In Vitro Cellular & Developmental Biology. Animal最新文献

{"title":"Chlorogenic acid suppresses the expression of matrix metalloproteinase-7 and cell invasiveness to almost the same extent as isofraxidin in human colorectal cancer cells.","authors":"Takayoshi Tokiwa, Taisuke Yamazaki, Takashi Yokoyama","doi":"10.1007/s11626-024-00993-1","DOIUrl":"10.1007/s11626-024-00993-1","url":null,"abstract":"<p><p>The expression of matrix metalloproteinase (MMP)-7 is reported to be correlated with invasion and metastasis of colorectal cancer (CRC). Therefore, the inhibition of MMP-7 would be beneficial for the suppression or prevention of CRC cell invasion and metastasis. The stem bark of Acanthopanax senticosus, a widely used medicinal herb, contains isofraxidin (IF) and chlorogenic acid (CGA) as major components. Previously we reported that IF suppressed the expression of MMP-7 and cell invasion in human hepatoma cells. In this study, we investigated the effects of CGA on cell invasion, MMP-7 mRNA expression and the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and compared it with those of IF in human CRC cells (HT-29). We found that CGA significantly suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced cell invasion, MMP-7 expression and the expression of activated form of MMP-7 to almost the same extent as IF. Meanwhile, we also found that TPA-induced expression of MMP-7 mRNA and ERK1/2 phosphorylation were significantly suppressed when cells were exposed to the ERK1/2 inhibitor U0126 and that CGA was a little more potent than IF at inhibiting TPA-induced ERK1/2 phosphorylation. Taken together, the present results indicate that CGA suppresses cell invasion, MMP-7 expression and ERK1/2 phosphorylation to almost the same extent as IF and suggest that not only IF but also CGA suppresses cell invasion by inhibiting MMP-7 expression via the inhibition of at least ERK1/2 phosphorylation and Acanthopanax senticosus, which contains two components with anti-MMP-7 activity, may be a beneficial herb with anti-invasive effects against human CRC cells.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"205-213"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853967","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":"Preliminary study on the potential damage of cigarette smoke extract in 3D human chondrocyte culture.","authors":"Yessica Zamudio-Cuevas, Javier Fernández-Torres, Octavio Gamaliel Aztatzi-Aguilar, Pedro Raymundo Martínez-Cabello, Ambar López-Macay, Victor Ilizaliturri-Sánchez, Bertha Vargas-Sandoval, Roberto Sánchez-Sánchez, Karina Martínez-Flores","doi":"10.1007/s11626-024-00999-9","DOIUrl":"10.1007/s11626-024-00999-9","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a chronic degenerative disease characterized by the progressive loss of articular cartilage. The role of cigarette smoke (CS) in OA is debated, with some studies suggesting a protective effect while others indicate it may pose a risk. Our preliminary findings suggest a link between smoking in young adults and severe knee OA, though the extent of this contribution is unclear. This study investigates the impact of cigarette smoke extract (CSE) on human chondrocytes. Human chondrocyte cultures were exposed to varying concentrations (0-10%) of CSE for 7 d. We evaluated cell viability, extracellular matrix (ECM) components, metalloproteinase expression and cytokines levels, and antioxidant enzymes (SOD1 and CAT) using calcein staining, immunohistochemistry and ELISA. Oxidative stress (OS) was assessed by measuring hydrogen peroxide (H₂O₂) and nitric oxide (NO) levels. Results were analyzed using ANOVA with Tukey post hoc tests, and Pearson correlation coefficients were calculated. Cell viability decreased at 10% CSE, and ECM components were diminished. MMP9 and MMP13 expression significantly increased at 5% and 10% CSE. H₂O₂ levels peaked at 1%, while IL-1β peaked at 2.5%. Antioxidant expression (SOD1 and CAT) decreased at higher concentrations, and heat shock protein 70 (HSP70) was notably expressed. MMPs expression was negatively correlated with both viability and ECM components. CSE induces cellular damage, alters ECM composition, and upregulates MMP expression via OS and IL-1β, while diminishing antioxidant defenses. These findings suggest that smoking may disrupt articular cartilage homeostasis, highlighting the need for further investigation into oxidative stress and inflammatory mediators.