In Vitro Cellular & Developmental Biology. Animal最新文献

{"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}

{"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}

{"title":"Decorin inhibits the migration and invasion of the LPS + high glucose-induced primary trophoblast cell through ADAMTS12.","authors":"Qiuling Chen, Taoyan Hu, Hui Luo","doi":"10.1007/s11626-026-01166-y","DOIUrl":"10.1007/s11626-026-01166-y","url":null,"abstract":"<p><p>Decorin was identified as the most relevant biomarker in type 2 diabetes or obesity-related diseases, but its function in gestational obesity or gestational diabetes mellitus (GDM) remains unknown. RT-qPCR or western blot were employed to validate the expression of Decorin and ADAMTS12 in the umbilical cord blood or placental tissues of the aforementioned groups. Subsequently, an LPS + high glucose-induced primary trophoblast cell model was established to verify the expression of DCN and ADAMTS12 in trophoblasts. Based on this model, silencing (si) of Decorin, or Decorin recombinant protein (DCN-r) combined with si-ADAMTS12 intervention, was performed to investigate its effects on trophoblast cell proliferation, migration, invasion, and other characteristics. Compared to the normal pregnancy group, the levels of DCN and ADAMTS12 showed an increasing trend in the gestational obesity group and the GDM group. Notably, DCN and ADAMTS12 were markedly higher in the GDM with obesity group compared to either the gestational obesity or GDM-alone groups. LPS + high glucose inhibited the migration and invasion of primary trophoblast cells while promoting increased levels of DCN and ADAMTS12. Under LPS + high-glucose intervention, DCN-r further suppressed trophoblast cell migration and invasion while enhancing ADAMTS12 expression, whereas si-DCN reversed these effects. Additionally, si-ADAMTS12 attenuated the LPS + high glucose-induced decline in trophoblast cell migration and invasion and blocked the promoting effects of DCN recombinant protein. Silencing ADAMTS12 can inhibit the promotive effect of DCN on the migration and invasion capabilities of LPS + high glucose-induced primary trophoblast cells. Clinical trial number: not applicable.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"639-648"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13246882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147511747","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":"Formononetin as a potential therapeutic agent for asthma: evidence from in vivo and in vitro models of attenuated inflammation via cAMP/PKA pathway inhibition.","authors":"Fuyi Zhang, Zimei Lai","doi":"10.1007/s11626-026-01160-4","DOIUrl":"10.1007/s11626-026-01160-4","url":null,"abstract":"<p><p>This study aims to elucidate the ameliorative effects and potential mechanisms of formononetin (FN) on airway inflammation in asthmatic rats. An ovalbumin-induced asthmatic rat model was established and treated with FN. Lung function, histopathology, apoptosis, inflammatory cytokine levels, and lipid profiles were assessed. In parallel, LPS-stimulated BEAS-2B cells were treated with FN and the cAMP/PKA pathway activator coleonol (CLE). Cell proliferation, inflammatory cytokine expression, and cAMP/PKA pathway activity were evaluated. FN significantly improved lung function, reduced airway inflammation and pathological damage, and inhibited apoptosis in asthmatic rats. It also decreased serum levels of IgE, IFN-γ, IL-4, and TNF-α, and improved lipid metabolism by lowering TC, TG, and LDL-C while increasing HDL-C. In BEAS-2B cells, FN promoted proliferation and suppressed inflammation under LPS stimulation. These effects were mediated through the inhibition of the cAMP/PKA signaling pathway, as evidenced by reduced cAMP levels and PKA phosphorylation. The protective effects of FN were partially reversed by CLE. FN ameliorates airway inflammation in asthma by modulating lipid metabolism and suppressing the cAMP/PKA signaling pathway, as demonstrated in both rat models and human bronchial epithelial cells. These findings highlight FN as a promising therapeutic candidate for asthma treatment.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"649-660"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146219599","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":"The chitosan collagen salvianolic membrane mitigates intervertebral disc degeneration through suppression of the Wnt/β-catenin signaling.","authors":"Zhaozhong Yu, Jun Kuang, Xuan Wan, Chaoyi Liang, Fan Wu, Zhimin Shu, Weidong Liang, Xiaoming Wan, Jianbin Gong","doi":"10.1007/s11626-026-01163-1","DOIUrl":"10.1007/s11626-026-01163-1","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IVDD), a natural aging process, leads to intervertebral disc pain, with lumbar resection providing pain relief but potential postoperative complications affecting outcomes. The chitosan-collagen-salvianolic (CCS) membrane has shown promise in reducing scar formation after lumbar resection, though the mechanisms remain unclear. A lumbar laminectomy model was used, with materials applied to the surgical site. Tissue samples were collected at 4 and 8 wk post-surgery for histological evaluation to assess pathological changes and apoptosis. Western blot analysis examined protein expression in the Wnt/β-catenin signaling pathway in scar tissue. Rabbit vascular adventitia fibroblast (VAF) cells were isolated, and a Wnt3a overexpression vector was created. Various composite membrane materials and pathway inhibitors were tested, with assessments of cell invasion, apoptosis, viability, cytokine levels, and protein expression. Results showed that lumbar laminectomy activated the Wnt/β-catenin pathway. The CCS membrane facilitated healing by inhibiting this pathway. It enhanced VAF cell activity, reduced apoptosis, and suppressed Wnt3a pathway activity. Additionally, it protected cells from Wnt3a overexpression-induced damage while maintaining normal function. In conclusion, the CCS composite membrane promoted bone tissue repair after lumbar laminectomy by inhibiting Wnt/β-catenin pathway activation and preserving extracellular matrix fibroblast function.