PMID- 27327778
OWN - NLM
STAT- MEDLINE
DCOM- 20171211
LR  - 20211204
IS  - 1521-0499 (Electronic)
IS  - 0190-2148 (Linking)
VI  - 42
IP  - 5
DP  - 2016 Jun
TI  - The protective role of protein L-isoaspartyl (D-aspartate) O-methyltransferase 
      for maintenance of mitochondrial morphology in A549 cell.
PG  - 245-62
LID - 10.1080/01902148.2016.1197984 [doi]
AB  - PURPOSE: The increasing amounts of evidence with abnormal aging process have been 
      involved in the pathogenesis of chronic obstructive pulmonary disease (COPD) and 
      idiopathic pulmonary fibrosis (IPF). Mice with deficient protein L-isoaspartate 
      (D-aspartate) O-methyl transferase 1 (PCMT1) expression reveal acceleration of 
      aging and result in the increased proportion of D-aspartate (D-Asp) residues and 
      dysfunction in proteins. Furthermore, mitochondrial morphology and functions are 
      associated with COPD and IPF pathogenesis. The purpose of the current study was 
      to investigate the role of PCMT1 on mitochondrial morphology using A549 cells. 
      MATERIALS AND METHODS: We investigated PCMT1, prohibitin1 (PHB1), mitochondrial 
      membrane proteins expression, mitochondrial morphology, and the proportion of 
      D-Asp residues in PHB1 in A549 cells with (PCMT1-KD) and without the context of 
      decreased PCMT1 expression (PCMT1-Cont) using electron microscopy, fluorescence 
      staining, Western blot analysis, and the ATP content per cells. To investigate 
      the effects of the PCMT1-KD cells, we developed double-transfected cell lines 
      containing either the cytosolic or the endoplasmic isoform of PCMT1. RESULTS: We 
      found a significantly higher proportion of D-Asp residues in PHB1 in PCMT1-KD 
      cells than that in PCMT1-Cont cells. The PCMT1-KD cells without cigarette smoke 
      extract exposure were characterized by a significantly increased proportion of 
      the D-Asp residues in PHB1, damaged mitochondrial ultrastructure, and a tendency 
      toward the fission direction of the mitochondrial dynamics followed by a 
      significant decrease in the cellular ATP content. CONCLUSIONS: The increased 
      proportion of the D-Asp residues may contribute to COPD pathogenesis, via 
      irreversible protein conformational changes, followed by mitochondrial 
      dysfunction.
FAU - Ogasawara, Masahito
AU  - Ogasawara M
AD  - a Department of Pharmacology , Ehime University Graduate School of Medicine , 
      Toon City , Japan.
FAU - Otani, Mieko
AU  - Otani M
AD  - b Laboratory of Molecular Cell Biology , Department of Life Sciences Pharmacy , 
      School of Pharmaceutical Sciences, Kobe Gakuin University , Chuo-ku, Kobe City , 
      Japan.
FAU - Takano, Masaoki
AU  - Takano M
AD  - b Laboratory of Molecular Cell Biology , Department of Life Sciences Pharmacy , 
      School of Pharmaceutical Sciences, Kobe Gakuin University , Chuo-ku, Kobe City , 
      Japan.
FAU - Shudou, Masachika
AU  - Shudou M
AD  - c Integrated Center for Science , Shigenobu Station, Ehime University Graduate 
      School of Medicine , Toon City , Japan.
FAU - Inaba, Yohei
AU  - Inaba Y
AD  - d Department of Environment Health , National Institute of Public Health , 
      Minami, Wako City , Saitama , Japan.
FAU - Nirasawa, Satoru
AU  - Nirasawa S
AD  - e Biological Resources and Post-Harvest Division , Japan International Research 
      Center for Agricultural Sciences , Tsukuba City , Ibaraki , Japan.
FAU - Takahashi, Saori
AU  - Takahashi S
AD  - f Akita Research Institute of Food and Brewing , Akita City , Japan.
FAU - Kiyoi, Takeshi
AU  - Kiyoi T
AD  - c Integrated Center for Science , Shigenobu Station, Ehime University Graduate 
      School of Medicine , Toon City , Japan.
FAU - Tanaka, Yuki
AU  - Tanaka Y
AD  - c Integrated Center for Science , Shigenobu Station, Ehime University Graduate 
      School of Medicine , Toon City , Japan.
FAU - Kameda, Kenji
AU  - Kameda K
AD  - c Integrated Center for Science , Shigenobu Station, Ehime University Graduate 
      School of Medicine , Toon City , Japan.
FAU - Kunugita, Naoki
AU  - Kunugita N
AD  - d Department of Environment Health , National Institute of Public Health , 
      Minami, Wako City , Saitama , Japan.
FAU - Maeyama, Kazutaka
AU  - Maeyama K
AD  - a Department of Pharmacology , Ehime University Graduate School of Medicine , 
      Toon City , Japan.
FAU - Sano, Keiji
AU  - Sano K
AD  - b Laboratory of Molecular Cell Biology , Department of Life Sciences Pharmacy , 
      School of Pharmaceutical Sciences, Kobe Gakuin University , Chuo-ku, Kobe City , 
      Japan.
FAU - Yamashita, Masahiro
AU  - Yamashita M
AD  - g Department of Respiratory Medicine , Iwate Medical University School of 
      Medicine , Morioka City , Japan.
FAU - Yamauchi, Kohei
AU  - Yamauchi K
AD  - g Department of Respiratory Medicine , Iwate Medical University School of 
      Medicine , Morioka City , Japan.
LA  - eng
PT  - Journal Article
DEP - 20160621
PL  - England
TA  - Exp Lung Res
JT  - Experimental lung research
JID - 8004944
RN  - 0 (PHB protein, human)
RN  - 0 (Prohibitins)
RN  - 0 (Repressor Proteins)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - EC 2.1.1.77 (Protein D-Aspartate-L-Isoaspartate Methyltransferase)
SB  - IM
MH  - A549 Cells
MH  - Adenosine Triphosphate/metabolism
MH  - Endoplasmic Reticulum Stress
MH  - Humans
MH  - Mitochondria/*enzymology/ultrastructure
MH  - Mitochondrial Dynamics
MH  - Oxidative Stress
MH  - Prohibitins
MH  - Protein D-Aspartate-L-Isoaspartate Methyltransferase/*metabolism
MH  - Repressor Proteins/*metabolism
OTO - NOTNLM
OT  - d-aspartic acid residue
OT  - isomerization
OT  - protein damage
EDAT- 2016/06/22 06:00
MHDA- 2017/12/12 06:00
CRDT- 2016/06/22 06:00
PHST- 2016/06/22 06:00 [entrez]
PHST- 2016/06/22 06:00 [pubmed]
PHST- 2017/12/12 06:00 [medline]
AID - 10.1080/01902148.2016.1197984 [doi]
PST - ppublish
SO  - Exp Lung Res. 2016 Jun;42(5):245-62. doi: 10.1080/01902148.2016.1197984. Epub 
      2016 Jun 21.