| RRC ID |
54766
|
| 著者 |
Umehara T, Mori R, Mace KA, Murase T, Abe Y, Yamamoto T, Ikematsu K.
|
| タイトル |
Identification of Specific miRNAs in Neutrophils of Type 2 Diabetic Mice: Overexpression of miRNA-129-2-3p Accelerates Diabetic Wound Healing.
|
| ジャーナル |
Diabetes
|
| Abstract |
Neutrophils are involved in the first stage of acute inflammation. After injury, they are mobilized and recruited to the injured tissue. In diabetes, wound healing is delayed and aberrant, leading to excessive recruitment and retention of neutrophils that fail to promote angiogenesis and prolong inflammation. However, the exact pathological mechanisms of diabetic-derived neutrophils in chronic inflammation remain unclear. Here, miRNA profiling of neutrophils from bone marrow in type 2 diabetic mice was performed using a microarray. miRNAs regulate the posttranscriptional expression of target mRNAs and are important in countering inflammation-related diseases. Our study revealed that miRNAs exhibit differential expression in diabetic-derived neutrophils compared with non-diabetic-derived neutrophils, especially miR-129 family members. miR-129-2-3p directly regulated the translation of Casp6 and Ccr2, which are involved in inflammatory responses and apoptosis. Furthermore, miR-129-2-3p overexpression at the wound site of type 2 diabetic mice accelerated wound healing. These results suggest possible involvement of miR-129-2-3p in diabetic-derived neutrophil dysfunction and that retention kinetics of neutrophils and chronic inflammation may be initiated through miR-129-2-3p-regulated genes. This study characterizes changes in global miRNA expression in diabetic-derived neutrophils and systematically identifies critical target genes involved in certain biological processes related to the pathology of diabetic wound healing.
|
| 巻・号 |
68(3)
|
| ページ |
617-630
|
| 公開日 |
2019-3-1
|
| DOI |
10.2337/db18-0313
|
| PII |
db18-0313
|
| PMID |
30523028
|
| MeSH |
3T3 Cells
Animals
B-Lymphocytes / metabolism
Diabetes Mellitus, Experimental / metabolism*
Diabetes Mellitus, Type 2 / metabolism*
Diabetes Mellitus, Type 2 / physiopathology
HL-60 Cells
Humans
In Situ Hybridization
Inflammation / metabolism
Macrophages / metabolism
Male
Mice
Mice, Mutant Strains
MicroRNAs / metabolism*
Mutation / genetics
Neutrophils / metabolism*
Real-Time Polymerase Chain Reaction
T-Lymphocytes / metabolism
Wound Healing / genetics
Wound Healing / physiology*
|
| IF |
7.199
|
| 引用数 |
6
|
| リソース情報 |
| ヒト・動物細胞 |
HL60(RCB0041) |
