Journal of Cellular Physiology最新文献_第2页

A combination of major histocompatibility complex (MHC) I overexpression and type I interferon induce mitochondrial dysfunction in human skeletal myoblasts. 主要组织相容性复合体（MHC）Ⅰ过表达和Ⅰ型干扰素共同诱导人类骨骼肌母细胞线粒体功能障碍。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-09 DOI: 10.1002/jcp.31458

Anastasia Thoma, Razan Alomosh, Holly L Bond, Tania Akter-Miah, Nasser Al-Shanti, Hans Degens, Vanja Pekovic-Vaughan, Adam P Lightfoot

{"title":"A combination of major histocompatibility complex (MHC) I overexpression and type I interferon induce mitochondrial dysfunction in human skeletal myoblasts.","authors":"Anastasia Thoma, Razan Alomosh, Holly L Bond, Tania Akter-Miah, Nasser Al-Shanti, Hans Degens, Vanja Pekovic-Vaughan, Adam P Lightfoot","doi":"10.1002/jcp.31458","DOIUrl":"https://doi.org/10.1002/jcp.31458","url":null,"abstract":"The overexpression of major histocompatibility complex (MHC) I on the surface of muscle fibers is a characteristic hallmark of the idiopathic inflammatory myopathies (IIMs), collectively termed myositis. Alongside MHC-I overexpression, subtypes of myositis, display a distinct type I interferon (IFN) signature. This study examined the combinational effects of elevated MHC-I and type I IFNs (IFNα/β) on mitochondrial function, as mitochondrial dysfunction is often seen in IIMs. Human skeletal muscle myoblasts were transfected with an MHC-I isoform using the mammalian HLA-A2/Kb vector. Mitochondrial respiration, mitochondrial membrane potential, and reactive oxygen/nitrogen species generation were assessed with or without IFNα and IFNβ. We show that MHC-I overexpression in human skeletal muscle myoblasts led to decreased basal glycolysis and mitochondrial respiration, cellular spare respiratory capacity, adenosine triphosphate-linked respiration, and an increased proton leak, which were all exaggerated by type I IFNs. Mitochondrial membrane depolarization was induced by MHC-I overexpression both in absence and presence of type I IFNs. Human myoblasts overexpressing MHC-I showed elevated nitric oxide generation that was abolished when combined with IFN. MHC-I on its own did not result in an increased reactive oxygen species (ROS) production, but IFN on their own, or combined with MHC-I overexpression did induce elevated ROS generation. Surprisingly, we observed no gross changes in mitochondrial reticular structure or markers of mitochondrial dynamics. We present new evidence that MHC-I overexpression and type I IFNs aggravate the effects each has on mitochondrial function in human skeletal muscle cells, providing novel insights into their mechanisms of action and suggesting important implications in the further study of myositis pathogenesis.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Investigation into the significant role of dermal-epidermal interactions in skin ageing utilising a bioengineered skin construct. 利用一种生物工程皮肤结构，研究真皮-表皮相互作用在皮肤老化中的重要作用。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-08 DOI: 10.1002/jcp.31463

Lydia Costello, Kirsty Goncalves, Paola De Los Santos Gomez, Ben Hulette, Teresa Dicolandrea, Michael J Flagler, Robert Isfort, John Oblong, Charlie Bascom, Stefan Przyborski

{"title":"Investigation into the significant role of dermal-epidermal interactions in skin ageing utilising a bioengineered skin construct.","authors":"Lydia Costello, Kirsty Goncalves, Paola De Los Santos Gomez, Ben Hulette, Teresa Dicolandrea, Michael J Flagler, Robert Isfort, John Oblong, Charlie Bascom, Stefan Przyborski","doi":"10.1002/jcp.31463","DOIUrl":"https://doi.org/10.1002/jcp.31463","url":null,"abstract":"Increased prevalence of skin ageing is a growing concern due to an ageing global population and has both sociological and psychological implications. The use of more clinically predictive in vitro methods for dermatological research is becoming commonplace due to initiatives and the cost of clinical testing. In this study, we utilise a well-defined and characterised bioengineered skin construct as a tool to investigate the cellular and molecular dynamics involved in skin ageing from a dermal perspective. Through incorporation of ageing fibroblasts into the dermal compartment we demonstrate the significant impact of dermal-epidermal crosstalk on the overlying epidermal epithelium. We characterise the paracrine nature of dermal-epidermal communication and the impact this has during skin ageing. Soluble factors, such as inflammatory cytokines released as a consequence of senescence associated secretory phenotype (SASP) from ageing fibroblasts, are known to play a pivotal role in skin ageing. Here, we demonstrate their effect on epidermal morphology and thickness, but not keratinocyte differentiation or tissue structure. Through a novel in vitro strategy utilising bioengineered tissue constructs, this study offers a unique reductionist approach to study epidermal and dermal compartments in isolation and tandem.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

