Cell Regeneration最新文献_第8页

Microfluidic devices as model platforms of CNS injury-ischemia to study axonal regeneration by regulating mitochondrial transport and bioenergetic metabolism. 微流控装置作为中枢神经系统损伤缺血模型平台，通过调节线粒体运输和生物能量代谢来研究轴突再生。

Cell Regeneration Pub Date : 2022-10-03 DOI: 10.1186/s13619-022-00138-3

Ning Huang, Zu-Hang Sheng

{"title":"Microfluidic devices as model platforms of CNS injury-ischemia to study axonal regeneration by regulating mitochondrial transport and bioenergetic metabolism.","authors":"Ning Huang, Zu-Hang Sheng","doi":"10.1186/s13619-022-00138-3","DOIUrl":"https://doi.org/10.1186/s13619-022-00138-3","url":null,"abstract":"Central nervous system (CNS) neurons typically fail to regenerate their axons after injury leading to neurological impairment. Axonal regeneration is a highly energy-demanding cellular program that requires local mitochondria to supply most energy within injured axons. Recent emerging lines of evidence have started to reveal that injury-triggered acute mitochondrial damage and local energy crisis contribute to the intrinsic energetic restriction that accounts for axon regeneration failure in the CNS. Characterizing and reprogramming bioenergetic signaling and mitochondrial maintenance after axon injury-ischemia is fundamental for developing therapeutic strategies that can restore local energy metabolism and thus facilitate axon regeneration. Therefore, establishing reliable and reproducible neuronal model platforms is critical for assessing axonal energetic metabolism and regeneration capacity after injury-ischemia. In this focused methodology article, we discuss recent advances in applying cutting-edge microfluidic chamber devices in combination with state-of-the-art live-neuron imaging tools to monitor axonal regeneration, mitochondrial transport, bioenergetic metabolism, and local protein synthesis in response to injury-ischemic stress in mature CNS neurons.","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":" ","pages":"33"},"PeriodicalIF":0.0,"publicationDate":"2022-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9527262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40386465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

A mouse model of vitiligo based on endogenous auto-reactive CD8 + T cell targeting skin melanocyte. 基于内源性自身反应性CD8 + T细胞靶向皮肤黑素细胞的小鼠白癜风模型。

Cell Regeneration Pub Date : 2022-10-02 DOI: 10.1186/s13619-022-00132-9

Daoming Chen, Zijian Xu, Jun Cui, Ting Chen

{"title":"A mouse model of vitiligo based on endogenous auto-reactive CD8 + T cell targeting skin melanocyte.","authors":"Daoming Chen, Zijian Xu, Jun Cui, Ting Chen","doi":"10.1186/s13619-022-00132-9","DOIUrl":"https://doi.org/10.1186/s13619-022-00132-9","url":null,"abstract":"Vitiligo is the most common human skin depigmenting disorder. It is mediated by endogenous autoreactive CD8 + T cells that destruct skin melanocytes. This disease has an estimated prevalence of 1% of the global population and currently has no cure. Animal models are indispensable tools for understanding vitiligo pathogenesis and for developing new therapies. Here, we describe a vitiligo mouse model which recapitulates key clinical features of vitiligo, including epidermis depigmentation, CD8 + T cell infiltration in skin, and melanocyte loss. To activate endogenous autoreactive cytotoxic CD8 + T cells targeting melanocytes, this model relies on transient inoculation of B16F10 melanoma cells and depletion of CD4 + regulatory T cells. At cellular level, epidermal CD8 + T cell infiltration and melanocyte loss start as early as Day 19 after treatment. Visually apparent epidermis depigmentation occurs 2 months later. This protocol can efficiently induce vitiligo in any C57BL/6 background mouse strain, using only commercially available reagents. This enables researchers to carry out in-depth in vivo vitiligo studies utilizing mouse genetics tools, and provides a powerful platform for drug discovery.","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":" ","pages":"31"},"PeriodicalIF":0.0,"publicationDate":"2022-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9526765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40388653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Cilia regeneration requires an RNA splicing factor from the ciliary base. 纤毛再生需要来自纤毛基部的RNA剪接因子。

Cell Regeneration Pub Date : 2022-10-01 DOI: 10.1186/s13619-022-00130-x

Kaiming Xu, Guangshuo Ou

引用次数: 1

CTCF acetylation at lysine 20 is required for the early cardiac mesoderm differentiation of embryonic stem cells. CTCF赖氨酸20乙酰化是胚胎干细胞早期心脏中胚层分化所必需的。

Cell Regeneration Pub Date : 2022-09-19 DOI: 10.1186/s13619-022-00131-w

Shixin Gong, Gongcheng Hu, Rong Guo, Jie Zhang, Yiqi Yang, Binrui Ji, Gang Li, Hongjie Yao

引用次数: 1

Rise of the human-mouse chimeric brain models. 人鼠嵌合脑模型的兴起。

Cell Regeneration Pub Date : 2022-09-03 DOI: 10.1186/s13619-022-00135-6

Peng Jiang, Mahabub Maraj Alam

引用次数: 3

The therapeutic prospects and challenges of human neural stem cells for the treatment of Alzheimer's Disease. 人类神经干细胞治疗阿尔茨海默病的前景和挑战。

