PMID- 31526566
OWN - NLM
STAT- MEDLINE
DCOM- 20200622
LR  - 20200622
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 519
IP  - 3
DP  - 2019 Nov 12
TI  - Ninjurin 1 mediates peripheral nerve regeneration through Schwann cell maturation 
      of NG2-positive cells.
PG  - 462-468
LID - S0006-291X(19)31712-7 [pii]
LID - 10.1016/j.bbrc.2019.09.007 [doi]
AB  - Ninjurin 1 (Ninj1) is identified as a peripheral nerve injury-induced protein. 
      However, the role of Ninj1 in nerve regeneration is unclear. Schwann cells (SCs) 
      and microvasculature are critical for peripheral nerve regeneration. SCs 
      precursors and microvascular pericytes (PCs), which are nerve/glial antigen 2 
      (NG2)-positive cells are observed in peripheral nervous system. In this study, we 
      investigated the role of Ninj1 in peripheral nerve regeneration using 
      NG2(+)cell-specific inducible deletion of Ninj1 mouse model. The number of 
      NG2(+)cells, which were associated with and without microvessels was increased 
      after sciatic nerve crush injury. There was a significant increase in the 
      expression of Ninj1 and EphA7 in the injured nerve tissue. This increase was 
      mostly observed in NG2(+)cells. Genetic tracing of NG2(+)cells was performed 
      using tamoxifen (Tam) treatment on NG2CreERT:R26R-tdTomato mice. The sciatic 
      nerve was injured following the Tam-treatment, then tdTomato-expressing SCs were 
      mostly observed in regenerated SCs at 21 days after nerve injury. Ninj1 gene 
      knockout (Ninj1 KO) in NG2(+)cells was induced using NG2CreERT:Ninj1loxp mice. 
      Tam-treated-NG2CreERT or Tam-nontreated NG2CreERT:Ninj1loxp mice were used as 
      controls. Following Tam-treatment, the sciatic nerve in each group was injured. 
      Ninj1KO significantly attenuated the expression of the myelin binding protein 
      (MBP) as well as the number of myelinated axons. The expression of MBP in 
      cultured SCs was significantly reduced by SiRNA-mediated Ninj1 knockdown (KD). 
      Ninj1KD also attenuated the differentiation of SCs by isolated 
      EphA7(+)multipotent PCs. The current data indicate that Ninj1 plays a vital role 
      in peripheral nerve regeneration. This is observed particularly in the 
      myelination process of NG2(+)cells including SCs precursors and multipotent PCs.
CI  - Copyright (c) 2019 Elsevier Inc. All rights reserved.
FAU - Tomita, Yui
AU  - Tomita Y
AD  - Department of Biochemistry, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan; Department of Radiology, Asahikawa, 2-1-1 Midorigaoka-higashi, 
      Asahikawa, 078-8510, Japan.
FAU - Horiuchi, Kiwamu
AU  - Horiuchi K
AD  - Department of Cardiovascular Regeneration and Innovation, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan; Department of Medicine, Division 
      of Cardiovascular, Respiratory and Neurology, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Kano, Kohei
AU  - Kano K
AD  - Department of Cardiovascular Regeneration and Innovation, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan; Department of Medicine, Division 
      of Cardiovascular, Respiratory and Neurology, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Tatsukawa, Takamitsu
AU  - Tatsukawa T
AD  - Department of Biochemistry, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan; Department of Vascular Surgery, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Matsuo, Risa
AU  - Matsuo R
AD  - Department of Biochemistry, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan; Department of Dermatology, Asahikawa Medical University, 
      Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Hayasaka, Taiki
AU  - Hayasaka T
AD  - Department of Cardiovascular Regeneration and Innovation, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan; Department of Medicine, Division 
      of Cardiovascular, Respiratory and Neurology, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Yoshida, Yuri
AU  - Yoshida Y
AD  - Department of Biochemistry, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan; Department of Vascular Surgery, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Kabara, Maki
AU  - Kabara M
AD  - Department of Cardiovascular Regeneration and Innovation, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Yasuda, Satoshi
AU  - Yasuda S
AD  - Department of Biochemistry, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan.
FAU - Nakajima, Keiichi
AU  - Nakajima K
AD  - Department of Biochemistry, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan.
FAU - Nakagawa, Naoki
AU  - Nakagawa N
AD  - Department of Medicine, Division of Cardiovascular, Respiratory and Neurology, 
      Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Takehara, Naofumi
AU  - Takehara N
AD  - Department of Medicine, Division of Cardiovascular, Respiratory and Neurology, 
      Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Okizaki, Atsutaka
AU  - Okizaki A
AD  - Department of Radiology, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan.
FAU - Hasebe, Naoyuki
AU  - Hasebe N
AD  - Department of Cardiovascular Regeneration and Innovation, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan; Department of Medicine, Division 
      of Cardiovascular, Respiratory and Neurology, Asahikawa, 2-1-1 
      Midorigaoka-higashi, Asahikawa, 078-8510, Japan.
FAU - Kawabe, Jun-Ichi
AU  - Kawabe JI
AD  - Department of Biochemistry, Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 
      078-8510, Japan; Department of Cardiovascular Regeneration and Innovation, 
      Asahikawa, 2-1-1 Midorigaoka-higashi, Asahikawa, 078-8510, Japan. Electronic 
      address: kawabeju@asahikawa-med.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190913
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Antigens)
RN  - 0 (Cell Adhesion Molecules, Neuronal)
RN  - 0 (Myelin Proteins)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Ninj1 protein, mouse)
RN  - 0 (Proteoglycans)
RN  - 0 (chondroitin sulfate proteoglycan 4)
SB  - IM
MH  - Animals
MH  - Antigens/genetics/*metabolism
MH  - Cell Adhesion Molecules, Neuronal/genetics/*metabolism
MH  - Cell Line
MH  - Female
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Myelin Proteins/genetics/metabolism
MH  - Nerve Growth Factors/genetics/*metabolism
MH  - Nerve Regeneration/*physiology
MH  - Pericytes/cytology/metabolism
MH  - Peripheral Nerve Injuries/genetics/metabolism/*physiopathology
MH  - Proteoglycans/genetics/*metabolism
MH  - Schwann Cells/*metabolism
OTO - NOTNLM
OT  - Angiogenesis
OT  - NG2
OT  - Neurogenesis
OT  - Ninjurin1
OT  - Peripheral nerve
OT  - Schwann cells
EDAT- 2019/09/19 06:00
MHDA- 2020/06/23 06:00
CRDT- 2019/09/19 06:00
PHST- 2019/08/17 00:00 [received]
PHST- 2019/08/27 00:00 [revised]
PHST- 2019/09/04 00:00 [accepted]
PHST- 2019/09/19 06:00 [pubmed]
PHST- 2020/06/23 06:00 [medline]
PHST- 2019/09/19 06:00 [entrez]
AID - S0006-291X(19)31712-7 [pii]
AID - 10.1016/j.bbrc.2019.09.007 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2019 Nov 12;519(3):462-468. doi: 
      10.1016/j.bbrc.2019.09.007. Epub 2019 Sep 13.