RETRACTION: Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis. 回放：通过经皮损伤诱发腰椎面关节骨关节炎，建立下背部疼痛的实验动物模型。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31455

{"title":"RETRACTION: Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis.","authors":"","doi":"10.1002/jcp.31455","DOIUrl":"https://doi.org/10.1002/jcp.31455","url":null,"abstract":"Retraction: J.-S. Kim, K. Ahmadinia, X. Li, J. L. Hamilton, S. Andrews, C. A. Haralampus, G. Xiao, H.-M. Sohn, J.-W. You, Y.-S. Seo, G. S. Stein, A. J. Van Wijnen, S.-G. Kim, and H.-J. Im, \"Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis,\" Journal of Cellular Physiology 230, no. 11 (2015): 2837-2847, https://doi.org/10.1002/jcp.25015. The above article, published online on 9 April 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, the journal has been made aware of discrepancies in the reported sample sizes for each of the three experimental groups in Figure 4A, with the indicated numbers exceeding the actual sample sizes. Additionally, image elements of the experimental data in Figure 7A and B were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Taurine reduces glycolysis of pig skeletal muscle by inhibiting HIF-1α signaling. 牛磺酸通过抑制 HIF-1α 信号传导减少猪骨骼肌的糖酵解。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31461

Xiaoling Chen, An Wenting, Huang Zhiqing, Gang Jia, Hua Zhao

{"title":"Taurine reduces glycolysis of pig skeletal muscle by inhibiting HIF-1α signaling.","authors":"Xiaoling Chen, An Wenting, Huang Zhiqing, Gang Jia, Hua Zhao","doi":"10.1002/jcp.31461","DOIUrl":"https://doi.org/10.1002/jcp.31461","url":null,"abstract":"The aim of this study was to investigate the effect of taurine on skeletal muscle glycolysis in pigs. The results showed that dietary supplementation of taurine significantly reduced the activities of hexokinase (HK), phosphofructose kinase (PFK), and pyruvate kinase (PK) in finishing pigs. Meanwhile, taurine reduced the protein and mRNA expression levels of hypoxia inducible factor 1α (HIF-1α) and the mRNA expression of glycolytic enzyme related genes (such as HK type II, HK Ⅱ; pyruvate kinase M2, PKM2; lactate dehydrogenase A, LDHA). In addition, taurine reduced the expression of HIF-1α, lactate content, and the expression of glycolysis related genes in porcine myotubes. These results suggest that taurine may regulate glycolysis in skeletal muscle of finishing pigs through the HIF-1α signaling pathway. To further investigate the mechanism by which taurine affects skeletal glycolysis, HIF-1α activator dimethyloxalyl glycine (DMOG) was used to treat porcine myotubes, our results showed that DMOG significantly increased the protein and mRNA expression levels of HIF-1α, lactate content, and glycolytic enzyme (HK, PFK, PK, and LDH) activity, but taurine treatment significantly inhibited this effect. Taken together, these results of in vivo and in vitro experiments revealed that taurine reduces skeletal muscle glycolysis by inhibiting HIF-1α signaling.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Compensatory reactions of B cells in response to chronic HIV-1 Tat exposure. B 细胞对长期暴露于 HIV-1 Tat 的补偿反应

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31459

Anna A Valyaeva, Maria A Tikhomirova, Junyi Feng, Anastasia A Zharikova, Daria M Potashnikova, Yana R Musinova, Andrey A Mironov, Yegor S Vassetzky, Eugene V Sheval

