Inflammation-associated miR-155 activates differentiation of muscular satellite cells

Autor: Maki Itokazu, Toshiyuki Takehara, Tatsufumi Mori, Takeshi Teramura, Yuta Onodera, Kanji Fukuda
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
Critical Care and Emergency Medicine
Cellular differentiation
Gene Expression
lcsh:Medicine
Pathology and Laboratory Medicine
Biochemistry
Geographical Locations
Mice
Japan
Cell Movement
Animal Cells
Morphogenesis
Medicine and Health Sciences
Receptor
Notch1
lcsh:Science
Immune Response
Cells
Cultured
Cellular Senescence
Trauma Medicine
Multidisciplinary
Stem Cells
Cell Differentiation
Muscle Differentiation
Up-Regulation
Cell biology
Nucleic acids
Cellular Types
Stem cell
medicine.symptom
Traumatic Injury
Research Article
Asia
Satellite Cells
Skeletal Muscle
Immunology
Inflammation
Biology
miR-155
03 medical and health sciences
Signs and Symptoms
Multinucleate
Downregulation and upregulation
Diagnostic Medicine
microRNA
Genetics
medicine
Animals
Non-coding RNA
Cell Proliferation
Cell growth
CCAAT-Enhancer-Binding Protein-beta
lcsh:R
Biology and Life Sciences
Cell Biology
Gene regulation
MicroRNAs
030104 developmental biology
Musculoskeletal Injury
People and Places
RNA
lcsh:Q
Developmental Biology
Zdroj: PLoS ONE, Vol 13, Iss 10, p e0204860 (2018)
PLoS ONE
ISSN: 1932-6203
Popis: Tissue renewal and muscle regeneration largely rely on the proliferation and differentiation of muscle stem cells called muscular satellite cells (MuSCs). MuSCs are normally quiescent, but they are activated in response to various stimuli, such as inflammation. Activated MuSCs proliferate, migrate, differentiate, and fuse to form multinucleate myofibers. Meanwhile, inappropriate cues for MuSC activation induce premature differentiation and bring about stem cell loss. Recent studies revealed that stem cell regulation is disrupted in various aged tissues. We found that the expression of microRNA (miR)-155, which is an inflammation-associated miR, is upregulated in MuSCs of aged muscles, and this upregulation activates the differentiation process through suppression of C/ebpβ, which is an important molecule for maintaining MuSC self-renewal. We also found that Notch1 considerably repressed miR-155 expression, and loss of Notch1 induced miR-155 overexpression. Our findings suggest that miR-155 can act as an activator of muscular differentiation and might be responsible for accelerating aging-associated premature differentiation of MuSCs.
Databáze: OpenAIRE
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