Cell and Tissue Research最新文献_第7页

Rheb1 is required for limb growth through regulating chondrogenesis in growth plate. 肢体生长需要 Rheb1 通过调节生长板中的软骨形成。

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-03-01 Epub Date: 2024-01-23 DOI: 10.1007/s00441-024-03861-2

Yuwei Zhang, Jiaxin Wen, Ruijun Lai, Jiahuan Zhang, Kai Li, Yue Zhang, Anling Liu, Xiaochun Bai

{"title":"Rheb1 is required for limb growth through regulating chondrogenesis in growth plate.","authors":"Yuwei Zhang, Jiaxin Wen, Ruijun Lai, Jiahuan Zhang, Kai Li, Yue Zhang, Anling Liu, Xiaochun Bai","doi":"10.1007/s00441-024-03861-2","DOIUrl":"10.1007/s00441-024-03861-2","url":null,"abstract":"Ras homology enriched in the brain (Rheb) is well established as a critical regulator of cell proliferation and differentiation in response to growth factors and nutrients. However, the role of Rheb1 in limb development remains unknown. Here, we found that Rheb1 was dynamically expressed during the proliferation and differentiation of chondrocytes in the growth plate. Given that Prrx1+ limb-bud-like mesenchymal cells are the source of limb chondrocytes and are essential for endochondral ossification, we conditionally deleted Rheb1 using Prrx1-Cre and found a limb dwarfism in Prrx1-Cre; Rheb1fl/fl mice. Normalized to growth plate height, the conditional knockout (cKO) mice exhibited a significant decrease in column count of proliferative zones which was increased in hypertrophic zones resulting in decreased growth plate size, indicating abnormal endochondral ossification. Interestingly, although Rheb1 deletion profoundly inhibited the transcription factor Sox9 in limb cartilage; levels of runx2 and collagen type 2 were both increased. These novel findings highlight the essential role of Rheb1 in limb growth and indicate a complex regulation of Rheb1 in chondrocyte proliferation and differentiation.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10904423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139520006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Suppression of MALAT1 promotes human synovial mesenchymal stem cells enhance chondrogenic differentiation and prevent osteoarthritis of the knee in a rat model via regulating miR-212-5p/MyD88 axis. 通过调节 miR-212-5p/MyD88 轴，抑制 MALAT1 可促进人滑膜间充质干细胞增强软骨分化并预防大鼠模型中的膝骨关节炎。

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-03-01 Epub Date: 2024-01-31 DOI: 10.1007/s00441-024-03863-0

Zhengyu Gao, Cuicui Guo, Shuai Xiang, Haining Zhang, Yingzhen Wang, Hao Xu

{"title":"Suppression of MALAT1 promotes human synovial mesenchymal stem cells enhance chondrogenic differentiation and prevent osteoarthritis of the knee in a rat model via regulating miR-212-5p/MyD88 axis.","authors":"Zhengyu Gao, Cuicui Guo, Shuai Xiang, Haining Zhang, Yingzhen Wang, Hao Xu","doi":"10.1007/s00441-024-03863-0","DOIUrl":"10.1007/s00441-024-03863-0","url":null,"abstract":"Osteoarthritis (OA) is one of the most common diseases of the skeleton. Long non-coding RNAs (lncRNAs) are emerging as key players in OA pathogenesis. This work sets out to determine the function of lncRNA MALAT1 in OA and the mechanisms by which it does so. Mesenchymal stem cells isolated from the human synovial membrane are called hSMSCs. The hSMSCs' surface markers were studied using flow cytometry. To determine whether or not hSMSC might differentiate, researchers used a number of different culture settings and labeling techniques. The expression levels of associated genes and proteins were determined using quantitative real-time polymerase chain reaction (RT-qPCR), western blotting (WB), and immunostaining. A dual luciferase reporter experiment and RNA immunoprecipitation (RIP) test demonstrated the direct association between miR-212-5p and MALAT1 or MyD88. MALAT1 was downregulated during the chondrogenic differentiation of hSMSCs, and underexpression of MALAT1 promotes chondrogenesis in hSMSCs. Using dual luciferase reporter and RIP assays facilitated the identification of MALAT1 as a competitive endogenous RNA (ceRNA) that sequesters miR-212-5p. Additionally, the expression of MYD88 was regulated by MALAT1 through direct binding with miR-212-5p. Significantly, the effects of MALAT1 on the chondrogenic differentiation of hSMSCs were counteracted by miR-212-5p/MYD88. Furthermore, our in vivo investigation revealed that the inhibition of MALAT1 mitigated osteoarthritis progression in rat models. In conclusion, the promotion of chondrogenic differentiation in hSMSCs and the protective effect on cartilage tissue in OA can be achieved by suppressing MALAT1, which regulates the miR-212-5p/MyD88 axis.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139641696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Localization of nitric oxide-producing hemocytes in Aedes and Culex mosquitoes infected with bacteria. 感染细菌的伊蚊和库蚊中产生一氧化氮的血细胞的定位。