{"title":"Compensatory reactions of B cells in response to chronic HIV-1 Tat exposure.","authors":"Anna A Valyaeva, Maria A Tikhomirova, Junyi Feng, Anastasia A Zharikova, Daria M Potashnikova, Yana R Musinova, Andrey A Mironov, Yegor S Vassetzky, Eugene V Sheval","doi":"10.1002/jcp.31459","DOIUrl":"https://doi.org/10.1002/jcp.31459","url":null,"abstract":"Patients infected with human immunodeficiency virus-1 (HIV-1) have an increased incidence of B-cell lymphoma, even though HIV-1 does not infect B cells. The development of B-cell lymphomas appears to be related to the action of the HIV-1 transactivator protein (Tat), which is released from HIV-infected cells and penetrates uninfected B cells, affecting host cell gene expression. Upon chronic HIV-1 infection, Tat acts on the cells for a long time, probably allowing the cells to adapt to the presence of the viral protein. The aim of this work was to identify and study the mechanism of adaptation of cells to prolonged (chronic) exposure to HIV-1 Tat. We performed a comparative analysis of cells expressing Tat under the action of either an inducible promoter or a constitutive promoter, allowing us to model acute and chronic Tat effects, respectively. We found that the acute action of Tat leads to the suppression of cell proliferation, probably due to the downregulation of genes associated with replication and protein synthesis. In the case of chronic action of Tat, cell proliferation was restored and the expression of genes associated with the implementation of protective (antiviral) functions of the cell was increased. Analysis using proteasome inhibitors showed that in the case of chronic action, intense Tat proteolysis occurred, which could be the main mechanism of B-cell adaptation. Thus, B cells have a powerful mechanism to adapt to the entry of HIV-1 Tat, the efficiency of which may determine the frequency of lymphomagenesis in HIV-1-infected patients.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

RETRACTION: PNU-74654 enhances the antiproliferative effects of 5-FU in breast cancer and antagonizes thrombin-induced cell growth via the Wnt pathway. 返回：PNU-74654 可增强 5-FU 对乳腺癌的抗增殖作用，并通过 Wnt 通路拮抗凝血酶诱导的细胞生长。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31462

{"title":"RETRACTION: PNU-74654 enhances the antiproliferative effects of 5-FU in breast cancer and antagonizes thrombin-induced cell growth via the Wnt pathway.","authors":"","doi":"10.1002/jcp.31462","DOIUrl":"https://doi.org/10.1002/jcp.31462","url":null,"abstract":"Retraction: F. Rahmani, F. Amerizadeh, S. M. Hassanian, M. Hashemzehi, S.-N. Nasiri, H. Fiuji, G. A. Ferns, M. Khazaei, and A. Avan, \"PNU-74654 Enhances the Antiproliferative Effects of 5-FU in Breast Cancer and Antagonizes Thrombin-induced Cell Growth via the Wnt Pathway,\" Journal of Cellular Physiology 234, no. 8 (2019): 14123-14132, https://doi.org/10.1002/jcp.28104. The above article, published online on 11 January 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by a third party on the data presented in the article. Specifically, image elements in Figure 1c were previously published by the same author group in a different scientific context. Additionally, the panels representing the histological staining corresponding to the \"Control\" and \"5-FU\" groups in Figure 3b were found to originate from the same biological sample. Finally, splicing sites have been detected within Figure 6b. The concerns were not satisfactorily addressed by the authors upon request. Accordingly, retraction is warranted as the editors have lost trust in the data presented in the article and in its conclusions. The corresponding author Majid Khazaei disagrees with the decision of retraction. No confirmation was obtained by the remaining co-authors.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

RETRACTION: Basic Fibroblast Growth Factor Accelerates Matrix Degradation via a Neuro-endocrine Pathway in Human Adult Articular Chondrocytes. 回放：碱性成纤维细胞生长因子通过神经内分泌途径加速人类成人关节软骨细胞的基质降解。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31453

{"title":"RETRACTION: Basic Fibroblast Growth Factor Accelerates Matrix Degradation via a Neuro-endocrine Pathway in Human Adult Articular Chondrocytes.","authors":"","doi":"10.1002/jcp.31453","DOIUrl":"https://doi.org/10.1002/jcp.31453","url":null,"abstract":"Retraction: H.-J. Im, X. Li, P. Muddasani, G.-H. Kim, F. Davis, J. Rangan, C. B. Forsyth, M. Ellman, and E. J. Thonar, \"Basic Fibroblast Growth Factor Accelerates Matrix Degradation via a Neuro-endocrine Pathway in Human Adult Articular Chondrocytes,\" Journal of Cellular Physiology 215, no. 2 (2008): 452-463, https://doi.org/10.1002/jcp.21317. The above article, published online on 24 October 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, image elements of the experimental data in Figure 6 A were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

RETRACTION: Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint. 回放：环境对昼夜节律的干扰易使小鼠膝关节发生骨关节炎样改变。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31457

