PMID- 32800547
OWN - NLM
STAT- MEDLINE
DCOM- 20210310
LR  - 20210310
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 531
IP  - 3
DP  - 2020 Oct 20
TI  - Tumor necrosis factor-alpha aggravates gliosis and inflammation of activated 
      retinal Muller cells.
PG  - 383-389
LID - S0006-291X(20)31499-6 [pii]
LID - 10.1016/j.bbrc.2020.07.102 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha), a major inflammatory factor released from 
      activated retinal glial cells, is implicated in the pathogenesis of glaucoma. In 
      this study, we investigated whether and how TNF-alpha may affect functional 
      conditions of activated retinal Muller cells. Our results showed that in the 
      group I metabotropic glutamate receptor (mGluR I) agonist DHPG-activated cultured 
      Muller cells, TNF-alpha treatment aggravated cell gliosis, as evidenced by 
      significantly increased expression of glial fibrillary acidic protein (GFAP). 
      TNF-alpha treatment of the DHPG-activated Muller cells decreased cell proliferation 
      and induced cell apoptosis. In normal Muller cells, TNF-alpha treatment increased the 
      mRNA levels of leukocyte inhibitory factor (LIF), intercellular cell adhesion 
      molecule (ICAM), vascular cell adhesion molecule (VCAM), and chemokine C-C-motif 
      ligand 2 (CCL2), which could be significantly attenuated when Muller cells were 
      pre-activated. However, TNF-alpha-induced elevation in mRNA levels of inflammatory 
      factors, such as TNF-alpha, inducible nitric oxide synthase (iNOS), and interleukin-6 
      (IL-6), in normal Muller cells still kept higher levels when Muller cells were 
      pre-activated. Furthermore, the TNF-alpha-induced changes of cytokines were partially 
      mediated by NF-kappaB signaling pathway. Our results suggest that TNF-alpha may promote 
      gliosis and inflammatory response of activated Muller cells, thus aggravating RGC 
      injury in glaucoma.
CI  - Copyright (c) 2020 Elsevier Inc. All rights reserved.
FAU - Hu, Xin
AU  - Hu X
AD  - Department of Ophthalmology, State Key Laboratory of Medical Neurobiology, MOE 
      Frontiers Center for Brain Science, Institutes of Brain Science, Fudan 
      University, Shanghai, 200032, China.
FAU - Xu, Meng-Xi
AU  - Xu MX
AD  - Department of Ophthalmology, State Key Laboratory of Medical Neurobiology, MOE 
      Frontiers Center for Brain Science, Institutes of Brain Science, Fudan 
      University, Shanghai, 200032, China.
FAU - Zhou, Han
AU  - Zhou H
AD  - Department of Ophthalmology, State Key Laboratory of Medical Neurobiology, MOE 
      Frontiers Center for Brain Science, Institutes of Brain Science, Fudan 
      University, Shanghai, 200032, China.
FAU - Cheng, Shuo
AU  - Cheng S
AD  - Department of Ophthalmology, State Key Laboratory of Medical Neurobiology, MOE 
      Frontiers Center for Brain Science, Institutes of Brain Science, Fudan 
      University, Shanghai, 200032, China.
FAU - Li, Fang
AU  - Li F
AD  - Department of Ophthalmology, State Key Laboratory of Medical Neurobiology, MOE 
      Frontiers Center for Brain Science, Institutes of Brain Science, Fudan 
      University, Shanghai, 200032, China.
FAU - Miao, Yanying
AU  - Miao Y
AD  - Department of Ophthalmology, State Key Laboratory of Medical Neurobiology, MOE 
      Frontiers Center for Brain Science, Institutes of Brain Science, Fudan 
      University, Shanghai, 200032, China.
FAU - Wang, Zhongfeng
AU  - Wang Z
AD  - Department of Ophthalmology, State Key Laboratory of Medical Neurobiology, MOE 
      Frontiers Center for Brain Science, Institutes of Brain Science, Fudan 
      University, Shanghai, 200032, China. Electronic address: zfwang@fudan.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200813
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Cytokines)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 534-82-7 (Methoxyhydroxyphenylglycol)
RN  - UEH9K539KJ (3,4-dihydroxyphenylglycol)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Cell Proliferation/drug effects
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Cytokines/metabolism
MH  - Ependymoglial Cells/drug effects/metabolism/*pathology
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Gliosis/complications/*pathology
MH  - Inflammation/complications/*pathology
MH  - Methoxyhydroxyphenylglycol/analogs & derivatives/pharmacology
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Signal Transduction/drug effects
MH  - Tumor Necrosis Factor-alpha/*toxicity
OTO - NOTNLM
OT  - Glaucoma
OT  - Gliosis
OT  - Inflammation
OT  - Muller cells
OT  - Tumor necrosis factor-alpha
COIS- Declaration of competing interest The authors declare that they have no conflict 
      of interest with the manuscript.
EDAT- 2020/08/18 06:00
MHDA- 2021/03/11 06:00
CRDT- 2020/08/18 06:00
PHST- 2020/07/21 00:00 [received]
PHST- 2020/07/22 00:00 [accepted]
PHST- 2020/08/18 06:00 [pubmed]
PHST- 2021/03/11 06:00 [medline]
PHST- 2020/08/18 06:00 [entrez]
AID - S0006-291X(20)31499-6 [pii]
AID - 10.1016/j.bbrc.2020.07.102 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2020 Oct 20;531(3):383-389. doi: 
      10.1016/j.bbrc.2020.07.102. Epub 2020 Aug 13.