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-03-01 Epub Date: 2024-01-19 DOI: 10.1007/s00441-024-03862-1

Stella Bergmann, Emily Graf, Pascal Hoffmann, Stefanie C Becker, Michael Stern

{"title":"Localization of nitric oxide-producing hemocytes in Aedes and Culex mosquitoes infected with bacteria.","authors":"Stella Bergmann, Emily Graf, Pascal Hoffmann, Stefanie C Becker, Michael Stern","doi":"10.1007/s00441-024-03862-1","DOIUrl":"10.1007/s00441-024-03862-1","url":null,"abstract":"Mosquitoes are significant vectors of various pathogens. Unlike vertebrates, insects rely solely on innate immunity. Hemocytes play a crucial role in the cellular part of the innate immune system. The gaseous radical nitric oxide (NO) produced by hemocytes acts against pathogens and also functions as a versatile transmitter in both the immune and nervous systems, utilizing cyclic guanosine monophosphate (cGMP) as a second messenger. This study conducted a parallel comparison of NO synthase (NOS) expression and NO production in hemocytes during Escherichia coli K12 infection in four vector species: Aedes aegypti, Aedes albopictus, Culex pipiens molestus, and Culex pipiens quinquefasciatus. Increased NOS expression by NADPH diaphorase (NADPHd) staining and NO production by immunofluorescence against the by-product L-citrulline were observed in infected mosquito hemocytes distributed throughout the abdomens. NADPHd activity and citrulline labeling were particularly found in periostial hemocytes near the heart, but also on the ventral nerve chord (VNC). Pericardial cells of Ae. aegypti and Cx. p. molestus showed increased citrulline immunofluorescence, suggesting their involvement in the immune response. Oenocytes displayed strong NADPHd and citrulline labeling independent of infection status. This comparative study, consistent with findings in other species, suggests a widespread phenomenon of NO's role in hemocyte responses during E. coli infection. Found differences within and between genera highlight the importance of species-specific investigations.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10904431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139490921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Yap/Taz activity is associated with increased expression of phosphoglycerate dehydrogenase that supports myoblast proliferation. Yap/Taz 活性与支持肌母细胞增殖的磷酸甘油酸脱氢酶的表达增加有关。

IF 3.2 3区生物学

Cell and Tissue Research Pub Date : 2024-03-01 Epub Date: 2024-01-06 DOI: 10.1007/s00441-023-03851-w

Marius Meinhold, Sander Verbrugge, Andi Shi, Martin Schönfelder, Lore Becker, Richard T Jaspers, Peter S Zammit, Henning Wackerhage