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"625-638"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147490993","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":"Cabozantinib activates TFEB-mediated autophagy to exert anti-tumor effects in hepatocellular carcinoma.","authors":"Cheng Chen, Yongjie Hu, Chenggang Zhang, Xiaocui Zhou","doi":"10.1007/s11626-026-01161-3","DOIUrl":"10.1007/s11626-026-01161-3","url":null,"abstract":"<p><p>Autophagy signaling plays a crucial yet complex role in hepatocellular carcinoma (HCC), influencing tumor progression and treatment response. Cabozantinib is an orally administered multi-kinase inhibitor used in the treatment of various advanced cancers, including renal cell carcinoma and HCC. However, its precise mechanisms of action in HCC require further elucidation. Our study first revealed elevated levels of phosphorylated TFEB (p-TFEB, Ser142) in human HCC tissues and cell lines, indicating impaired TFEB-mediated autophagic flux in hepatocellular carcinoma. Treatment with Cabozantinib induced dose-dependent cytotoxicity, oxidative stress (increased ROS and decreased GSH), and mitochondrial dysfunction (reduced Complex IV activity and ATP production). Furthermore, Cabozantinib promoted autophagy activation, as evidenced by increased autophagosome formation, elevated LC3-II/I conversion and Beclin1 expression, and decreased p62 levels. Mechanistically, Cabozantinib inhibited TFEB phosphorylation at Ser142 and enhanced its nuclear translocation. Critically, TFEB knockdown abolished Cabozantinib-induced autophagy, confirming that the pro-autophagic effects are TFEB-dependent. These findings demonstrate that Cabozantinib exerts its anti-tumor activity in HCC through activating TFEB-mediated autophagy pathway by inducing oxidative stress and mitochondrial damage.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"661-672"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638769","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":"The active plant compounds demonstrated positive activity on mouse intestinal organoids as an inflammation model system.","authors":"Selinay Şenkal-Turhan, Özüm Begüm Böke, Ezgi Bulut-Okumuş, Hazar Eren Soydan, Neşe Başak Türkmen, Ayça Şenol, Kaan Kadayıfcı, Neslihan Akmaz, Ayşegül Doğan","doi":"10.1007/s11626-026-01165-z","DOIUrl":"10.1007/s11626-026-01165-z","url":null,"abstract":"<p><p>Diet has an important impact on intestinal homeostasis, and the establishment of appropriate experimental models to study the effect of food compounds is of interest. The organoid model can be used to check the positive protective role of active food compounds on intestinal tissue. In the current study, mouse intestinal organoids were used to model air-liquid interface (ALI), lipopolysaccharide (LPS)-induced inflammation, and macrophage co-culture-based inflammation modelling. The activity of hesperidin, capsaicin, allicin, and 18β-glycyrrhetinic acid (18β-GA) was determined in organoid culture. Morphology, crypt number, area, and intensity were analyzed. mRNA expression analysis and immunostaining analysis were performed for inflammation and proliferation markers. The ALI model exerted a suitable organoid culture system to mimic intestinal growth based on our results. Hesperidin, capsaicin, and allicin demonstrated positive effects on LPS-induced inflammation. All of the food compounds showed positive effects in macrophage co-culture for organoid structure and growth but not for macrophage proliferation and viability. All compounds reduced the inflammatory gene expression and increased stem cell marker and proliferation-related gene expression in the ALI model. In addition, capsaicin showed positive effects on organoid growth and maturation. This study generated an experimental model system to test food components and might be used in further research.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"573-588"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147432556","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":"VEGFA is essential for the potentiation of ATRA on BMP9-induced osteogenesis of preadipocytes and osteoporotic fracture healing.","authors":"Hao Wang, Jingjiang Wang, Jiangyu Xiang, Yang Liu","doi":"10.1007/s11626-026-01170-2","DOIUrl":"10.1007/s11626-026-01170-2","url":null,"abstract":"<p><p>The induction of osteogenic differentiation in preadipocytes may serve as a potential therapeutic approach for treating osteoporosis and osteoporotic fractures. All-trans retinoic acid (ATRA) promotes the bone morphogenetic protein 9 (BMP9)-induced osteogenic differentiation of preadipocytes. The present study further investigated whether