PMID- 15319282
OWN - NLM
STAT- MEDLINE
DCOM- 20050324
LR  - 20210206
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 104
IP  - 13
DP  - 2004 Dec 15
TI  - Lysophosphatidic acid accelerates the development of human mast cells.
PG  - 4080-7
AB  - Mast cells (MCs) initiate immune responses from mucosal surfaces and perivascular 
      spaces. Stem cell factor (SCF) regulates MC development and viability, but the 
      role of innate serum factors in MC development is unexplored. Cultured cord 
      blood-derived human MCs (hMCs) express mRNA transcripts for all 4 known receptors 
      for lysophosphatidic acid (LPA), an abundant serum-associated lipid growth 
      factor. In an SCF-dependent serum-free culture system, LPA (2.5-10 microM) 
      increased the total number of hMCs by approximately 10-fold compared with 
      cultures maintained in the absence of LPA under otherwise identical conditions. 
      LPA was comitogenic with SCF but did not prolong MC survival. LPA-mediated 
      proliferation was blocked by VPC-32179, a competitive antagonist of LPA(1) and 
      LPA(3) receptors, and by pertussis toxin, and it was also attenuated by GW9662, a 
      selective antagonist of peroxisome proliferator-activated receptor (PPAR)-gamma. 
      LPA accelerated the acquisition of hMC granules and increased Kit expression. 
      hMCs derived in the presence of LPA were functional, as evidenced by their 
      immunoglobulin E (IgE)-dependent histamine release and by their characteristic 
      proliferative responses to interleukin-3 (IL-3), IL-4, and IL-9 in combination 
      with SCF. Thus, LPA acts through LPA receptor and PPAR-gamma-dependent pathways 
      to accelerate hMC proliferation and differentiation, and it modulates their 
      phenotype without providing cytoprotection. LPA could facilitate MC hyperplasia 
      in inflammation associated with either innate or adaptive immunity.
FAU - Bagga, Savita
AU  - Bagga S
AD  - Department of Medicine, Harvard Medical School, Boston, MA, USA.
FAU - Price, Kursteen S
AU  - Price KS
FAU - Lin, Debby A
AU  - Lin DA
FAU - Friend, Daniel S
AU  - Friend DS
FAU - Austen, K Frank
AU  - Austen KF
FAU - Boyce, Joshua A
AU  - Boyce JA
LA  - eng
GR  - AI-31599/AI/NIAID NIH HHS/United States
GR  - AI-48802/AI/NIAID NIH HHS/United States
GR  - AI-52353/AI/NIAID NIH HHS/United States
GR  - HL-36110/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20040819
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (DNA Primers)
RN  - 0 (Lysophospholipids)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Lysophosphatidic Acid)
SB  - IM
MH  - Apoptosis
MH  - Base Sequence
MH  - Cell Division
MH  - DNA Primers
MH  - Fetal Blood
MH  - Humans
MH  - Infant, Newborn
MH  - Leukocytes, Mononuclear/cytology/drug effects/immunology
MH  - Lysophospholipids/*pharmacology
MH  - Mast Cells/*cytology/drug effects/immunology
MH  - RNA, Messenger/genetics
MH  - Receptors, Lysophosphatidic Acid/genetics/immunology
MH  - Umbilical Cord
EDAT- 2004/08/21 05:00
MHDA- 2005/03/25 09:00
CRDT- 2004/08/21 05:00
PHST- 2004/08/21 05:00 [pubmed]
PHST- 2005/03/25 09:00 [medline]
PHST- 2004/08/21 05:00 [entrez]
AID - S0006-4971(20)49051-2 [pii]
AID - 10.1182/blood-2004-03-1166 [doi]
PST - ppublish
SO  - Blood. 2004 Dec 15;104(13):4080-7. doi: 10.1182/blood-2004-03-1166. Epub 2004 Aug 
      19.