{"title":"Yap/Taz activity is associated with increased expression of phosphoglycerate dehydrogenase that supports myoblast proliferation.","authors":"Marius Meinhold, Sander Verbrugge, Andi Shi, Martin Schönfelder, Lore Becker, Richard T Jaspers, Peter S Zammit, Henning Wackerhage","doi":"10.1007/s00441-023-03851-w","DOIUrl":"10.1007/s00441-023-03851-w","url":null,"abstract":"In skeletal muscle, the Hippo effector Yap promotes satellite cell, myoblast, and rhabdomyoblast proliferation but prevents myogenic differentiation into multinucleated muscle fibres. We previously noted that Yap drives expression of the first enzyme of the serine biosynthesis pathway, phosphoglycerate dehydrogenase (Phgdh). Here, we examined the regulation and function of Phgdh in satellite cells and myoblasts and found that Phgdh protein increased during satellite cell activation. Analysis of published data reveal that Phgdh mRNA in mouse tibialis anterior muscle was highly expressed at day 3 of regeneration after cardiotoxin injection, when markers of proliferation are also robustly expressed and in the first week of synergist-ablated muscle. Finally, siRNA-mediated knockdown of PHGDH significantly reduced myoblast numbers and the proliferation rate. Collectively, our data suggest that Phgdh is a proliferation-enhancing metabolic enzyme that is induced when quiescent satellite cells become activated.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10904560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139110754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Long noncoding RNA XIST inhibition promotes Leydig cell apoptosis by acting as a competing endogenous RNA for microRNA-145a-5p that targets SIRT1 in late-onset hypogonadism. 在晚发性性腺功能减退症中，长非编码 RNA XIST 作为靶向 SIRT1 的 microRNA-145a-5p 的竞争性内源性 RNA，其抑制作用可促进睾丸细胞凋亡。

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-03-01 Epub Date: 2024-02-14 DOI: 10.1007/s00441-024-03860-3

Jing Wang, Yiqiong Yang, Yang Xu, Zhipeng Xu, Xiaozhi Zhao, Ruipeng Jia, Yutian Dai

{"title":"Long noncoding RNA XIST inhibition promotes Leydig cell apoptosis by acting as a competing endogenous RNA for microRNA-145a-5p that targets SIRT1 in late-onset hypogonadism.","authors":"Jing Wang, Yiqiong Yang, Yang Xu, Zhipeng Xu, Xiaozhi Zhao, Ruipeng Jia, Yutian Dai","doi":"10.1007/s00441-024-03860-3","DOIUrl":"10.1007/s00441-024-03860-3","url":null,"abstract":"Leydig cell (LCs) apoptosis is responsible for decreased serum testosterone levels during late-onset hypogonadism (LOH). Our study was designed to illustrate the regulatory effect of lncRNA XIST on LCs and to clarify its molecular mechanism of action in LOH. The Leydig cells (TM3) was treated by 300 μM H2O2 for 8 h to establish Leydig cell oxidative stress model in vitro. The expression levels of lncRNA XIST in the testicular tissues of patients with LOH were measured using fluorescence in situ hybridization (FISH). The interaction between lncRNA XIST/SIRT1 and miR-145a-5p was assessed using starBase and dual-luciferase reporter gene assays. Apoptotic cells and Caspase3 activity were determined by flow cytometry (FCM) assay. Testosterone concentration was determined by ELISA. Moreover, histological assessment of testicles in mice was performed by using HE staining and the TUNEL assay was used to determine apoptosis. We found that the lncRNA XIST was downregulated in the testicular tissues of LOH patients and mice and in H2O2-induced TM3 cells. XIST siRNA significantly promoted apoptosis, enhanced Caspase3 activity and reduced testosterone levels in H2O2-stimulated TM3 cells. Further studies showed that the miR-145a-5p inhibitor reversed the effect of XIST-siRNA on H2O2-induced Leydig cell apoptosis. MiR-145a-5p negatively regulated SIRT1 expression, and SIRT1-siRNA reversed the effects of the miR-145a-5p inhibitor on H2O2 stimulated TM3 cells. The in vivo experiments indicated that silencing of the lncRNA XIST aggravated LOH symptoms in mice. Inhibition of lncRNA XIST induces Leydig cell apoptosis through the miR-145a-5p/SIRT1 axis in the progression of LOH.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139729101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tissue distribution of cysteine string protein/DNAJC5 in C. elegans analysed by CRISPR/Cas9-mediated tagging of endogenous DNJ-14 通过 CRISPR/Cas9 介导的内源性 DNJ-14 标记分析半胱氨酸串联蛋白/DNAJC5 在优雅子中的组织分布情况

