PMID- 17404035
OWN - NLM
STAT- MEDLINE
DCOM- 20070508
LR  - 20071115
IS  - 0077-8923 (Print)
IS  - 0077-8923 (Linking)
VI  - 1095
DP  - 2007 Jan
TI  - Inhibition of serine-threonine protein phosphatases in monocyte chemoattractant 
      protein-1 expression in Helicobacter pylori-stimulated gastric epithelial cells.
PG  - 220-7
AB  - The reversible phosphorylation of proteins controlled by protein kinases and 
      protein phosphatases is a major mechanism that regulates a wide variety of 
      cellular processes, such as inflammation. It has been reported that the activity 
      of at least 30% of all proteins can be regulated by phosphorylation in eukaryotic 
      cells. Among these proteins, mitogen-activated protein kinases (MAPK) and several 
      transcription factors play pivotal roles in inflammation. We previously 
      demonstrated that Helicobacter pylori in a Korean isolate (HP99) induced 
      proinflammatory chemokine expression by activating MAPK and transcription 
      factors, nuclear factor-kappaB (NF-kappaB), and activator protein-1 (AP-1) in 
      gastric epithelial AGS cells. In an attempt to determine the role of 
      phosphorylation-dephosphorylation in HP99-induced inflammation, we analyzed the 
      expression of protein phosphatases, the activation of MAPK and transcription 
      factors, and the production of chemokine MCP-1 in AGS cells stimulated with HP99 
      (at a bacteria-cell ratio of 300:1) and cultured in the presence or absence of a 
      nonspecific serine-threonine protein phosphatase inhibitor, okadaic acid (OA). 
      Our results showed that HP99 induced the expression of protein phosphatases, PP1 
      and PP2A in AGS cells as early as 30 min. HP99 induced the activation of MAPK and 
      AP-1, and the production of monocyte chemoattractant protein-1 (MCP-1), which 
      were augmented by pretreatment with 100 nM of OA. Gastric epithelial cells 
      induced the expression of PP1 and PP2A in response to HP99 presumably as a 
      defense mechanism against inflammatory chemokine expression by inhibiting the 
      activation of MAPK and AP-1.
FAU - Chung, Hae-Yun
AU  - Chung HY
AD  - Department of Food and Nutrition, Yonsei University College of Human Ecology, 
      Seoul 120-749, Korea.
FAU - Cha, Boram
AU  - Cha B
FAU - Kim, Hyeyoung
AU  - Kim H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (Chemokine CCL2)
RN  - EC 3.1.3.16 (Phosphoprotein Phosphatases)
SB  - IM
MH  - Cell Line, Tumor
MH  - Chemokine CCL2/*biosynthesis/genetics/physiology
MH  - Gastric Mucosa/*enzymology/*microbiology/pathology
MH  - Gastritis/enzymology/microbiology/pathology
MH  - Gene Expression Regulation, Bacterial
MH  - Helicobacter Infections/enzymology/pathology
MH  - Helicobacter pylori/*physiology
MH  - Humans
MH  - Phosphoprotein Phosphatases/*antagonists & inhibitors
EDAT- 2007/04/04 09:00
MHDA- 2007/05/09 09:00
CRDT- 2007/04/04 09:00
PHST- 2007/04/04 09:00 [pubmed]
PHST- 2007/05/09 09:00 [medline]
PHST- 2007/04/04 09:00 [entrez]
AID - 1095/1/220 [pii]
AID - 10.1196/annals.1397.026 [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2007 Jan;1095:220-7. doi: 10.1196/annals.1397.026.