The role of P16Ink4a in adult skeletal muscle stem cells
The role of P16Ink4a in adult skeletal muscle stem cells
批准号:
10661698
负责人:
Brian Feeley
金额:
$44.53万
依托单位国家:
美国
项目类别:
财政年份:
2021
资助国家:
美国
项目状态:
未结题
起止时间:
2021-08-17 至 2026-05-31
关键词:
AdhesionsAdultAgingAtomic Force MicroscopyBehaviorBiomechanicsBiomedical EngineeringCDKN2A geneCell AdhesionCell physiologyCellsComplexCytoskeletonDataDegenerative DisorderDiseaseEnvironmentExtracellular MatrixFeedbackFibronectinsGeneticGoalsHeterogeneityImageIn VitroIntegrinsKnock-outMalignant NeoplasmsMeasuresMechanicsMediatingMolecularMusMuscleMuscle satellite cellMyoblastsPhenotypePlayProcessProliferatingPropertyPublishingRegenerative capacityRegulationReporterReportingRoleSamplingSeriesSignal TransductionSkeletal MuscleTestingTimeTissuesTraction Force MicroscopyTraumaTumor Suppressor ProteinsWorkadult stem cellcell motilityextracellulargenetic approachin vivoinsightmechanotransductionmigrationnovelpharmacologicreceptorregenerativerepairedresponseresponse to injurysatellite cellself-renewalsenescencestem cell functionstem cellstissue regenerationtissue repairtransmission process
中文摘要
项目摘要
细胞迁移、增殖和细胞命运决定的协调对于干细胞功能和组织至关重要。
修复.我们已经确定,P16Ink4a,经典的促衰老和衰老调节剂,参与了衰老过程。
调节健康成人肌肉干细胞。我们发现P16Ink4a在细胞迁移和细胞命运决定中的作用
通过细胞骨架和收缩机制。这在以前没有报道过。长期目标是
了解P16Ink4a如何被诱导并调节非老年人健康祖细胞的细胞骨架功能
组织中第一个目标将结合联合收割机时间调节和细胞特异性遗传策略,以确定
健康成人肌肉干细胞中的P16Ink4a。第二个目标将剖析功能和分子
通过P16Ink4a调节细胞力学、迁移和细胞命运的机制。第三个目标将审查
P16Ink4a在细胞自主调节自身微环境中的作用。了解P16Ink4a的作用
对祖细胞功能的研究将对衰老、衰老、癌症和肌肉退化产生重要影响
疾病
英文摘要
PROJECT SUMMARY
Coordination of cell migration, proliferation and cell fate determination is critical for stem cell function and tissue
repair. We have identified that P16Ink4a, the classic pro-senescence and aging regulator, participates in the
regulation of healthy adult muscle stem cells. We find a role for P16Ink4a in cell migration and cell fate decisions
via the cytoskeleton and contractile machinery. This has not been reported previously. The long-term goal is to
understand how P16Ink4a is induced and regulates cytoskeletal function of healthy progenitor cells in non-aged
tissues. The first aim will combine temporal regulated and cell specific genetic strategies to determine the role of
P16Ink4a in healthy adult muscle stem cells. The second aim will dissect the functional and molecular
mechanism that regulates cell mechanics, migration and cell fate via P16Ink4a. The third aim will examine the
role of P16Ink4a in cell autonomous regulation of its own microenvironment. Understanding the role of P16Ink4a
in progenitor cell function will lead to important insights for aging, senescence, cancer and muscle degenerative
diseases.
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会议论文
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海外基金