{"title":"Role of the Ror family receptors in Wnt5a signaling","authors":"Koki Kamizaki, Yasuhiro Minami, Michiru Nishita","doi":"10.1007/s11626-024-00885-4","DOIUrl":"https://doi.org/10.1007/s11626-024-00885-4","url":null,"abstract":"<p>Ror-family receptors, Ror1 and Ror2, are type I transmembrane proteins that possess an extracellular cysteine-rich domain, which is conserved throughout the Frizzled-family receptors and is a binding site for Wnt ligands. Both Ror1 and Ror2 function primarily as receptors or co-receptors for Wnt5a to activate the β-catenin-independent, non-canonical Wnt signaling, thereby regulating cell polarity, migration, proliferation, and differentiation depending on the context. Ror1 and Ror2 are expressed highly in many tissues during embryogenesis but minimally or scarcely in adult tissues, with some exceptions. In contrast, Ror1 and Ror2 are expressed in many types of cancers, and their high expression often contributes to the progression of the disease. Therefore, Ror1 and Ror2 have been proposed as potential targets for the treatment of the malignancies. In this review, we provide an overview of the regulatory mechanisms of Ror1/Ror2 expression and discuss how Wnt5a-Ror1/Ror2 signaling is mediated and regulated by their interacting proteins.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140576690","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}
Abdul Wazith M. J., Taju G., Abdul Majeed S., Mithra S., Nafeez Ahmed A., Badhusha A., Rajkumar V., Sahul Hameed A. S.
{"title":"A comparative study on targeted gene expression in zebrafish and its gill cell line exposed to chlorpyrifos","authors":"Abdul Wazith M. J., Taju G., Abdul Majeed S., Mithra S., Nafeez Ahmed A., Badhusha A., Rajkumar V., Sahul Hameed A. S.","doi":"10.1007/s11626-024-00892-5","DOIUrl":"https://doi.org/10.1007/s11626-024-00892-5","url":null,"abstract":"<p>Chlorpyrifos (CPF) is an organophosphorus-based insecticide, which is known to pose a serious risk to aquatic animals. However, the mechanisms of CPF toxicity in animals still remain unclear. The present investigation aimed to compare the potential effects of CPF in zebrafish (<i>Danio rerio</i>) and its gill cell line (<i>DrG</i> cells). Based on the in vivo study, the LC<sub>50</sub> was calculated as 18.03 µg/L and the chronic toxic effect of CPF was studied by exposing the fish to 1/10th (1.8 µg/L) and 1/5th (3.6 µg/L) of the LC<sub>50</sub> value. Morphological changes were observed in fish and <i>Dr</i>G cells which were exposed to sublethal concentrations of CPF. The results of MTT and NR assays showed significant decline in the survival of cells exposed to CPF at 96 h. The production of reactive oxygen species in <i>Dr</i>G cells and expression levels of antioxidant markers, inflammatory response genes (<i>cox2a</i> and <i>cox2b</i>), <i>cyp1a</i>, proapoptotic genes (<i>bax</i>), antiapoptotic gene (<i>bcl2</i>), apoptotic genes (<i>cas3</i> and <i>p53</i>), and neuroprotective gene (<i>ache</i>) were determined in vivo using zebrafish and in vitro using <i>DrG</i> cells after exposure to CPF. Significant changes were found in the ROS production (<i>Dr</i>G cells) and in the expression of inflammatory, proapoptotic, and apoptotic genes. This study showed that <i>DrG</i> cells are potential alternative tools to replace the use of whole fish for toxicological studies.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140576793","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":"Inhibition of circ_0073932 attenuates myocardial ischemia‒reperfusion injury via miR-493-3p/FAF1/JNK","authors":"Yang Su, Lili Zhao, Dongli Lei, Xiaoming Yang","doi":"10.1007/s11626-024-00900-8","DOIUrl":"https://doi.org/10.1007/s11626-024-00900-8","url":null,"abstract":"<p>Oxidative stress and apoptosis play crucial roles in myocardial ischemia‒reperfusion injury (MIRI). In this study, we investigated the role of circ_0073932 in MIRI as well as its molecular mechanism. A hypoxia/reoxygenation (H/R) cardiomyocyte model was established with H9C2 cardiomyocytes, and RT–qPCR was used to measure gene expression. We observed that circ_0073932 expression was abnormally increased in the H/R cardiomyocyte model and in blood samples from MIRI patients. Inhibition of circ_0073932 suppressed H/R-induced cell apoptosis, oxidative stress (ROS, LDH and MDA), and p-JNK expression. Dual luciferase reporter assays showed that circ_0073932 targeted the downregulation of miR-493-3p, and miR-493-3p targeted the downregulation of FAF1. Furthermore, si-circ_0073932, an miR-493-3p inhibitor, oe-FAF1, or si-FAF1 were transfected into H9C2 cardiomyocytes to investigate the roles of these factors in MIRI. Our results showed that compared with the H/R group, si-circ_0073932 inhibited H/R-induced cell apoptosis, oxidative stress (ROS, LDH and MDA), and p-JNK expression. These results were reversed by the miR-493-3p inhibitor or oe-FAF1. Finally, a rat model of MIRI was established, and si-circ_0073932 was administered. Inhibition of circ_0073932 reduced the area of myocardial infarction and decreased the levels of apoptosis and oxidative stress by inhibiting the JNK signaling pathway. Our study indicated that circ_0073932 mediates MIRI via miR-493-3p/FAF1/JNK in vivo and in vitro, revealing novel insights into the pathogenesis of MIRI and providing a new target for the clinical treatment of MIRI.