PMID- 30152001
OWN - NLM
STAT- MEDLINE
DCOM- 20191025
LR  - 20191025
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 148
IP  - 3
DP  - 2019 Feb
TI  - Cathepsin C modulates myelin oligodendrocyte glycoprotein-induced experimental 
      autoimmune encephalomyelitis.
PG  - 413-425
LID - 10.1111/jnc.14581 [doi]
AB  - Multiple sclerosis (MS) is an autoimmune disease characterized by immune-mediated 
      inflammation, which attacks the myelin sheath. MS pursues a relapsing and 
      remitting course with varying intervals between symptoms. The main clinical 
      pathological features include inflammation, myelin sheath destruction and plaque 
      formation in the central nervous system (CNS). We previously reported that 
      cystatin F (CysF) expression is induced in demyelinating lesions that are 
      accompanied by active remyelination (referred to as shadow plaques) but is 
      down-regulated in chronic demyelinated lesions (plaques) in the spinal cord of MS 
      patients and in several murine models of demyelinating disease. CysF is a 
      cathepsin protease inhibitor whose major target is cathepsin C (CatC), which is 
      co-expressed in demyelinating regions in Plp(4e/-) mice, a model of chronic 
      demyelination. Here, we report the time course of CatC and CysF expression and 
      describe the symptoms in a mouse experimental autoimmune encephalomyelitis (EAE) 
      model using CatC knockdown (KD) and CatC over-expression (OE) mice. In myelin 
      oligodendrocyte glycoprotein (MOG)-EAE, CatC positive cells were found to 
      infiltrate the CNS at an early stage prior to any clinical signs, in comparison 
      to WT mice. CysF expression was not observed at this early stage, but appeared 
      later within shadow plaques. CatC expression was found in chronic demyelinated 
      lesions but was not associated with CysF expression, and CatCKD EAE mouse showed 
      delayed demyelination. Whereas, CatCOE in microglia significantly increased 
      severity of demyelination in the MOG-EAE model. Thus, these results demonstrate 
      that CatC plays a major role in MOG-EAE.
CI  - (c) 2018 International Society for Neurochemistry.
FAU - Durose, Wilaiwan Wisessmith
AU  - Durose WW
AUID- ORCID: 0000-0001-9463-9689
AD  - Division of Neurobiology and Bioinformatics, National Institute for Physiological 
      Sciences, Okazaki, Japan.
AD  - Department of Physiological Sciences, The Graduate University of Advance Studies 
      (SOKENDAI), Okazaki, Japan.
AD  - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol 
      University, Nakhonpathom, Thailand.
FAU - Shimizu, Takahiro
AU  - Shimizu T
AD  - Division of Neurobiology and Bioinformatics, National Institute for Physiological 
      Sciences, Okazaki, Japan.
AD  - Department of Physiological Sciences, The Graduate University of Advance Studies 
      (SOKENDAI), Okazaki, Japan.
FAU - Li, JiaYi
AU  - Li J
AD  - Division of Neurobiology and Bioinformatics, National Institute for Physiological 
      Sciences, Okazaki, Japan.
AD  - Department of Physiological Sciences, The Graduate University of Advance Studies 
      (SOKENDAI), Okazaki, Japan.
FAU - Abe, Manabu
AU  - Abe M
AD  - Brain Research Institute, Niigata University, Niigata, Japan.
FAU - Sakimura, Kenji
AU  - Sakimura K
AD  - Brain Research Institute, Niigata University, Niigata, Japan.
FAU - Chetsawang, Banthit
AU  - Chetsawang B
AD  - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol 
      University, Nakhonpathom, Thailand.
FAU - Tanaka, Kenji F
AU  - Tanaka KF
AD  - Division of Neurobiology and Bioinformatics, National Institute for Physiological 
      Sciences, Okazaki, Japan.
AD  - Department of Neuropsychiatry, Keio University, Tokyo, Japan.
FAU - Suzumura, Akio
AU  - Suzumura A
AD  - Department of Neuroimmunology, Research Institute of Environmental Medicine, 
      Nagoya University, Nagoya, Japan.
FAU - Tohyama, Koujiro
AU  - Tohyama K
AD  - Department of Physiology, School of Dentistry, Iwate Medical University, Morioka, 
      Japan.
FAU - Ikenaka, Kazuhiro
AU  - Ikenaka K
AD  - Division of Neurobiology and Bioinformatics, National Institute for Physiological 
      Sciences, Okazaki, Japan.
AD  - Department of Physiological Sciences, The Graduate University of Advance Studies 
      (SOKENDAI), Okazaki, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181203
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Cystatins)
RN  - 0 (Myelin-Oligodendrocyte Glycoprotein)
RN  - 0 (cystatin F, mouse)
RN  - EC 3.4.14.1 (Cathepsin C)
SB  - IM
MH  - Animals
MH  - Brain/*metabolism/pathology
MH  - Cathepsin C/*metabolism
MH  - Cystatins/metabolism
MH  - Encephalomyelitis, Autoimmune, Experimental/*metabolism/pathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Myelin Sheath/metabolism
MH  - Myelin-Oligodendrocyte Glycoprotein/immunology
MH  - Nerve Degeneration/*metabolism/pathology
MH  - Spinal Cord/*metabolism/pathology
OTO - NOTNLM
OT  - cathepsin C
OT  - cystatin F
OT  - demyelination
OT  - experimental autoimmune encephalomyelitis (EAE)
OT  - multiple sclerosis
EDAT- 2018/08/29 06:00
MHDA- 2019/10/28 06:00
CRDT- 2018/08/29 06:00
PHST- 2018/01/15 00:00 [received]
PHST- 2018/08/15 00:00 [revised]
PHST- 2018/08/16 00:00 [accepted]
PHST- 2018/08/29 06:00 [pubmed]
PHST- 2019/10/28 06:00 [medline]
PHST- 2018/08/29 06:00 [entrez]
AID - 10.1111/jnc.14581 [doi]
PST - ppublish
SO  - J Neurochem. 2019 Feb;148(3):413-425. doi: 10.1111/jnc.14581. Epub 2018 Dec 3.