logo

  • P-ISSN2233-4203
  • E-ISSN2093-8950
  • ESCI, SCOPUS, KCI

논문 상세

Home > 논문 상세
  • P-ISSN 2233-4203
  • E-ISSN 2093-8950

Investigation on Lipopolysaccharide Activated Microglia by Phosphoproteomics and Phosphoinositide Lipidomics

Mass Spectrometry Letters / Mass Spectrometry Letters, (P)2233-4203; (E)2093-8950
2014, v.5 no.3, pp.70-78
https://doi.org/10.5478/MSL.2014.5.3.70
Young Jun Kim (Konkuk University)
Hackyoung Kim (Konkuk University)
Kwangmo Noh (Konkuk University)
  • 다운로드 수
  • 조회수

Abstract

Microglia are the confined immune cells of the central nervous system (CNS). In response to injury or infection,microglia readily become activated and release proinflammatory mediators that are believed to contribute to microglia-mediatedneurodegeneration. In the present study, inflammation was induced in the immortalized murine microglial cell line BV-2 bylipopolysaccharide (LPS) treatment. We firstly performed phosphoproteomics analysis and phosphoinositide lipidomics analysiswith LPS activated microglia in order to compare phosphorylation patterns in active and inactive microglia and to detect the patternof changes in phosphoinositide regulation upon activation of microglia. Mass spectrometry analysis of the phosphoproteomeof the LPS treatment group compared to that of the untreated control group revealed a notable increase in the diversity ofcellular phosphorylation upon LPS treatment. Additionally, a lipidomics analysis detected significant increases in the amounts ofphosphoinositide species in the LPS treatment. This investigation could provide an insight for understanding molecular mechanismsunderlying microglia-mediated neurodegenerative diseases.

keywords
Microglia, Lipopolysaccharide (LPS), Neuroinflammation, Phosphoproteomics, Lipidomics, Phosphoinositide


참고문헌

1

Dheen, S. T.. (2007). . Curr. Med. Chem, 14, 1189-1197.

2

Streit, W. J.. (2004). . J. Neuroinflammation, 1, 14-.

3

Kim, S. U.. (2005). . J. Neurosci. Res, 81, 302-313.

4

Lu, D. Y.. (2007). . Br. J. Pharmacol, 151, 396-405.

5

McGeer, P. L.. (1988). . Neurology, 38, 1285-1291.

6

Block, M. L.. (2007). . Nat. Rev. Neurosci, 8, 57-69.

7

Tufekci, K. U.. (2011). . Parkinsons Dis, , 487450-.

8

Carson, M. J.. (2006). . Clin. Neurosci. Res, 6, 237-245.

9

Herbert, M. R.. (2005). . Neuroscientist, 11, 417-440.

10

Liu, B.. (2003). . J. Pharmacol. Exp. Ther, 304, 1-7.

11

Boulet, I.. (1992). . Oncogene, 7, 703-710.

12

Bhat, N. R.. (1998). . J. Neurosci, 18, 1633-1641.

13

Chen, C. C.. (1998). . J Biol. Chem, 273, 19424-19430.

14

Henn, A.. (2009). . ALTEX, 26, 83-94.

15

Han, D.. (2013). . Proteomics, 13, 2984-2988.

16

Han, D.. (2014). . BMC Genomics, 15, 95-.

17

Jeon, H.. (2010). . J. Neuroimmunol, 229, 63-72.

18

Wenk, M. R.. (2003). . Nat. Biotechnol, 21, 813-817.

19

Milne, S. B.. (2005). . J. Lipid Res, 46, 1796-1802.

20

Simonsen, A.. (2001). . Curr. Opin. Cell Biol, 13, 485-492.

21

Parker, P.. (2004). . J. Biochem. Soc. Trans, 32, 893-898.

22

Pettitt, T. R.. (2006). . J. Lipid. Res, 47, 1588-1596.

23

Lee, S. Y.. . Neurochem. Int., 57, 600-607.

24

Jin, R.. . Biochem. Biophys. Res. Commun., 399, 458-464.

25

Wisniewski, J. R.. (2009). . Nat. Methods, 6, 359-362.

26

Keller, A.. (2002). . Anal. Chem, 74, 5383-5392.

투고일Received
2014-07-19
수정일Revised
2014-08-27
게재확정일Accepted
2014-09-12
출판일Published
2014-09-01
상단으로 이동

Mass Spectrometry Letters