Life medicine最新文献_第3页

The evolution of ovarian somatic cells characterized by transcriptome and chromatin accessibility across rodents, monkeys, and humans.

Life medicine Pub Date : 2024-07-31 eCollection Date: 2024-10-01 DOI: 10.1093/lifemedi/lnae028

Qiancheng Zhang, Fengyuan Sun, Ruifeng Zhang, Donghong Zhao, Ran Zhu, Xin Cheng, Xin Long, Xinling Hou, Rui Yan, Yu Cao, Fan Guo, Long Yan, Yuqiong Hu

{"title":"The evolution of ovarian somatic cells characterized by transcriptome and chromatin accessibility across rodents, monkeys, and humans.","authors":"Qiancheng Zhang, Fengyuan Sun, Ruifeng Zhang, Donghong Zhao, Ran Zhu, Xin Cheng, Xin Long, Xinling Hou, Rui Yan, Yu Cao, Fan Guo, Long Yan, Yuqiong Hu","doi":"10.1093/lifemedi/lnae028","DOIUrl":"10.1093/lifemedi/lnae028","url":null,"abstract":"The ovary plays a crucial role in the reproductive system of female mammals by producing mature oocytes through folliculogenesis. Non-human model organisms are extensively utilized in research on human ovarian biology, thus necessitating the investigation of conservation and divergence in molecular mechanisms across species. In this study, we employed integrative single-cell analysis of transcriptome and chromatin accessibility to identify the evolutionary conservation and divergence patterns of ovaries among humans, monkeys, mice, rats, and rabbits. Our analyses revealed that theca cells exhibited the most significant changes during evolution based on scRNA-seq and scATAC-seq datasets. Furthermore, we discovered common cis-regulatory architectures in theca cells across species by conducting joint analyses of scRNA-seq and scATAC-seq datasets. These findings have potential applications in non-human biomedical and genetic research to validate molecular mechanisms found in human organisms. Additionally, our investigation into non-coding genomic regions identified intergenic highly transcribed regions (igHTRs) that may contribute to the evolution of species-specific phenotypic traits. Overall, our study provides valuable insights into understanding the molecular characteristics of adult ovaries while offering new perspectives for studying human ovarian physiology and diseases.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"3 5","pages":"lnae028"},"PeriodicalIF":0.0,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054586","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: 0

Natural flavonoid glycosides Chrysosplenosides I & A rejuvenate intestinal stem cell aging via activation of PPARγ signaling.

Life medicine Pub Date : 2024-06-28 eCollection Date: 2024-06-01 DOI: 10.1093/lifemedi/lnae025

Jinbao Ye, La Yan, Yu Yuan, Fang Fu, Lu Yuan, Xinxin Fan, Juanyu Zhou, Yuedan Zhu, Xingzhu Liu, Gang Ren, Haiyang Chen

{"title":"Natural flavonoid glycosides Chrysosplenosides I & A rejuvenate intestinal stem cell aging via activation of PPARγ signaling.","authors":"Jinbao Ye, La Yan, Yu Yuan, Fang Fu, Lu Yuan, Xinxin Fan, Juanyu Zhou, Yuedan Zhu, Xingzhu Liu, Gang Ren, Haiyang Chen","doi":"10.1093/lifemedi/lnae025","DOIUrl":"10.1093/lifemedi/lnae025","url":null,"abstract":"The decline in intestinal stem cell (ISC) function is a hallmark of aging, contributing to compromised intestinal regeneration and increased incidence of age-associated diseases. Novel therapeutic agents that can rejuvenate aged ISCs are of paramount importance for extending healthspan. Here, we report on the discovery of Chrysosplenosides I and A (CAs 1 & 2), flavonol glycosides from the Xizang medicinal plant Chrysosplenium axillare Maxim., which exhibit potent anti-aging effects on ISCs. Our research, using Drosophila models, reveals that CAs 1 & 2 treatments not only restrain excessive ISC proliferation, thereby preserving intestinal homeostasis, but also extend the lifespan of aging Drosophila. In aged mouse intestinal organoids, CAs 1 & 2 enhance the growth and budding of intestinal organoids, indicating improved regenerative capacity. Mechanistic investigations show that CAs 1 & 2 exert their effects by activating the peroxisome proliferator-activated receptor-gamma (PPARγ) and concurrently inhibiting the epidermal growth factor receptor (EGFR) signaling pathways. Our findings position CAs 1 & 2 as promising candidates for ameliorating ISC aging and suggest that targeting PPARγ, in particular, may offer a therapeutic strategy to counteract age-related intestinal dysfunction.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"3 3","pages":"lnae025"},"PeriodicalIF":0.0,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054598","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: 0

Oral microbiota in aging and diseases.