</p><h3 data-test=\"abstract-sub-heading\">Graphic Abstract</h3><p>Suppression of circ_0073932 can inhibit myocardial apoptosis and regulate oxidative stress in MIRI through the miR-493-3p/FAF1/JNK</p>\u0000","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140602588","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}
Minping Zhang, Li Chen, Qunping Xu, Xiaohua Yang, Xiang Liu, Luanmei Liu
{"title":"Vitamin D3 reduces the symptoms of ovarian hyperstimulation syndrome in mice and inhibits the release of granulosa cell angiogenic factor through pentraxin 3","authors":"Minping Zhang, Li Chen, Qunping Xu, Xiaohua Yang, Xiang Liu, Luanmei Liu","doi":"10.1007/s11626-024-00898-z","DOIUrl":"https://doi.org/10.1007/s11626-024-00898-z","url":null,"abstract":"<p>It has been reported that the effective inhibition of vascular endothelial growth factor (VEGF) can prevent the progression of ovarian hyperstimulation syndrome (OHSS). The present study aimed to investigate the mechanism underlying the effect of vitamin D<sub>3</sub> (VD3) on OHSS in mouse models and granulosa cells. The effects of VD3 administration (16 and 24 IU) on ovarian permeability were determined using Evans blue. In addition, ovarian pathology, corpus luteum count, inflammatory responses, and hormone and VEGFA levels were assessed using pathological sections and ELISA. Molecular docking predicted that pentraxin 3 (PTX3) could be a potential target of VD3, and therefore, the effects of human chorionic gonadotropin (hCG) and VD3 as well as PTX3 overexpression on the production and secretion of VEGFA in granulosa cells were also investigated using western blotting and immunofluorescence. Twenty-four IU VD3 significantly reversed the increase in ovarian weight and permeability in mice with OHSS. Additionally, VD3 diminished congestion and the number of corpus luteum in the ovaries and reduced the secretion levels of inflammatory factors and those of estrogen and progesterone. Notably, VD3 downregulated VEGFA and CD31 in ovarian tissues, while the expression levels of PTX3 varied among different groups. Furthermore, VD3 restored the hCG-induced enhanced VEGFA and PTX3 expression levels in granulosa cells, whereas PTX3 overexpression abrogated the VD3-mediated inhibition of VEGFA production and secretion. The present study demonstrated that VD3 could inhibit the release of VEGFA through PTX3, thus supporting the beneficial effects of VD3 administration on ameliorating OHSS symptoms.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140576697","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}
Fernanda Becker Weber, Camila Leite Santos, Amanda da Silva, Izaviany Schmitz, Ester Rezena, Carlos-Alberto Gonçalves, André Quincozes-Santos, Larissa Daniele Bobermin
{"title":"Differences between cultured astrocytes from neonatal and adult Wistar rats: focus on in vitro aging experimental models.","authors":"Fernanda Becker Weber, Camila Leite Santos, Amanda da Silva, Izaviany Schmitz, Ester Rezena, Carlos-Alberto Gonçalves, André Quincozes-Santos, Larissa Daniele Bobermin","doi":"10.1007/s11626-024-00896-1","DOIUrl":"10.1007/s11626-024-00896-1","url":null,"abstract":"<p><p>Astrocytes play key roles regulating brain homeostasis and accumulating evidence has suggested that glia are the first cells that undergo functional changes with aging, which can lead to a decline in brain function. In this context, in vitro models are relevant tools for studying aged astrocytes and, here, we investigated functional and molecular changes in cultured astrocytes obtained from neonatal or adult animals submitted to an in vitro model of aging by an additional period of cultivation of cells after confluence. In vitro aging induced different metabolic effects regarding glucose and glutamate uptake, as well as glutamine synthetase activity, in astrocytes obtained from adult animals compared to those obtained from neonatal animals. In vitro aging also modulated glutathione-related antioxidant defenses and increased reactive oxygen species and cytokine release especially in astrocytes from adult animals. Interestingly, in vitro aged astrocytes from adult animals exposed to pro-oxidant, inflammatory, and antioxidant stimuli showed enhanced oxidative and inflammatory responses. Moreover, these functional changes were correlated with the expression of the senescence marker p21, cytoskeleton markers, glutamate transporters, inflammatory mediators, and signaling pathways such as nuclear factor κB (NFκB)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1). Alterations in these genes are remarkably associated with a potential neurotoxic astrocyte phenotype. Therefore, considering the experimental limitations due to the need for long-term maintenance of the animals for studying aging, astrocyte cultures obtained from adult animals further aged in vitro can provide an improved experimental model for understanding the mechanisms associated with aging-related astrocyte dysfunction.