PMID- 27670946
OWN - NLM
STAT- MEDLINE
DCOM- 20170629
LR  - 20171206
IS  - 1753-4267 (Electronic)
IS  - 1753-4259 (Linking)
VI  - 22
IP  - 8
DP  - 2016 Nov
TI  - Autophagy is induced by anti-neutrophil cytoplasmic Abs and promotes neutrophil 
      extracellular traps formation.
PG  - 658-665
LID - 10.1177/1753425916668981 [doi]
AB  - Dysregulated neutrophil extracellular traps (NETs) formation contributes to the 
      pathogenesis of anti-neutrophil cytoplasmic Ab (ANCA)-associated vasculitis 
      (AAV). Increasing evidence indicates that autophagy is involved in the process of 
      NETs formation. In this study, we aimed to investigate whether ANCA could induce 
      autophagy in the process of NETs formation. Autophagy was detected using live 
      cell imaging, microtubule-associated protein light chain 3B (LC3B) accumulation 
      and Western blotting. The results showed that autophagy vacuolization was 
      detected in neutrophils treated with ANCA-positive IgG by live cell imaging. This 
      effect was enhanced by rapamycin, the autophagy inducer, and weakened by 
      3-methyladenine (3-MA), the autophagy inhibitor. In line with these results, the 
      autophagy marker, LC3B, showed a punctate distribution pattern in the neutrophils 
      stimulated with ANCA-positive IgG. In the presence of rapamycin, LC3B 
      accumulation was further increased; however, this effect was attenuated by 3-MA. 
      Moreover, incubated with ANCA-positive IgG, the NETosis rate significantly 
      increased compared with the unstimulated group. And, the rate significantly 
      increased or decreased in the neutrophils pretreated with rapamycin or 3-MA, 
      respectively, as compared with the cells incubated with ANCA-positive IgG. 
      Overall, this study demonstrates that autophagy is induced by ANCA and promotes 
      ANCA-induced NETs formation.
FAU - Sha, Li-Li
AU  - Sha LL
AD  - 1 Renal Division, Department of Medicine, Peking University First Hospital; 
      Peking University Institute of Nephrology; Key Laboratory of Renal Disease, 
      Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention 
      and Treatment (Peking University), Ministry of Education, China.
AD  - 2 Guizhou Medical University, China.
FAU - Wang, Huan
AU  - Wang H
AD  - 1 Renal Division, Department of Medicine, Peking University First Hospital; 
      Peking University Institute of Nephrology; Key Laboratory of Renal Disease, 
      Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention 
      and Treatment (Peking University), Ministry of Education, China.
FAU - Wang, Chen
AU  - Wang C
AD  - 1 Renal Division, Department of Medicine, Peking University First Hospital; 
      Peking University Institute of Nephrology; Key Laboratory of Renal Disease, 
      Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention 
      and Treatment (Peking University), Ministry of Education, China.
FAU - Peng, Hong-Ying
AU  - Peng HY
AD  - 2 Guizhou Medical University, China.
FAU - Chen, Min
AU  - Chen M
AD  - 1 Renal Division, Department of Medicine, Peking University First Hospital; 
      Peking University Institute of Nephrology; Key Laboratory of Renal Disease, 
      Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention 
      and Treatment (Peking University), Ministry of Education, China.
FAU - Zhao, Ming-Hui
AU  - Zhao MH
AD  - 1 Renal Division, Department of Medicine, Peking University First Hospital; 
      Peking University Institute of Nephrology; Key Laboratory of Renal Disease, 
      Ministry of Health of China; Key Laboratory of Chronic Kidney Disease Prevention 
      and Treatment (Peking University), Ministry of Education, China.
AD  - 3 Peking-Tsinghua Center for Life Sciences, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160926
PL  - United States
TA  - Innate Immun
JT  - Innate immunity
JID - 101469670
RN  - 0 (Antibodies, Antineutrophil Cytoplasmic)
RN  - 0 (MAP1LC3B protein, human)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 5142-23-4 (3-methyladenine)
RN  - JAC85A2161 (Adenine)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - Adenine/analogs & derivatives/pharmacology
MH  - Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis/drug 
      therapy/*immunology
MH  - Antibodies, Antineutrophil Cytoplasmic/*metabolism
MH  - *Autophagy/drug effects
MH  - Cells, Cultured
MH  - Extracellular Traps/*metabolism
MH  - Healthy Volunteers
MH  - Humans
MH  - Microtubule-Associated Proteins/metabolism
MH  - Neutrophils/drug effects/*immunology
MH  - Sirolimus/pharmacology
OTO - NOTNLM
OT  - ANCA
OT  - Autophagy
OT  - neutrophil extracellular traps
OT  - vasculitis
EDAT- 2016/09/28 06:00
MHDA- 2017/07/01 06:00
CRDT- 2016/09/28 06:00
PHST- 2016/09/28 06:00 [pubmed]
PHST- 2017/07/01 06:00 [medline]
PHST- 2016/09/28 06:00 [entrez]
AID - 1753425916668981 [pii]
AID - 10.1177/1753425916668981 [doi]
PST - ppublish
SO  - Innate Immun. 2016 Nov;22(8):658-665. doi: 10.1177/1753425916668981. Epub 2016 
      Sep 26.