fenyu Fu, Shiqiang Yu, Yinbo Wang, Lei Chen, Zhilong Xiu","doi":"10.1007/s11626-026-01172-0","DOIUrl":"10.1007/s11626-026-01172-0","url":null,"abstract":"<p><p>Corticosterone (CORT) is a glucocorticoid hormone whose prolonged elevation during stress can generate excessive reactive oxygen species (ROS), leading to hippocampal neuron dysfunction. Puerarin, a natural isoflavone extracted from Pueraria lobata, has known antioxidant and neuroprotective properties. However, its effects on CORT-induced neurotoxicity have not been well characterized. In this study, we investigated the effects of puerarin on CORT-induced damage in primary mouse hippocampal neurons. We found that CORT (100-800 μM) dose-dependently reduced neuronal viability, whereas cultured astrocytes remained viable except at the highest concentration (800 μM), indicating a relative resistance of astrocytes to CORT. CORT treatment also significantly impaired neurite outgrowth, increased lactate dehydrogenase (LDH) release, elevated intracellular ROS levels, and decreased antioxidant enzyme activities in neurons. Importantly, pretreatment with puerarin markedly ameliorated these CORT-induced effects: puerarin preserved neurite length, suppressed LDH leakage and ROS accumulation, and restored activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). These results demonstrate that puerarin can attenuate CORT-induced hippocampal neuron dysfunction in vitro. Our findings suggest that puerarin has potential therapeutic value for oxidative stress-related neural impairment in stress-related disorders.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"614-624"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148029695","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}