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140318190","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":"PRDX6 alleviated heart failure by inhibiting doxorubicin-induced ferroptosis through the JAK2/STAT1 pathway inactivation.","authors":"Jie Xiong, Rong Zhou, Xu Deng","doi":"10.1007/s11626-024-00889-0","DOIUrl":"10.1007/s11626-024-00889-0","url":null,"abstract":"<p><p>Peroxiredoxin 6 (PRDX6) is a protective biomarker associated with ferroptosis in heart failure (HF). This study investigated the specific mechanism of PRDX6 on doxorubicin (DOX)-induced ferroptosis in HF. Wistar rats and H9c2 cells were induced by DOX to construct HF models. Pathological changes and collagen deposition in myocardium were investigated using HE and Masson staining. PRDX6 levels, indexes of ferroptosis, and JAK2/STAT1 pathway were detected by qRT-PCR, Western blot, and biochemical kits. DOX promoted heart weight/body weight, increased inflammation and collagen deposition, increased PTGS2 and MDA levels, and decreased SLC7A11, GPX4, FTH1, and PRDX6 levels in myocardium. PRDX6 overexpression reduced PTGS2, MDA, Fe<sup>2+</sup>, and LDH levels, inhibited JAK2 and STAT1 phosphorylation, and increased SLC7A11, GPX4, and FTH1 levels in DOX-added H9c2 cells. RO8191 and erastin reversed the inhibition of PRDX6 on ferroptosis through the JAK2/STAT1 pathway. Overall, PRDX6 alleviated HF by inhibiting DOX-induced ferroptosis through the JAK2/STAT1 pathway inactivation.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140293437","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":"Eco-friendly green synthesis of N‑pyrazole amino chitosan using PEG-400 as an anticancer agent against gastric cancer cells via inhibiting EGFR.","authors":"Limin Zhang, Chunfeng Li","doi":"10.1007/s11626-024-00890-7","DOIUrl":"10.1007/s11626-024-00890-7","url":null,"abstract":"<p><p>The present study was conducted to develop a green process that provides access to the development of Schiff base derivatives of chitosan with the heterocyclic moiety as a novel class of anti-gastric cancer agent. In the present study, we have synthesized these derivatives by reacting various pyrazoles with chitosan using CAN in PEG400. The compounds were synthesized in 20 min in excellent yield by using CAN at 5% in PEG400 at 80°C in the shortest reaction time of 20 min. The PEG400 could be efficiently recycled for the three consecutive runs. The developed compounds were tested for EGFR-TK inhibition using a Kinase-Glo Plus luminescence kinase assay kit where they exhibited significant activity revealing compound 2d as the most potent analog, while other compounds showed mild to moderate inhibitory activity. MTT assay was conducted to determine the effect of the three most potent EGFR inhibitors (2b, 2c, and 2d) on the proliferation of gastric cancer cells (SGC-7901). The results showed compound 2d as the most potent anticancer agent against SGC7901 cells. The effect of compound 2d was also quantified on the apoptosis and cell phase of SGC7901 cells using flow cytometry assay at various concentrations ranging from 0, 10, 20, and 30 µM. Results suggest that compound 2d showed significant inhibition of SGC-7901 by inducing apoptosis and arresting G0/G1 cell phase. The western blot analysis also revealed that compound 2d significantly inhibited the overexpression of EGFR in SGC-7901 cells. The study successfully demonstrated the development of N‑pyrazole amino chitosan as a novel class of agent against gastric cancer via inhibition of EGFR.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140335510","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":"CDC-like kinase 3 deficiency aggravates hypoxia-induced cardiomyocyte apoptosis through AKT signaling pathway.","authors":"Xiue Ma, Liming Gao, Rucun Ge, Tianyou Yuan, Bowen Lin, Lixiao Zhen","doi":"10.1007/s11626-024-00886-3","DOIUrl":"10.1007/s11626-024-00886-3","url":null,"abstract":"<p><p>Hypoxia-induced cardiomyocyte apoptosis is one major pathological change of acute myocardial infarction (AMI), but the underlying mechanism remains unexplored. CDC-like kinase 3 (CLK3) plays crucial roles in cell proliferation, migration and invasion, and nucleotide metabolism, however, the role of CLK3 in AMI, especially hypoxia-induced apoptosis, is largely unknown. The expression of CLK3 was elevated in mouse myocardial infarction (MI) models and neonatal rat ventricular myocytes (NRVMs) under hypoxia. Furthermore, CLK3 knockdown significantly promoted apoptosis and inhibited NRVM survival, while CLK3 overexpression promoted NRVM survival and inhibited apoptosis under hypoxic conditions. Mechanistically, CLK3 regulated the phosphorylation status of AKT, a key player in the regulation of apoptosis. Furthermore, overexpression of AKT rescued hypoxia-induced apoptosis in NRVMs caused by CLK3 deficiency. Taken together, CLK3 deficiency promotes hypoxia-induced cardiomyocyte apoptosis through AKT signaling pathway.