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"214-227"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142893513","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":"Compatibility of Calycosin-Tanshinone IIA improves Ang II-induced renal artery endothelial cell dysfunction through lncRNA-mRNA co-expression network.","authors":"YanYun Jiang, Cong Han, WanLi Xu, YuQiu Li, Yao Liu","doi":"10.1007/s11626-024-00990-4","DOIUrl":"10.1007/s11626-024-00990-4","url":null,"abstract":"<p><p>This study aimed to investigate the effect of the compatibility of Calycosin and Tanshinone IIA on dysfunction of rat renal artery endothelial cells (RRAECs) induced by angiotensin II (Ang II) and to elucidate the underlying molecular mechanisms. We utilized cell culture to optimize Calycosin and Tanshinone IIA concentrations and assessed autophagy, apoptosis, ATP levels, and cell migration using MDC staining, Annexin V-FITC/PI staining, ATP assay, and Transwell assays, respectively. RNA-seq identified differentially expressed lncRNAs and mRNAs, which were validated by qRT-PCR. The compatibility of Calycosin and Tanshinone IIA significantly enhanced the proliferative capacity of Ang II-induced RRAECs, increased autophagosome formation, reduced cell apoptosis, elevated ATP production, and enhanced cell migration ability. RNA sequencing analysis revealed 146 differentially expressed lncRNAs and 43 differentially expressed mRNAs, and co-expression network analysis identified interactions between 28 lncRNAs and 7 mRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses indicated that these differentially expressed mRNAs were primarily involved in the regulation of ATPase activity and metabolic processes related to serine family amino acids, triglycerides, arachidonic acid, etc., as well as the MAPK signaling pathway. The compatibility of Calycosin and Tanshinone IIA improved Ang II-induced dysfunction in RRAECs by modulating the lncRNA-mRNA co-expression network, providing new molecular targets and therapeutic strategies for the prevention and treatment of hypertensive renal damage.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"189-204"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143407411","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":"OPA3 inhibits the cGAS-STING pathway mediated by mtDNA stress to promote colorectal cancer progression.","authors":"Yuqiang Yin, Zhenxin Ma, Siwen Yuan, Kangfeng Xu, Xiaofeng Wang","doi":"10.1007/s11626-024-01000-3","DOIUrl":"10.1007/s11626-024-01000-3","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is an extremely harmful malignant tumor. Optic atrophy 3 (OPA3) is highly expressed in multiple tumors, but its action in CRC is still unknown. This research aims to explore the role of OPA3 and its related molecular mechanisms for CRC. Firstly, we overexpressed and knocked down OPA3 to examine its effect on CRC cell (HT29 cell) growth. CRC cell viability, migration, invasion, and levels of proliferation markers and cell cycle-associated proteins were measured. Then, we treated cells with carbonyl cyanide m-chlorophenyl hydrazone (CCCP) to explore mitochondrial dysfunction and mtDNA stress in HT29 cells. Next, we overexpressed cGAS and STING to examine their correlation with OPA3. The results showed that OPA3 overexpression enhanced CRC cell viability, migration, invasion, and the levels of PCNA, Cyclin A2, and Cyclin B1. Knockdown of OPA3 had the opposite effects. Moreover, OPA3 knockdown facilitated mitochondrial dysfunction and mtDNA stress in CRC cells. OPA3 overexpression also inhibited CCCP-induced mitochondrial stress disorder. Additionally, OPA3 knockdown elevated the protein levels of p-STING and cGAS and the mRNA level of STING target genes. Furthermore, overexpression of either cGAS or STING partially alleviated the enhancement of HT29 cell proliferation, migration, and invasion mediated by OPA3 