論文

査読有り 国際誌
2019年3月

Identification of Specific miRNAs in Neutrophils of Type 2 Diabetic Mice: Overexpression of miRNA-129-2-3p Accelerates Diabetic Wound Healing.

Diabetes
  • Takahiro Umehara
  • ,
  • Ryoichi Mori
  • ,
  • Kimberly A Mace
  • ,
  • Takehiko Murase
  • ,
  • Yuki Abe
  • ,
  • Takuma Yamamoto
  • ,
  • Kazuya Ikematsu

68
3
開始ページ
617
終了ページ
630
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.2337/db18-0313

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.

リンク情報
DOI
https://doi.org/10.2337/db18-0313
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/30523028
ID情報
  • DOI : 10.2337/db18-0313
  • PubMed ID : 30523028

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