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140027998","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":"Influence of the storage conditions of embryo culture media on mouse development","authors":"Marten Davenport, Yingming Wang, Lev M. Fedorov","doi":"10.1007/s11626-024-00884-5","DOIUrl":"https://doi.org/10.1007/s11626-024-00884-5","url":null,"abstract":"<p>The culture of preimplantation embryos in vitro is an important method for human and mouse reproductive technology. This study aims to investigate the influence of different conditions of culture media on the preimplantation stage of mouse embryos cultured in vitro, and monitor the post-implantation development of new mice after embryo transfer to surrogate females. We demonstrated here that mouse embryos cultured in vitro in fresh M16, KSOM, Global, and HTF embryo culture media from one cell to the blastocyst stage and the subsequent embryo transfer to surrogate females are able to proceed through post-implantation development and, after birth, develop into healthy mice. However, culture of embryos in differently aged media shows various (often unpredictable) results. To find the optimal storage conditions of culture media, we suggest that the freezing and long-term storage of these media at − 80°C will not influence the quality of the media. To test this hypothesis, we grew embryos from one cell to blastocysts in vitro in the selected media after thawing and subsequently transferring them to surrogate females. Embryo culture in these four media after thawing does not affect preimplantation and postnatal mouse development. Thus, we have shown that storage of embryo culture media at low temperature (− 80°C) does not impact the quality of the media, and subsequently, it can be used for the culture of embryos for the full preimplantation period, the same as in fresh media.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140167659","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}
Donghua Liu, Wang Tang, Dongming Tang, Haixia Yan, Feng Jiao
{"title":"Ocu-miR-10a-5p promotes the chondrogenic differentiation of rabbit BMSCs by targeting BTRC-mediated Wnt/β-catenin signaling pathway","authors":"Donghua Liu, Wang Tang, Dongming Tang, Haixia Yan, Feng Jiao","doi":"10.1007/s11626-024-00888-1","DOIUrl":"https://doi.org/10.1007/s11626-024-00888-1","url":null,"abstract":"<p>MicroRNAs (miRNAs) play an important role in articular cartilage damage in osteoarthritis (OA). However, the biological role of miRNAs in the chondrogenic differentiation of bone marrow mesenchymal stem cell (BMSC) remains largely unclear. Rabbit bone marrow mesenchymal stem cells (rBMSCs) were isolated, cultured, and identified. Afterwards, rBMSCs were induced to chondrogenic differentiation, examined by Alcian Blue staining. Differentially expressed miRNAs were identified in rBMSCs between induced and non-induced groups by miRNA sequencing analysis, part of which was validated via PCR assay. Cell viability and apoptosis were assessed by CCK-8 assay and Hoechst staining. Saffron O staining was utilized to assess chondrocyte hyperplasia. The expression of specific chondrogenic markers, including COL2A1, SOX9, Runx2, MMP-13, Aggrecan, and BMP-2, were measured at mRNA and protein levels. The association between beta-transducin repeat containing E3 ubiquitin protein ligase (BTRC) and miR-10a-5p in the miRNA family from rabbit (ocu-miR-10a-5p) was determined by luciferase reporter assay. A total of 76 differentially expressed miRNAs, including 52 downregulated and 24 upregulated miRNAs, were identified in rBMSCs from the induced group. Inhibition of ocu-miR-10a-5p suppressed rBMSC viability and chondrogenic differentiation, as well as downregulated the expression of β-catenin, SOX9, COL2A1, MMP-13, and Runx2. BTRC was predicted and confirmed as a target of ocu-miR-10a-5p. Overexpression of BTRC rescued the promoting impacts of overexpressed ocu-miR-10a-5p on chondrogenic differentiation of rBMSCs and β-catenin expression. Taken together, our data suggested that ocu-miR-10a-5p facilitated rabbit BMSC survival and chondrogenic differentiation by activating Wnt/β-catenin signaling through BTRC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140167655","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}