PMID- 24682924
OWN - NLM
STAT- MEDLINE
DCOM- 20150528
LR  - 20211021
IS  - 1559-1166 (Electronic)
IS  - 0895-8696 (Linking)
VI  - 54
IP  - 2
DP  - 2014
TI  - Induction of matrix metalloproteinase-3 (MMP-3) expression in the microglia by 
      lipopolysaccharide (LPS) via upregulation of glycoprotein nonmetastatic melanoma 
      B (GPNMB) expression.
PG  - 234-42
LID - 10.1007/s12031-014-0280-0 [doi]
AB  - Substantial evidence suggests that inflammation is an important contributor to 
      many neurodegenerative disorders. Activated microglial cells play an important 
      role in releasing pro-inflammatory factors, including tumor necrosis factor-alpha 
      (TNF-alpha) and interleukin-1beta (IL-1beta) for inducing inflammation. Recently, some 
      reports have suggested that glycoprotein nonmetastatic melanoma B (GPNMB) is 
      highly expressed in microglia after LPS treatment. However, the role of GPNMB in 
      activated microglia is not clearly understood. In this study, we used RT-PCR and 
      Western blotting to detect GPNMB and matrix metalloproteinase-3 (MMP-3) 
      expressions in activated microglia. GPNMB small interfering RNA (siRNA) or MMP-3 
      inhibitor was applied on microglial BV2 cells, and ELISA was performed to measure 
      the expressions of TNF-alpha and IL-1beta in BV2 cells. Levels of iNOS and NO in BV2 
      cells were also determined. We found that the levels of GPNMB and MMP-3 were 
      significantly increased in BV2 cells after LPS treatment. Moreover, we found that 
      GPNMB significantly upregulated the expression of MMP-3 in BV2 cells, and high 
      expression of MMP-3 was dependent on the level of GPNMB. Inhibition of GPNMB or 
      MMP-3 expression by GPNMB siRNA or MMP-3 inhibitor dramatically suppressed the 
      expressions of TNF-alpha, IL-1beta, iNOS, and NO in activated microglia. All of these 
      results suggest that GPNMB is involved in the inflammatory responses of 
      microglia.
FAU - Shi, Fangyuan
AU  - Shi F
AD  - Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry 
      of Education, College of Life Science, Northwest University, Xi'an, 710069, 
      China.
FAU - Duan, Shuangyan
AU  - Duan S
FAU - Cui, Jihong
AU  - Cui J
FAU - Yan, Xingrong
AU  - Yan X
FAU - Li, Hongmin
AU  - Li H
FAU - Wang, Yingjuan
AU  - Wang Y
FAU - Chen, Fulin
AU  - Chen F
FAU - Zhang, Lihua
AU  - Zhang L
FAU - Liu, Jun
AU  - Liu J
FAU - Xie, Xin
AU  - Xie X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140330
PL  - United States
TA  - J Mol Neurosci
JT  - Journal of molecular neuroscience : MN
JID - 9002991
RN  - 0 (Eye Proteins)
RN  - 0 (Gpnmb protein, mouse)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 3.4.24.17 (Matrix Metalloproteinase 3)
RN  - EC 3.4.24.17 (Mmp3 protein, mouse)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Eye Proteins/genetics/*metabolism
MH  - Interleukin-1beta/genetics/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Matrix Metalloproteinase 3/genetics/*metabolism
MH  - Membrane Glycoproteins/genetics/*metabolism
MH  - Mice
MH  - Microglia/drug effects/*metabolism
MH  - Nitric Oxide Synthase Type II/genetics/metabolism
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
MH  - *Up-Regulation
EDAT- 2014/04/01 06:00
MHDA- 2015/05/29 06:00
CRDT- 2014/04/01 06:00
PHST- 2014/02/21 00:00 [received]
PHST- 2014/03/03 00:00 [accepted]
PHST- 2014/04/01 06:00 [entrez]
PHST- 2014/04/01 06:00 [pubmed]
PHST- 2015/05/29 06:00 [medline]
AID - 10.1007/s12031-014-0280-0 [doi]
PST - ppublish
SO  - J Mol Neurosci. 2014;54(2):234-42. doi: 10.1007/s12031-014-0280-0. Epub 2014 Mar 
      30.