Life medicine最新文献

CD157 selectively identifies hPSCs with enhanced hepatic differentiation capacity CD157 可选择性地识别肝脏分化能力增强的 hPSCs

Life medicine Pub Date : 2024-06-05 DOI: 10.1093/lifemedi/lnae026

Shuang Li, Dacheng Jiang, Xin Li, Yongxu Zhao, Xiaosong Gu, Chunping Jiang, Qiurong Ding

引用次数: 0

SHOC2 plays an oncogenic or tumor suppressive role by differentially targeting the MAPK and mTORC1 signals in liver cancer SHOC2 在肝癌中通过不同程度地靶向 MAPK 和 mTORC1 信号发挥致癌或抑癌作用

Life medicine Pub Date : 2024-05-23 DOI: 10.1093/lifemedi/lnae023

Xiahong You, Longyu Dou, Mingjia Tan, Xiufang Xiong, Yi Sun

{"title":"SHOC2 plays an oncogenic or tumor suppressive role by differentially targeting the MAPK and mTORC1 signals in liver cancer","authors":"Xiahong You, Longyu Dou, Mingjia Tan, Xiufang Xiong, Yi Sun","doi":"10.1093/lifemedi/lnae023","DOIUrl":"https://doi.org/10.1093/lifemedi/lnae023","url":null,"abstract":"\u0000 SHOC2 is a scaffold protein that activates the RAS-MAPK signal. Our recent study showed that SHOC2 is also a negative regulator of the mTORC1 signal in lung cancer cells. Whether and how SHOC2 differentially regulates the RAS-MAPK vs. the mTORC1 signals in liver cancer remains unknown. Here we showed that SHOC2 is overexpressed in human liver cancer tissues, and SHOC2 overexpression promotes growth and survival of liver cancer cells via activation of the RAS-MAPK signal, although the mTORC1 signal is inactivated. SHOC2 knockdown suppresses the growth of liver cancer cells mainly through inactivating the RAS-MAPK signal. Thus, in the cell culture models, SHOC2 regulation of growth is dependent of the RAS-MAPK, but not the mTORC1 signal. Interestingly, in a mouse liver cancer model induced by diethylnitrosamine (DEN)-high fat diet (HFD), hepatocyte-specific Shoc2 deletion inactivates the Ras-Mapk signal, but has no effect in liver tumorigenesis. However, in the Pten loss-induced liver cancer model, Shoc2 deletion further activates mTorc1 without affecting the Ras-Mapk signal, and promotes liver tumorigenesis. Collectively, it appears that SHOC2 could act as either an oncogene (via activating the MAPK signal) or a tumor suppressor (via inactivating the mTORC1 signal) in the manner dependent of the dominancy of the MAPK vs. mTORC1 signals.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"52 23","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141103059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Establishment of epithelial inflammatory injury model using adult kidney organoids 利用成人肾脏器官组织建立上皮炎症损伤模型

Life medicine Pub Date : 2024-05-09 DOI: 10.1093/lifemedi/lnae022

Haoran Du, Liqiang Guo, Jiabei Lian, Huanlu Qiu, Yunuo Mao, Fan Yi, Huili Hu

引用次数: 0

Regulatory cellular and molecular networks in the bone microenvironment during aging 衰老过程中骨骼微环境的细胞和分子调控网络

Life medicine Pub Date : 2024-05-02 DOI: 10.1093/lifemedi/lnae019

Lingli Zhang, Zhikun Wang, Yuan Zhang, Rui Ji, Zhiben Li, Jun Zou, Bo Gao

{"title":"Regulatory cellular and molecular networks in the bone microenvironment during aging","authors":"Lingli Zhang, Zhikun Wang, Yuan Zhang, Rui Ji, Zhiben Li, Jun Zou, Bo Gao","doi":"10.1093/lifemedi/lnae019","DOIUrl":"https://doi.org/10.1093/lifemedi/lnae019","url":null,"abstract":"\u0000 Age-induced abnormalities in bone metabolism disrupt the equilibrium between bone resorption and formation. This largely stems from disturbances in bone homeostasis, in which signaling pathways exert a significant regulatory influence. Aging compromises the functionality of the bone marrow mesenchymal stem cells (BMSCs), ultimately resulting in tissue dysfunction and pathological aging. Age-related bone degradation primarily manifests as reduced bone formation and the increased accumulation of bone marrow fat. Cellular senescence diminishes bone cell vitality, thereby disrupting the balance of bone remodeling. Intensive osteoclast differentiation leads to the generation of more osteoclasts and increased bone resorption. This review provides insight into the impact of aging on bone, encompassing bone cell states during the aging process and bone signaling pathway transformations. It primarily delves into aging-related signaling pathways, such as the bone morphogenetic protein/Smad, Wnt/β-catenin, osteoprotegerin/receptor activator of NF-κB ligand/receptor activator of NF-κB, connexin43/miR21, and nuclear factor erythroid 2-related factor 2/antioxidant response element pathways, seeking to enhance our comprehension of crucial bone cells and their secretory phenotypes during aging. Furthermore, the precise molecular regulatory mechanisms underlying the interactions between bone signaling pathways and aging are investigated.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"78 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141022093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Follicular fluid-derived exosomes rejuvenate ovarian aging through miR-320a-3p-mediated FOXQ1 inhibition 卵泡液源性外泌体通过 miR-320a-3p 介导的 FOXQ1 抑制作用使卵巢衰老恢复活力