{"title":"RETRACTION: Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint.","authors":"","doi":"10.1002/jcp.31457","DOIUrl":"https://doi.org/10.1002/jcp.31457","url":null,"abstract":"Retraction: R. Kc, X. Li, R. M. Voigt, M. B. Ellman, K. C. Summa, M. H. Vitaterna, A. Keshavarizian, F. W. Turek, Q.-J. Meng, G. S. Stein, A. J. van Wijnen, D. Chen, C. B. Forsyth, and H.-J. Im, \"Environmental Disruption of Circadian Rhythm Predisposes Mice to Osteoarthritis-Like Changes in Knee Joint,\" Journal of Cellular Physiology 230, no. 9 (2015): 2174-2183, https://doi.org/10.1002/jcp.24946. The above article, published online on 5 February 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, image elements of the experimental data in Figure 4 A were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Emerging understandings of the role of exosomes in atherosclerosis. 对外泌体在动脉粥样硬化中作用的新认识。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-06 DOI: 10.1002/jcp.31454

Zena Wehbe, Maya Wehbe, Ali Al Khatib, Ali H Dakroub, Gianfranco Pintus, Firas Kobeissy, Ali H Eid

{"title":"Emerging understandings of the role of exosomes in atherosclerosis.","authors":"Zena Wehbe, Maya Wehbe, Ali Al Khatib, Ali H Dakroub, Gianfranco Pintus, Firas Kobeissy, Ali H Eid","doi":"10.1002/jcp.31454","DOIUrl":"https://doi.org/10.1002/jcp.31454","url":null,"abstract":"Atherosclerosis remains a major contributor to cardiovascular disease, the leading cause of global morbidity and mortality. Despite the elucidation of several molecular, biochemical, and cellular aspects that contribute to the etio-pathogenesis of atherosclerosis, much remains to be understood about the onset and progression of this disease. Emerging evidence supports a role for exosomes in the cellular basis of atherosclerosis. Indeed, exosomes of activated monocytes seem to accentuate a positive feedback loop that promotes recruitment of pro-inflammatory leukocytes. Moreover, in addition to their role in promoting proliferation and invasion of vascular smooth muscle cells, exosomes can also induce neovascularization within lesions and increase endothelial permeability, two important features of fibrous plaques. Depending on their sources and cargo, exosomes can also induce clot formation and contribute to other hallmarks of atherosclerosis. Taken together, it is becoming increasingly evident that a better understanding of exosome biology is integral to elucidating the pathogenesis of atherosclerosis, and may thus provide insight into a potentially new therapeutic target for this disease.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Ethionine-induced S-adenosylmethionine deficiency suppressed H3K27me3 and cell differentiation during neural tube development in mice. 乙硫宁诱导的 S-腺苷蛋氨酸缺乏会抑制小鼠神经管发育过程中的 H3K27me3 和细胞分化。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-06 DOI: 10.1002/jcp.31452

Li Zhang, Xiaona Zhang, Yurong Liu, Kaixin Wei, Huijing Ma, Li Xia, Rui Cao, Yuqing Sun, Ronghua Zheng, Xiuwei Wang, Bingmei Chang

{"title":"Ethionine-induced S-adenosylmethionine deficiency suppressed H3K27me3 and cell differentiation during neural tube development in mice.","authors":"Li Zhang, Xiaona Zhang, Yurong Liu, Kaixin Wei, Huijing Ma, Li Xia, Rui Cao, Yuqing Sun, Ronghua Zheng, Xiuwei Wang, Bingmei Chang","doi":"10.1002/jcp.31452","DOIUrl":"https://doi.org/10.1002/jcp.31452","url":null,"abstract":"S-adenosylmethionine (SAM) as a major methyl donor plays a key role in methylation modification in vivo, and its disorder was closely related to neural tube defects (NTDs). However, the exact mechanism between SAM deficiency and NTDs remained unclearly. Hence, we investigated the association between histone methylation modification and cell differentiation in NTDs mice induced by SAM deficiency. The levels of SAM and SAH (S-adenosylhomocysteine) were determined by enzyme linked immunosorbent assay (ELISA). The level of histone methylation, β-catenin were analyzed by Western blot, reversing transcription and quantitative PCR (RT-qPCR) and immunofluorescence. The results showed that the incidence rate of NTDs induced by ethionine were 46.2%. Post treatment of ethionine combined with SAM, the incidence rate of NTDs was reduced to 26.2%. The level of SAM was significantly decreased (p < 0.05) and a reduction in the SAM/SAH ratio was observed after entionine treatment. The SAM deficiency caused the reduction of H3K27me3 modifications and the elevated UTX activity (p < 0.05), and inhibited the expressions of β-catenin. The differentiations of NSCs into neurons and oligodendrocytes were inhibited under SAM deficiency (p < 0.05). These results indicated that the SAM deficiency led to reduce H3K27me3 modifications, prevented the β-catenin signaling pathway and NSCs differentiation, which provided an understanding of the novel function of epigenetic regulation in NTDs.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":null,"pages":null},"PeriodicalIF":4.5,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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