Life medicine Pub Date : 2024-06-28 eCollection Date: 2024-06-01 DOI: 10.1093/lifemedi/lnae024

Ya Ren, Mingxu Chen, Ziyang Wang, Jing-Dong J Han

{"title":"Oral microbiota in aging and diseases.","authors":"Ya Ren, Mingxu Chen, Ziyang Wang, Jing-Dong J Han","doi":"10.1093/lifemedi/lnae024","DOIUrl":"10.1093/lifemedi/lnae024","url":null,"abstract":"Human microbiomes are microbial populations that form a symbiotic relationship with humans. There are up to 1000 species on the surface of human skin and mucosal system, among which gut microbiota attracts the most interest. As the beginning of the digestive tract, oral cavity is also an important microbial habitat in the human body which is the first line of defense against pathogens entering the body. Many studies have revealed that oral microbial dysbiosis could not only contribute to oral diseases but also whole-body systemic diseases and health status. Oral microorganisms can enter the gastrointestinal tract with saliva and food, or enter the blood circulation through mouth breakage, thus causing systemic inflammation and aging-related diseases including some causal links to Alzheimer's disease. A series of changes take place in oral microbial composition during development, with different age stages marked by different dominant microbial species. Despite a lack of comprehensive studies on aging oral microbiota, through systemic inflammation, oral pathogenic microbes are likely to contribute inflammatory aging. As inflammaging is a key signature and one of the causes for accelerated aging, improving the structure of oral microbiome may be not only a new strategy for disease prevention and treatment, but also for aging intervention.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"3 3","pages":"lnae024"},"PeriodicalIF":0.0,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054604","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: 0

Versatile platelets contribute to rejuvenation.

Life medicine Pub Date : 2024-06-28 eCollection Date: 2024-06-01 DOI: 10.1093/lifemedi/lnae018

John M Perry, Meng Zhao

引用次数: 0

Establishment of novel colorectal cancer organoid model based on tumor microenvironment analysis.

Life medicine Pub Date : 2024-06-24 eCollection Date: 2024-08-01 DOI: 10.1093/lifemedi/lnae027

Zhidong Xu, Shengwen Meng, Ran Xu, De Ma, Emmanuel Enoch Dzakah, Hailun Zheng, Tingjing Yao, Chao Ni, Bing Zhao

引用次数: 0

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

Unlocking heart anti-aging potential: the SIRT2-STAT3-CDKN2B pathway as a bridge between fiction and reality.

Life medicine Pub Date : 2024-05-13 eCollection Date: 2024-06-01 DOI: 10.1093/lifemedi/lnae020

Chunyu Chen, Jingxuan Liu, Wei Yu

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

Cellular senescence induced by down-regulation of PTBP1 correlates with exon skipping of mitochondrial-related gene NDUFV3.

Life medicine Pub Date : 2024-05-03 eCollection Date: 2024-04-01 DOI: 10.1093/lifemedi/lnae021

Yu Yang, Haimei Wen, Yuxin Li, Xin Zeng, Gang Wei, Zhenglong Gu, Ting Ni

{"title":"Cellular senescence induced by down-regulation of PTBP1 correlates with exon skipping of mitochondrial-related gene NDUFV3.","authors":"Yu Yang, Haimei Wen, Yuxin Li, Xin Zeng, Gang Wei, Zhenglong Gu, Ting Ni","doi":"10.1093/lifemedi/lnae021","DOIUrl":"10.1093/lifemedi/lnae021","url":null,"abstract":"As the most prevalent type of alternative splicing in animal cells, exon skipping plays an important role in expanding the diversity of transcriptome and proteome, thereby participating in the regulation of diverse physiological and pathological processes such as development, aging, and cancer. Cellular senescence serving as an anti-cancer mechanism could also contribute to individual aging. Although the dynamic changes of exon skipping during cellular senescence were revealed, its biological consequence and upstream regulator remain poorly understood. Here, by using human foreskin fibroblasts (HFF) replicative senescence as a model, we discovered that splicing factor PTBP1 was an important contributor for global exon skipping events during senescence. Down-regulated expression of PTBP1 induced senescence-associated phenotypes and related mitochondrial functional changes. Mechanistically, PTBP1 binds to the third exon of mitochondrial complex I subunit coding gene NDUFV3 and protects the exon from skipping. We further confirmed that exon skipping of NDUFV3 correlates with and partially contributes to cellular senescence and related mitochondrial functional changes upon PTBP1 knockdown. Together, we revealed for the first time that mitochondrial-related gene NDUFV3 is a new downstream target for PTBP1-regulated exon skipping to mediate cellular senescence and mitochondrial functional changes.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"3 2","pages":"lnae021"},"PeriodicalIF":0.0,"publicationDate":"2024-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054538","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: 0