overexpression. In conclusion, OPA3 promotes CRC progression via inhibiting the cGAS-STING pathway, which is mediated by mtDNA stress. OPA3 may be a new potential target for CRC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"165-177"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142894246","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":"MiR-146a-5p downregulated TRAF6/NF-κB p65 pathway to attenuate the injury of HT-22 cells induced by oxygen-glucose deprivation/reoxygenation.","authors":"Yuan Deng, Ganlan Wang, Dan Hou, Lei Zhang, Chaoying Pei, Guoshuai Yang","doi":"10.1007/s11626-024-00986-0","DOIUrl":"10.1007/s11626-024-00986-0","url":null,"abstract":"<p><p>MicroRNA-146a-5p (miR-146a-5p) actively participates in the process of cerebral ischemia-reperfusion (CI/R) injury. Dysregulation of the tumor necrosis factor receptor-associated factor 6 (TRAF6)/nuclear factor kappa-B (NF-κB) p65 axis is closely associated with inflammatory response. This study aimed to investigate the potential involvement of miR-146a-5p and TRAF6/NF-κB p65 in mediating CI/R progression in vitro. HT-22 cells were challenged with oxygen-glucose deprivation/reoxygenation (OGD/R) to simulate CI/R in vitro. HT-22 cells were transfected with miR-146a-5p mimics or TRAF6 overexpression constructs. The impact of miR-146a-5p on apoptosis, inflammation, and TRAF6/NF-κB p65 activation were investigated. OGD/R inhibited HT-22 cell viability, induced apoptosis, reduced miR-146a-5p levels and activated the TRAF6/NF-κB p65 pathway. MiR-146a-5p mimics reduced pro-inflammatory factor release, limited apoptosis-related protein expression, and inactivated the TRAF6/NF-κB p65 pathway in OGD/R-challenged HT-22 cells. Mechanistically, miR-146a-5p was verified to bind to TRAF6 3'UTR. TRAF6 overexpression reversed the beneficial effects of miR-146a-5p mimics on apoptosis, inflammation, and TRAF6/NF-κB p65 activation. This work revealed that miR-146a-5p targeted TRAF6 and suppressed the TRAF6/NF-κB p65 pathway, thereby reducing OGD/R-induced inflammation and apoptosis in HT-22 cells. These findings suggest the potential of the miR-146a-5p/TRAF6/NF-κB p65 axis in the treatment of CI/R.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"178-188"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791671","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":"Impact and mechanism of the TBX-22 gene mutation G874A on the epithelial-mesenchymal transition in medial edge epithelial cells.","authors":"Chen Xu, Yali Hou, Li Ma, Dongsheng Zhang","doi":"10.1007/s11626-024-00932-0","DOIUrl":"10.1007/s11626-024-00932-0","url":null,"abstract":"<p><p>Cleft lip and palate (CL/P) are prevalent congenital anomalies with complex genetic causes. The G874A mutation of T-box transcription factor 22 (TBX-22) gene is notably associated with CL/P, while the underlying mechanism remains to be clarified. Studies have shown that the restriction of epithelial-mesenchymal transformation (EMT) process in medial edge epithelial cells (MEEs) is crucial for CL/P development. In our current research, primary MEEs, isolated and cultured from mouse embryos, were genetically introduced the TBX-22 G874A mutation and subsequently treated with TGF-β1. They were then utilized to test the hypothesis that the G874A mutation in TBX22 plays a role in the regulation of the EMT in MEEs. Our findings reveal that TBX22 reduces miR140-5p transcription by binding to its promoter, while miR140-5p downregulates TGFBR1 protein expression by targeting its mRNA 3'-UTR. In other words, TBX22 could indirectly positively regulates TGFBR1 expression post-transcriptionally. Functional cellular assays showed that the G874A mutation of TBX-22 counteracted TGF-β1-induced decrease in proliferation and migration. Western blotting results showed that the G874A mutation of TBX-22 inhibited EMT protein expression (α-SMA and Vimentin) and promoted E-cadherin in TGF-β1-induced MEEs. To summarize, our research reveals that the G874A mutation of TBX22 impedes the progression of EMT in MEEs through the upregulation of miR140-5p and the downregulation of TGFBR1. This highlights TGFBR1 as a viable target for the prevention of CL/P.