Cell Regeneration Pub Date : 2022-09-02 DOI: 10.1186/s13619-022-00128-5

Chunmei Yue, Su Feng, Yingying Chen, Naihe Jing

{"title":"The therapeutic prospects and challenges of human neural stem cells for the treatment of Alzheimer's Disease.","authors":"Chunmei Yue, Su Feng, Yingying Chen, Naihe Jing","doi":"10.1186/s13619-022-00128-5","DOIUrl":"https://doi.org/10.1186/s13619-022-00128-5","url":null,"abstract":"Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder associated with aging. Due to its insidious onset, protracted progression, and unclear pathogenesis, it is considered one of the most obscure and intractable brain disorders, and currently, there are no effective therapies for it. Convincing evidence indicates that the irreversible decline of cognitive abilities in patients coincides with the deterioration and degeneration of neurons and synapses in the AD brain. Human neural stem cells (NSCs) hold the potential to functionally replace lost neurons, reinforce impaired synaptic networks, and repair the damaged AD brain. They have therefore received extensive attention as a possible source of donor cells for cellular replacement therapies for AD. Here, we review the progress in NSC-based transplantation studies in animal models of AD and assess the therapeutic advantages and challenges of human NSCs as donor cells. We then formulate a promising transplantation approach for the treatment of human AD, which would help to explore the disease-modifying cellular therapeutic strategy for the treatment of human AD.","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":" ","pages":"28"},"PeriodicalIF":0.0,"publicationDate":"2022-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9437172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40340536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Intestinal cellular heterogeneity and disease development revealed by single-cell technology. 单细胞技术揭示肠道细胞异质性和疾病发展。

Cell Regeneration Pub Date : 2022-09-01 DOI: 10.1186/s13619-022-00127-6

Yalong Wang, Wanlu Song, Shicheng Yu, Yuan Liu, Ye-Guang Chen

引用次数: 6

Correction: Stepwise differentiation of functional pancreatic β cells from human pluripotent stem cells. 更正:从人类多能干细胞逐步分化功能性胰腺β细胞。

Cell Regeneration Pub Date : 2022-08-23 DOI: 10.1186/s13619-022-00134-7

Wenwen Jin, Wei Jiang

引用次数: 0

Chemical journey of somatic cells to pluripotency. 体细胞到多能性的化学过程。

Cell Regeneration Pub Date : 2022-08-03 DOI: 10.1186/s13619-022-00126-7

Deepti Abbey

引用次数: 0

Rif1 interacts with non-canonical polycomb repressive complex PRC1.6 to regulate mouse embryonic stem cells fate potential. Rif1与非规范多梳抑制复合体PRC1.6相互作用，调控小鼠胚胎干细胞命运潜能。

Cell Regeneration Pub Date : 2022-08-02 DOI: 10.1186/s13619-022-00124-9

Lu Li, Pishun Li, Jiale Chen, Li Li, Yunfan Shen, Yangzixuan Zhu, Jiayi Liu, Lu Lv, Song Mao, Fang Chen, Guang Hu, Kai Yuan

{"title":"Rif1 interacts with non-canonical polycomb repressive complex PRC1.6 to regulate mouse embryonic stem cells fate potential.","authors":"Lu Li, Pishun Li, Jiale Chen, Li Li, Yunfan Shen, Yangzixuan Zhu, Jiayi Liu, Lu Lv, Song Mao, Fang Chen, Guang Hu, Kai Yuan","doi":"10.1186/s13619-022-00124-9","DOIUrl":"https://doi.org/10.1186/s13619-022-00124-9","url":null,"abstract":"Mouse embryonic stem cells (mESCs) cycle in and out of a transient 2-cell (2C)-like totipotent state, driven by a complex genetic circuit involves both the coding and repetitive sections of the genome. While a vast array of regulators, including the multi-functional protein Rif1, has been reported to influence the switch of fate potential, how they act in concert to achieve this cellular plasticity remains elusive. Here, by modularizing the known totipotency regulatory factors, we identify an unprecedented functional connection between Rif1 and the non-canonical polycomb repressive complex PRC1.6. Downregulation of the expression of either Rif1 or PRC1.6 subunits imposes similar impacts on the transcriptome of mESCs. The LacO-LacI induced ectopic colocalization assay detects a specific interaction between Rif1 and Pcgf6, bolstering the intactness of the PRC1.6 complex. Chromatin immunoprecipitation followed by sequencing (ChIP-seq) analysis further reveals that Rif1 is required for the accurate targeting of Pcgf6 to a group of genomic loci encompassing many genes involved in the regulation of the 2C-like state. Depletion of Rif1 or Pcgf6 not only activates 2C genes such as Zscan4 and Zfp352, but also derepresses a group of the endogenous retroviral element MERVL, a key marker for totipotency. Collectively, our findings discover that Rif1 can serve as a novel auxiliary component in the PRC1.6 complex to restrain the genetic circuit underlying totipotent fate potential, shedding new mechanistic insights into its function in regulating the cellular plasticity of embryonic stem cells.","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":" ","pages":"25"},"PeriodicalIF":0.0,"publicationDate":"2022-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9343540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40662733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4