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-02-26 DOI: 10.1007/s00441-024-03875-w

{"title":"Tissue distribution of cysteine string protein/DNAJC5 in C. elegans analysed by CRISPR/Cas9-mediated tagging of endogenous DNJ-14","authors":"","doi":"10.1007/s00441-024-03875-w","DOIUrl":"https://doi.org/10.1007/s00441-024-03875-w","url":null,"abstract":"<h3>Abstract</h3> Cysteine string protein (CSP) is a member of the DnaJ/Hsp40 family of molecular chaperones. CSP is enriched in neurons, where it mainly localises to synaptic vesicles. Mutations in CSP-encoding genes in flies, worms, mice and humans result in neuronal dysfunction, neurodegeneration and reduced lifespan. Most attention has therefore focused on CSP’s neuronal functions, although CSP is also expressed in non-neuronal cells. Here, we used genome editing to fluorescently tag the Caenorhabditis elegans CSP orthologue, dnj-14, to identify which tissues preferentially express CSP and hence may contribute to the observed mutant phenotypes. Replacement of dnj-14 with wrmScarlet caused a strong chemotaxis defect, as seen with other dnj-14 null mutants. In contrast, inserting the reporter in-frame to create a DNJ-14-wrmScarlet fusion protein had no effect on chemotaxis, indicating that C-terminal tagging does not impair DNJ-14 function. WrmScarlet fluorescence appeared most obvious in the intestine, head/pharynx, spermathecae and vulva/uterus in the reporter strains, suggesting that DNJ-14 is preferentially expressed in these tissues. Crossing the DNJ-14-wrmScarlet strain with GFP marker strains confirmed the intestinal and pharyngeal expression, but only a partial overlap with neuronal GFP was observed. DNJ-14-wrmScarlet fluorescence in the intestine was increased in response to starvation, which may be relevant to mammalian CSPα’s role in microautophagy. DNJ-14’s enrichment in worm reproductive tissues (spermathecae and vulva/uterus) parallels the testis-specific expression of CSPβ and CSPγ isoforms in mammals. Furthermore, CSPα messenger RNA is highly expressed in the human proximal digestive tract, suggesting that CSP may have a conserved, but overlooked, function within the gastrointestinal system.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139968120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bone morphogenetic protein 6 (BMP6) antagonises experimental proliferative vitreoretinopathy established by TGF-β2 stimulation in retinal pigment epithelial cells through modulation of the p38 and JNK MAPK pathways 骨形态发生蛋白 6 (BMP6) 通过调节 p38 和 JNK MAPK 通路，拮抗视网膜色素上皮细胞在 TGF-β2 刺激下发生的实验性增殖性玻璃体视网膜病变

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-02-26 DOI: 10.1007/s00441-024-03870-1

