Dysregulation of a novel miR-23b/27b-p53 axis impairs muscle stem cell differentiation of humans with type 2 diabetes
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
Dysregulation of a novel miR-23b/27b-p53 axis impairs muscle stem cell differentiation of humans with type 2 diabetes. / Henriksen, Tora I; Davidsen, Peter K; Pedersen, Maria; Schultz, Heidi S; Hansen, Ninna S; Larsen, Therese J; Vaag, Allan; Pedersen, Bente K; Nielsen, Søren; Scheele, Camilla.
In: Molecular Metabolism, Vol. 6, No. 7, 2017, p. 770-779.Research output: Contribution to journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Dysregulation of a novel miR-23b/27b-p53 axis impairs muscle stem cell differentiation of humans with type 2 diabetes
AU - Henriksen, Tora I
AU - Davidsen, Peter K
AU - Pedersen, Maria
AU - Schultz, Heidi S
AU - Hansen, Ninna S
AU - Larsen, Therese J
AU - Vaag, Allan
AU - Pedersen, Bente K
AU - Nielsen, Søren
AU - Scheele, Camilla
PY - 2017
Y1 - 2017
N2 - OBJECTIVE: MicroRNAs (miRNAs) are increasingly recognized as fine-tuning regulators of metabolism, and are dysregulated in several disease conditions. With their capacity to rapidly change gene expression, miRNAs are also important regulators of development and cell differentiation. In the current study, we describe an impaired myogenic capacity of muscle stem cells isolated from humans with type 2 diabetes (T2DM) and assess whether this phenotype is regulated by miRNAs.METHODS: We measured global miRNA expression during in vitro differentiation of muscle stem cells derived from T2DM patients and healthy controls.RESULTS: The mir-23b/27b cluster was downregulated in the cells of the patients, and a pro-myogenic effect of these miRNAs was mediated through the p53 pathway, which was concordantly dysregulated in the muscle cells derived from humans with T2DM.CONCLUSIONS: Our results indicate that we have identified a novel pathway for coordination of myogenesis, the miR-23b/27b-p53 axis that, when dysregulated, potentially contributes to a sustained muscular dysfunction in T2DM.
AB - OBJECTIVE: MicroRNAs (miRNAs) are increasingly recognized as fine-tuning regulators of metabolism, and are dysregulated in several disease conditions. With their capacity to rapidly change gene expression, miRNAs are also important regulators of development and cell differentiation. In the current study, we describe an impaired myogenic capacity of muscle stem cells isolated from humans with type 2 diabetes (T2DM) and assess whether this phenotype is regulated by miRNAs.METHODS: We measured global miRNA expression during in vitro differentiation of muscle stem cells derived from T2DM patients and healthy controls.RESULTS: The mir-23b/27b cluster was downregulated in the cells of the patients, and a pro-myogenic effect of these miRNAs was mediated through the p53 pathway, which was concordantly dysregulated in the muscle cells derived from humans with T2DM.CONCLUSIONS: Our results indicate that we have identified a novel pathway for coordination of myogenesis, the miR-23b/27b-p53 axis that, when dysregulated, potentially contributes to a sustained muscular dysfunction in T2DM.
KW - Journal Article
U2 - 10.1016/j.molmet.2017.04.006
DO - 10.1016/j.molmet.2017.04.006
M3 - Journal article
C2 - 28702332
VL - 6
SP - 770
EP - 779
JO - Molecular Metabolism
JF - Molecular Metabolism
SN - 2212-8778
IS - 7
ER -
ID: 182890331