Life medicine Pub Date : 2024-03-25 DOI: 10.1093/lifemedi/lnae013

Yu Liu, Hongbei Mu, Yu Chen, Kexin Li, Q. Mei, Lingjuan Wang, Tianyu Tang, Qiuzi Shen, Huaibiao Li, Ling Zhang, Jing Li, W. Xiang

{"title":"Follicular fluid-derived exosomes rejuvenate ovarian aging through miR-320a-3p-mediated FOXQ1 inhibition","authors":"Yu Liu, Hongbei Mu, Yu Chen, Kexin Li, Q. Mei, Lingjuan Wang, Tianyu Tang, Qiuzi Shen, Huaibiao Li, Ling Zhang, Jing Li, W. Xiang","doi":"10.1093/lifemedi/lnae013","DOIUrl":"https://doi.org/10.1093/lifemedi/lnae013","url":null,"abstract":"\u0000 Ovarian aging is mainly characterized by a progressive decline in oocyte quantity and quality, which ultimately leads to female infertility. Various therapies have been established to cope with ovarian aging, among which exosome-based therapy is considered a promising strategy that can benefit ovarian functions via multiple pathways. Here, we isolated and characterized exosomes derived from ovarian follicular fluid and profiled the differential expression patterns of noncoding exosomal RNAs in young and aged women. Treatment with young mouse-derived exosomes efficiently rescued ovarian function in aged mice. The follicular fluid exosomes from young mice and miR-320-3p can also promote the proliferation of ovarian granulosa cells and improve mitochondrial function from old mice in vitro. Exosomes can increase the number of primordial and growing follicles, and improve the developmental ability of oocytes in the old mice in vivo. The mechanism may be involve that exosomes transfer miR-320-3p to granulosa cells, and inhibit the expression of FOXQ1. And hnRNPA2B1 controls miR-320-3p entry into exosomes. This work provides insights into the antiaging potential of follicular fluid-derived exosomes and the underlying molecular mechanisms, which may facilitate prevention of ovarian aging and an improvement in female fertility.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":" 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140384410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Brain organoids: from unguided to regionalized to nucleus-specific 脑器质性组织：从无引导到区域化再到特异性细胞核

Life medicine Pub Date : 2024-03-22 DOI: 10.1093/lifemedi/lnae014

Yangfei Xiang, In-Hyun Park

引用次数: 0

Tracing TMEM106B fibril deposition in aging and Parkinson’s disease with dementia brains 追踪衰老和帕金森病痴呆大脑中的 TMEM106B 纤维沉积情况

Life medicine Pub Date : 2024-03-07 DOI: 10.1093/lifemedi/lnae011

Wanbing Zhao, Yun Fan, Qinyue Zhao, Zhen Fan, Jue Zhao, Wenbo Yu, Wensheng Li, Dan Li, Cong Liu, Jian Wang

{"title":"Tracing TMEM106B fibril deposition in aging and Parkinson’s disease with dementia brains","authors":"Wanbing Zhao, Yun Fan, Qinyue Zhao, Zhen Fan, Jue Zhao, Wenbo Yu, Wensheng Li, Dan Li, Cong Liu, Jian Wang","doi":"10.1093/lifemedi/lnae011","DOIUrl":"https://doi.org/10.1093/lifemedi/lnae011","url":null,"abstract":"\u0000 Transmembrane protein 106B (TMEM106B), previously identified as a risk factor in frontotemporal lobar degeneration, has recently been detected to form fibrillar aggregates in the brains of patients with various neurodegenerative diseases (NDs) and normal elders. While, the specifics of when and where TMEM106B fibrils accumulate in human brains, as well as their connection to aging and disease progression, remain poorly understood. Here, we identified an antibody (NBP1-91311) that directly binds to TMEM106B fibrils extracted from the brain in vitro and to Thioflavin S positive TMEM106B fibrillar aggregates in brain sections. We discovered that TMEM106B fibrils deposit in the human brain in an age-dependent manner. Notably, the TMEM106B fibril load in the brains of Parkinson’s disease with dementia patients was significantly higher than in age-matched elders. Additionally, we found that TMEM106B fibrils predominantly accumulate in astrocytes and neurons and do not co-localize with the pathological deposition formed by other amyloid proteins such as α-synuclein, Aβ, and Tau. Our work provides a comprehensive analysis of the burden and cellular distribution of TMEM106B fibrils in human brains, underscoring the impact of both aging and disease conditions on TMEM106B fibril deposition. This highlights the potential significance of TMEM106B fibrils in various age-related NDs.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140260556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Osteoporosis under psychological stress: mechanisms and therapeutics 心理压力下的骨质疏松症：机制与疗法

Life medicine Pub Date : 2024-03-07 DOI: 10.1093/lifemedi/lnae009

Hao-Kun Xu, Jie-Xi Liu, Ze-Kai Zhou, Chen-Xi Zheng, B. Sui, Yuan Yuan, Liang Kong, Yan Jin, Ji Chen

引用次数: 0

When synthetic biology meets medicine 当合成生物学遇上医学

Life medicine Pub Date : 2024-03-06 DOI: 10.1093/lifemedi/lnae010

Yuge Feng, Cong Su, Guobin Mao, Baoting Sun, Yizhi Cai, Junbiao Dai, Yingxin Ma

引用次数: 0

Programmable G-to-Y base editing using engineered DNA glycosylase 利用工程 DNA 糖基化酶进行可编程 G-Y 碱基编辑

Life medicine Pub Date : 2024-02-17 DOI: 10.1093/lifemedi/lnae005

Huawei Tong, Tonghuai Li, Hui Yang

引用次数: 0