Xuan Liu, Ming Liu, Li Chen

{"title":"Bone morphogenetic protein 6 (BMP6) antagonises experimental proliferative vitreoretinopathy established by TGF-β2 stimulation in retinal pigment epithelial cells through modulation of the p38 and JNK MAPK pathways","authors":"Xuan Liu, Ming Liu, Li Chen","doi":"10.1007/s00441-024-03870-1","DOIUrl":"https://doi.org/10.1007/s00441-024-03870-1","url":null,"abstract":"The formation of the epiretinal fibrotic membrane by retinal pigment epithelial (RPE) cells is a primary pathological change for proliferative vitreoretinopathy (PVR). Bone morphogenetic protein 6 (BMP6) is an antifibrogenic factor in various cells. To date, it is still unknown whether BMP6 can interfere with the fibrogenesis of RPE cells during the progression of PVR. This work aimed to address the relationship between BMP6 and transforming growth factor-β2 (TGF-β2)-elicited fibrogenesis of RPE cells, an experimental model for studying PVR in vitro. The BMP6 level was down-regulated, while the TGF-β2 level was up-regulated in the vitreous humor of PVR patients. The BMP6 level was down-regulated in human RPE cells challenged with TGF-β2. The treatment of RPE cells with TGF-β2 resulted in significant increases in proliferation, migration, epithelial-to-mesenchymal transition (EMT), and extracellular matrix (ECM) remodelling. These effects were found to be inhibited by the overexpression of BMP6 or exacerbated by the knockdown of BMP6. BMP6 overexpression reduced the phosphorylation of p38 and JNK in TGF-β2-stimulated RPE cells, while BMP6 knockdown showed the opposite effects. The inhibition of p38 or JNK partially reversed the BMP6-silencing-induced promoting effects on TGF-β2-elicited fibrogenesis in RPE cells. Taken together, BMP6 demonstrates the ability to counteract the proliferation, migration, EMT, and ECM remodelling of RPE cells induced by TGF-β2. This is achieved through the regulation of the p38 and JNK MAPK pathways. These findings imply a potential connection between BMP6 and PVR, and highlight the potential application of BMP6 in therapeutic interventions for PVR.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139967551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Structure of putative epidermal sensory receptors in an acoel flatworm, Praesagittifera naikaiensis 鳗扁虫（Praesagittifera naikaiensis）假定表皮感觉受体的结构

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-02-02 DOI: 10.1007/s00441-024-03865-y

{"title":"Structure of putative epidermal sensory receptors in an acoel flatworm, Praesagittifera naikaiensis","authors":"","doi":"10.1007/s00441-024-03865-y","DOIUrl":"https://doi.org/10.1007/s00441-024-03865-y","url":null,"abstract":"<h3>Abstract</h3> Acoel flatworms possess epidermal sensory-receptor cells on their body surfaces and exhibit behavioral repertoires such as geotaxis and phototaxis. Acoel epidermal sensory receptors should be mechanical and/or chemical receptors; however, the mechanisms of their sensory reception have not been elucidated. We examined the three-dimensional relationship between epidermal sensory receptors and their innervation in an acoel flatworm, Praesagittifera naikaiensis. The distribution of the sensory receptors was different between the ventral and dorsal sides of worms. The nervous system was mainly composed of a peripheral nerve net, an anterior brain, and three pairs of longitudinal nerve cords. The nerve net was located closer to the body surface than the brain and the nerve cords. The sensory receptors have neural connections with the nerve net in the entire body of worms. We identified five homologs of polycystic kidney disease (PKD): PKD1-1, PKD1-2, PKD1-3, PKD1-4, and, PKD2, from the P. naikaiensis genome. All of these PKD genes were implied to be expressed in the epidermal sensory receptors of P. naikaiensis. PKD1-1 and PKD2 were dispersed across the entire body of worms. PKD1-2, PKD1-3, and PKD1-4 were expressed in the anterior region of worms. PKD1-4 was also expressed around the mouth opening. Our results indicated that P. naikaiensis possessed several types of epidermal sensory receptors to convert various environmental stimuli into electrical signals via the PKD channels and transmit the signals to afferent nerve and/or effector cells.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139663654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

METTL3 promotes microglial inflammation via MEF2C in spinal cord injury. METTL3通过MEF2C促进脊髓损伤中的小胶质细胞炎症

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-02-01 Epub Date: 2024-01-05 DOI: 10.1007/s00441-023-03855-6