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"125-130"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052376","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":"IL-27 attenuated macrophage injury and inflammation induced by Mycobacterium tuberculosis by activating autophagy.","authors":"Yushan Zhou, Yuxuan Zhang, Yanli Li, Liqiong Liu, Min Zhuang, Yi Xiao","doi":"10.1007/s11626-024-00989-x","DOIUrl":"10.1007/s11626-024-00989-x","url":null,"abstract":"<p><p>Interleukin-27 (IL-27) is a cytokine that is reported to be highly expressed in the peripheral blood of patients with pulmonary tuberculosis (PTB). IL-27-mediated signaling pathways, which exhibit anti- Mycobacterium tuberculosis (Mtb) properties, have also been demonstrated in macrophages infected with Mtb. However, the exact mechanism remains unclear. This study aimed to clarify the potential molecular mechanisms through which IL-27 enhances macrophage resistance to Mtb infection. Both normal and PTB patients provided bronchoalveolar lavage fluid (BALF). Peripheral blood mononuclear cells (PBMCs) were isolated from healthy individuals and stimulated with 50 ng/mL macrophage-colony stimulating factor (M-CSF) to obtain monocyte-derived macrophages (MDMs). Using 100 ng/mL phorbol 12-myristate 13-acetate (PMA), THP-1 cells were induced to differentiate into THP-1-derived macrophage-like cells (TDMs). Both MDMs and TDMs were subsequently infected with the Mtb strain H37Rv and treated with 50 ng/mL IL-27 prior to infection. The damage and inflammation of macrophages were examined using flow cytometry, enzyme-linked immunosorbent assay (ELISA), and Western blotting. Patients with PTB had elevated levels of IL-27 in their BALF. Preconditioning with IL-27 was shown to reduce H37Rv-induced MDMs and TDMs apoptosis while also decreasing the levels of Cleaved Caspase-3, Bax and the proinflammatory cytokines TNF-α, IL-1β, and IL-6, promoting the expression of Bcl-2 and the anti-inflammatory factors IL-10 and IL-4. Silencing of the IL-27 receptor IL-27Ra increased macrophage damage and inflammation triggered by H37Rv. Mechanistically, IL-27 activates autophagy by inhibiting TLR4/NF-κB signaling and activating the PI3K/AKT signaling pathway, thereby inhibiting H37Rv-induced macrophage apoptosis and the inflammatory response. Our study suggests that IL-27 alleviates H37Rv-induced macrophage injury and the inflammatory response by activating autophagy and that IL-27 may be a new target for the treatment of PTB.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"245-256"},"PeriodicalIF":1.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499539","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 inhibitory effect of salidroside on RANKL-induced osteoclast formation via NFκB suppression.","authors":"Adilsaikhan Mendjargal, Shijir Narmandakh, Munkhjargal Zinamyadar, Egshiglen Amartuvshin, Juramt Bold, Nandin Garmaa, Enebish Sundui, Amgalanbaatar Dorjkhuu, Avirmed Amgalanbaatar, Erdenezaya Odkhuu","doi":"10.1007/s11626-024-00981-5","DOIUrl":"10.1007/s11626-024-00981-5","url":null,"abstract":"<p><p>Bone fractures are a prevalent clinical issue, and recent studies highlighted the promising potential of natural bone healing agents in enhancing fracture repair and regeneration. The regulatory interaction mechanism between osteoblasts and osteoclasts is crucial for bone cell biology and bone disease. In Mongolian medicine, people have used the Rhodiola rosea (R. rosea) extract to accelerate bone healing in bone fractures. Salidroside is a bioactive compound of R. rosea. Salidroside is known to regulate bone metabolism and inhibit the activation of osteoclast cells, but how it affects the differentiation of osteoclasts is unknown. We examined the effect of R. rosea extract and its bioactive compound salidroside on the RANKL-induced osteoclast formation in RAW 264.7 cells. The present study observed that salidroside directly inhibits RANKL-induced TRAP-positive osteoclast formation. Immunoblotting analysis revealed that salidroside inhibited the expression of c-Fos and NFATc1, osteoclastogenic key transcription factors, by suppressing late activation of p65 NFκB. Further, the ethanol extracts of R. rosea significantly reduced the RANKL-induced osteoclasts in a dose-dependent manner. In conclusion, salidroside inhibits RANKL-induced osteoclast formation via suppressing the NFκB/c-Fos/NFATc1 signalling pathway. R. rosea, a primary source of salidroside, is helpful for bone healing via its inhibitory effect on osteoclast formation.