PMID- 19878709
OWN - NLM
STAT- MEDLINE
DCOM- 20100224
LR  - 20131121
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 165
IP  - 2
DP  - 2010 Jan 20
TI  - NG2, a member of chondroitin sulfate proteoglycans family mediates the 
      inflammatory response of activated microglia.
PG  - 386-94
LID - 10.1016/j.neuroscience.2009.10.022 [doi]
AB  - Activation of microglial cells, the resident immune cells of the CNS causes 
      neurotoxicity through the release of a wide array of inflammatory mediators 
      including proinflammatory cytokines, chemokines and reactive oxygen species. In 
      this study, we have investigated the expression of NG2 (also known as CSPG4), one 
      of the members of transmembrane chondroitin sulfate proteoglycans family, in 
      microglial cells and its role on inflammatory reaction of microglia by analyzing 
      the expression of the proinflammation cytokines (interleukin-1beta (IL-1beta) and 
      tumor necrosis factor-alpha (TNF-alpha)), chemokines (stromal cell-derived 
      factor-1alpha and monocyte chemotactic protein-1) and inducible nitric oxide 
      synthase (iNOS). NG2 expression was not detectable in microglial cells expressing 
      OX-42 in the brains of 1-day old postnatal rat pups and adult rats; it was, 
      however, induced in activated microglial cells in pups and adult rats injected 
      with lipopolysaccharide (LPS). In vitro analysis further confirmed that LPS 
      induced the expression of NG2 in primary microglial cells and this was inhibited 
      by dexamethasone. It has been well demonstrated that LPS induces the expression 
      of iNOS and proinflammatory cytokines in microglia. However in this study, LPS 
      did not induce the mRNA expression of iNOS and cytokines including IL-1beta, and 
      TNF-alpha in microglial cells transfected with CSPG4 siRNA. On the contrary, mRNA 
      expression of chemokines such as monocyte chemoattractant protein-1 (MCP-1) and 
      stromal cell-derived factor-1alpha (SDF-1alpha) was significantly increased in 
      LPS-activated microglial cells after CSPG4 siRNA transfection in comparison with 
      the control. The above results indicate that NG2 mediates the induction of iNOS 
      and inflammatory cytokine expression, but not the chemokine expression in 
      activated microglia.
FAU - Gao, Q
AU  - Gao Q
AD  - Department of Anatomy, Yong Loo Lin School of Medicine, National University of 
      Singapore, Singapore.
FAU - Lu, J
AU  - Lu J
FAU - Huo, Y
AU  - Huo Y
FAU - Baby, N
AU  - Baby N
FAU - Ling, E A
AU  - Ling EA
FAU - Dheen, S T
AU  - Dheen ST
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antigens)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Proteoglycans)
RN  - 0 (RNA, Messenger)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (chondroitin sulfate proteoglycan 4)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
SB  - IM
MH  - Aging
MH  - Animals
MH  - Animals, Newborn
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Antigens/*metabolism
MH  - Brain/drug effects/*immunology/*physiology
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CXCL12/metabolism
MH  - Dexamethasone/pharmacology
MH  - Interleukin-1beta/metabolism
MH  - Lipopolysaccharides/toxicity
MH  - Microglia/drug effects/*immunology/*physiology
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - Proteoglycans/*metabolism
MH  - RNA, Messenger/metabolism
MH  - RNA, Small Interfering/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2009/11/03 06:00
MHDA- 2010/02/25 06:00
CRDT- 2009/11/03 06:00
PHST- 2009/02/16 00:00 [received]
PHST- 2009/10/12 00:00 [revised]
PHST- 2009/10/12 00:00 [accepted]
PHST- 2009/11/03 06:00 [entrez]
PHST- 2009/11/03 06:00 [pubmed]
PHST- 2010/02/25 06:00 [medline]
AID - S0306-4522(09)01662-5 [pii]
AID - 10.1016/j.neuroscience.2009.10.022 [doi]
PST - ppublish
SO  - Neuroscience. 2010 Jan 20;165(2):386-94. doi: 10.1016/j.neuroscience.2009.10.022.