Dongliang Wang, Wei Qian, Duanrong Wu, Ya Wu, Kun Lu, Guoyou Zou

{"title":"METTL3 promotes microglial inflammation via MEF2C in spinal cord injury.","authors":"Dongliang Wang, Wei Qian, Duanrong Wu, Ya Wu, Kun Lu, Guoyou Zou","doi":"10.1007/s00441-023-03855-6","DOIUrl":"10.1007/s00441-023-03855-6","url":null,"abstract":"Spinal cord injury (SCI) is a significant contributor to disability in contemporary society, resulting in substantial psychological and economic burdens for patients and their family. Microglia-mediated inflammation is an important factor affecting the nerve repair of SCI patients. N6-methyladenosine (m6A) is a prevalent epigenetic modification in mammals, which shows a strong association with inflammation. However, the mechanism of m6A modification regulating microglia-mediated inflammation is still unclear. Here, we observed that METTL3, a m6A methylase, was increased in SCI mice and lipopolysaccharide (LPS)-exposed BV2 cells. Knockdown of METTL3 inhibited the increased expression of iNOS and IL-1β induced by LPS in vitro. Subsequently, MEF2C, myocyte-specific enhancer factor 2C, was decreased in SCI mice and LPS-exposed BV2 cells. Knockdown of MEF2C promoted the expression of iNOS and IL-1β. Sequence analysis showed that there were multiple highly confident m6A modification sites on the MEF2C mRNA. METTL3 antibody could pull down a higher level of MEF2C mRNA than the IgG in RNA binding protein immunoprecipitation assay. Knockdown of METTL3 promoted MEF2C protein expression and MEF2C mRNA expression, accompanied by a reduced m6A modification level on the MEF2C mRNA. Knockdown of MEF2C inhibited the anti-inflammatory effect of METTL3 siRNA. Our results suggest that METTL3 promotes microglia inflammation via regulating MEF2C mRNA m6A modification induced by SCI and LPS treatment.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139097409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neurotoxic stimulation alters prosaposin levels in the salivary systems of rats. 神经毒性刺激会改变大鼠唾液系统中的丙磺舒水平。

IF 3.6 3区生物学

Cell and Tissue Research Pub Date : 2024-02-01 Epub Date: 2023-12-12 DOI: 10.1007/s00441-023-03847-6

Farzana Khan, Sakirul Khan, Hiroaki Nabeka, Hitomi Mimuro, Akira Nishizono, Fumihiko Hamada, Seiji Matsuda

{"title":"Neurotoxic stimulation alters prosaposin levels in the salivary systems of rats.","authors":"Farzana Khan, Sakirul Khan, Hiroaki Nabeka, Hitomi Mimuro, Akira Nishizono, Fumihiko Hamada, Seiji Matsuda","doi":"10.1007/s00441-023-03847-6","DOIUrl":"10.1007/s00441-023-03847-6","url":null,"abstract":"Prosaposin (PSAP), a potent neurotrophic factor, is found in neuronal and non-neuronal tissues and various biological fluids. Neuropathological conditions often alter PSAP production in neural tissues. However, little is known about its alterations in non-neural tissues, particularly in the salivary glands, which are natural reservoirs of various neurotrophic factors. In this study, we explored whether neurotoxic stimulation by kainic acid (KA), a glutamate analog, altered PSAP levels in the salivary system of rats. The results revealed that KA injection did not alter total saliva production. However, KA-induced neurotoxic stimulation significantly increased the PSAP level in the secreted saliva but decreased it in the serum. In addition, KA-induced elevated immunoreactivities of PSAP and its receptors have been observed in the granular convoluted tubule (GCT) cells of the submandibular gland (SMG), a major salivary secretory organ. Indeed, a large number of PSAP-expressing immunogold particles were observed in the secretory granules of the SMG. Furthermore, KA-induced overexpression of PSAP was co-localized with secretogranin in secretory acini (mostly in GCT cells) and the ductal system of the SMG, suggesting the release of excess PSAP from the salivary glands into the oral cavity. In conclusion, the salivary system produces more PSAP during neurotoxic conditions, which may play a protective role in maintaining the secretory function of the salivary glands and may work in distant organs.","PeriodicalId":9712,"journal":{"name":"Cell and Tissue Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138794597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0