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"59-66"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545198","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, characterization, and sensory characteristics (taste and flavor) of an immortalized muscle cell line from the seven-band grouper Epinephelus septemfasciatus: implications for cultured seafood applications.","authors":"Sathish Krishnan, Selvakumari Ulagesan, Ji-Sung Moon, Youn-Hee Choi, Taek-Jeong Nam","doi":"10.1007/s11626-024-00971-7","DOIUrl":"10.1007/s11626-024-00971-7","url":null,"abstract":"<p><p>Grouper muscle satellite cells (GMSCs) from the seven-band grouper (Epinephelus septemfasciatus) were isolated, and their growth conditions were optimized (10% fetal bovine serum, 24°C, 10 ng/mL bFGF). The cells were immortalized at passage 14 and designated as grouper immortalized muscle satellite cells (GIMSCs). DNA barcoding confirmed the grouper origin of both GMSC and GIMSC lines. GIMSCs exhibited enhanced proliferation, accelerated differentiation, and robust myotube formation compared to pre-crisis GMSCs. Western blot analysis showed upregulation of key myogenic factors (Pax7, MyoD, MyoG) and structural proteins (Desmin) in GIMSC, indicating the differentiation potential. The immortalized GIMSC line maintained consistent morphology, growth rates, and viability across multiple passages. Biocompatibility studies showed GIMSCs were compatible with bio-inks (sodium alginate, gelatin, κ-carrageenan) at 250 to 10,000 µg/mL, retaining ~ 80% viability at the highest concentration. Taste sensory analysis revealed GMSCs had the highest umami and lowest saltiness and sourness, contrasting with the muscle of the seven-band grouper, which had higher saltiness and sourness. Flavor analysis identified pronounced fishy, hot fat, and ethereal flavors in the cells at higher level than in the muscle. These findings suggest GMSCs and GIMSCs are promising for producing cultured meat with enhanced umami taste and flavors, advancing cellular agriculture and sustainable food production.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"8-23"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286166","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":"Study on the mechanism of SAR1B in sodium acetate promoting milk fat synthesis.","authors":"Zhixia Wang, Haixin Fu, Na Zhang","doi":"10.1007/s11626-024-00974-4","DOIUrl":"10.1007/s11626-024-00974-4","url":null,"abstract":"<p><p>Acetate can promote milk fat synthesis in dairy cow mammary epithelial cells (BMECs). In this study, gene function analysis was used to explore the role of Ras family secretion-related GTP binding protein 1B (SAR1B) in milk fat synthesis of BMECs and its role and molecular mechanism in acetate-promoted milk fat synthesis. We found that the synthesis of lipid droplets and triglycerides was inhibited, and the expression levels of key genes and proteins in milk fat synthesis such as FASN and ACC were decreased in SAR1B knockout, which was reversed by overexpression of SAR1B. Addition of sodium acetate in BMECs can promote the expression of SAR1B, and SAR1B plays an important role in the synthesis of milk fat promoted by sodium acetate. We further investigated the underlying mechanism of SAR1B upregulation by sodium acetate, and found that sodium acetate could affect SAR1B expression through the positive regulation of SAR1B gene promoter activity by C/EBPβ and PPARγ. In conclusion, the results suggest that SAR1B can promote milk fat synthesis in BMECs, while C/EBPβ and PPARγ play important roles in sodium acetate to promote the expression of SAR1B.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":"24-35"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307693","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}