vascular endothelial growth factor A (VEGFA) may play a role in this process and the effect of ATRA and BMP9 on osteoporotic fracture healing in rats. The results indicated that ATRA and BMP9 synergistically upregulated VEGFA expression in preadipocytes. Furthermore, knockdown of VEGFA expression abolished the stimulatory effect of ATRA on the BMP9-induced early and late osteogenic differentiation of preadipocytes in vitro, as evidenced by a decrease in alkaline phosphatase (ALP) activity, osteopontin and osteocalcin expression as well as mineralization. The in vivo cell implantation assay showed that ATRA failed to augment BMP9-induced ectopic bone formation in the absence of VEGFA. Subsequently, an osteoporotic femoral fracture rat model was established and micro-CT scans, alongside quantitative analysis, revealed that ATRA effectively promoted BMP9-stimulated callus formation during osteoporotic fracture healing. Moreover, ATRA and BMP9 acted together to significantly elevate VEGFA expression in bone calluses. Mechanistically, ATRA and BMP9 synergistically stimulated the osteogenic transcription factor, runt-related transcription factor 2 (Runx2). Transcriptomic and bioinformatic analyses further revealed that the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway may be crucial for mediating the synergistic effects of ATRA and BMP9, as validated by detecting the phosphorylation of PI3K and Akt. However, the increases in Runx2 expression and Akt phosphorylation induced by the combination of ATRA and BMP9 were inhibited by VEGFA silencing. ATRA also failed to increase the BMP9-induced ALP activity in preadipocytes treated with an Akt inhibitor. These findings suggest that VEGFA may influence the potentiation effect of ATRA on the BMP9-mediated osteogenesis of preadipocytes and in osteoporotic fracture healing through Runx2 and the PI3K/Akt signaling pathway.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"713-726"},"PeriodicalIF":2.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147473629","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":"Correction: The effect of IGF-1 on cartilage injury in bone marrow mesenchymal stem cells through the BMP2-Smad1/5 signaling pathway.","authors":"HuiYue Ye, Liang Shao","doi":"10.1007/s11626-026-01179-7","DOIUrl":"10.1007/s11626-026-01179-7","url":null,"abstract":"","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"571-572"},"PeriodicalIF":1.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627788","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":"The differential expression of lipocalin-2 in pig tissues and its molecular mechanism of regulating cell viability, differentiation, adipogenesis, and glycometabolism in porcine intramuscular preadipocytes.","authors":"Xiaoying Dong, Yanfei Chen, Liubing Tang, Qinen Wu, Tingjun Li, Qiuxia Wei, Shengqiu Tang","doi":"10.1007/s11626-026-01158-y","DOIUrl":"10.1007/s11626-026-01158-y","url":null,"abstract":"<p><p>Lipocalin-2 (LCN-2) is an adipocytokine secreted mainly by adipose tissue. Increasing evidences suggest that LCN-2 is an inflammatory factor associated with insulin resistance, obesity, and its complications. The precise mechanism of the development of obesity-related disorders induced by LCN-2 is not very clear. This study evaluated the expression of LCN-2 in pig tissues and its molecular mechanism of regulating preadipocyte differentiation in porcine intramuscular preadipocytes. LCN-2 expression in tissues of Tongcheng pigs, intramuscular adipose tissue of Tongcheng pigs (fat type) and Landrace pigs (lean type) in embryonic stage and growth stage, and adipocyte differentiation-induced porcine intramuscular preadipocytes was detected using reverse transcription polymerase chain reaction (qRT-PCR). After LCN-2 treatment, cell viability was measured by the methyl thiazolyl tetrazolium (MTT) method, mRNA expression of CCAAT/enhancer binding protein-ɑ (C/EBPɑ), adipocyte determination and differentiation factor-1 (ADD1), fatty acid desaturase (FAD), fatty acid synthase (FAS), and glucose transporter (GLUT) 1,4 was determined by qRT-PCR, protein expression of LCN-2 and peroxisome proliferator-activated receptor-γ (PPARγ) was analyzed by Western blot. Results of qRT-PCR indicated that LCN-2 showed significantly higher expression in high-intramuscular fat (IMF) pigs compared to low-IMF pigs (P < 0.05). LCN-2 expression in porcine intramuscular preadipocytes was significantly upregulated after adipocytic differentiation induction (P < 0.05). Silencing of LCN-2 with LCN-2 siRNA (siLCN-2) inhibited cell viability, lipid droplets, protein expression of PPARγ, and mRNA expression of C/EBPa, ADD1, FAD, FAS, and GLUT 1,4. siLCN-2 treated cells also showed a lower content of triglyceride and release of glucose. Moreover, LCN-2-induced downregulation of cell viability, adipocytic differentiation, adipogenesis, and glycometabolism of porcine intramuscular preadipocytes was partially blocked by the PPARγ inhibitor (GW9662). It is indicated that LCN-2 silencing suppresses cell viability, adipocytic differentiation and adipogenesis, glycometabolism, and fat deposition of porcine intramuscular preadipocytes through suppression of the PPARγ signaling pathway.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"525-536"},"PeriodicalIF":2.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147473582","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}