PMID- 10036240
OWN - NLM
STAT- MEDLINE
DCOM- 19990504
LR  - 20091119
IS  - 0021-9533 (Print)
IS  - 0021-9533 (Linking)
VI  - 112 ( Pt 6)
DP  - 1999 Mar
TI  - PDGF (alpha)-receptor is unresponsive to PDGF-AA in aortic smooth muscle cells
      from the NG2 knockout mouse.
PG  - 905-15
AB  - A line of null mice has been produced which fails to express the transmembrane
      chondroitin sulfate proteoglycan NG2. Homozygous NG2 null mice do not exhibit
      gross phenotypic differences from wild-type mice, suggesting that detailed
      analyses are required to detect subtle alterations caused by the absence of NG2. 
      Accordingly, dissociated cultures of aortic smooth muscle cells from null mice
      were compared to parallel cultures from wild-type mice for their ability to
      proliferate and migrate in response to specific growth factors. Both null and
      wild-type smooth muscle cells exhibited identical abilities to proliferate and
      migrate in response to PDGF-BB. In contrast, only the wild-type cells responded
      to PDGF-AA in both types of assays. NG2 null cells failed to proliferate or
      migrate in response to PDGF-AA, implying a defect in the signaling cascade
      normally initiated by activation of the PDGF (alpha)-receptor. In agreement with 
      this idea, activation of the extracellular signal-regulated kinase (ERK) in
      response to PDGF-AA treatment occured only in wild-type cells. Failure to observe
      autophosphorylation of the PDGF (alpha)-receptor in PDGF-AA-treated null cells
      indicates that the absence of NG2 causes a defect in signal transduction at the
      level of (alpha)-receptor activation.
FAU - Grako, K A
AU  - Grako KA
AD  - The Burnham Institute, La Jolla Cancer Research Center, La Jolla, CA 92037, USA.
FAU - Ochiya, T
AU  - Ochiya T
FAU - Barritt, D
AU  - Barritt D
FAU - Nishiyama, A
AU  - Nishiyama A
FAU - Stallcup, W B
AU  - Stallcup WB
LA  - eng
GR  - F32 HL09541/HL/NHLBI NIH HHS/United States
GR  - R01 NS21990/NS/NINDS NIH HHS/United States
GR  - R01 NS32767/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Cell Sci
JT  - Journal of cell science
JID - 0052457
RN  - 0 (Antigens)
RN  - 0 (Platelet-Derived Growth Factor)
RN  - 0 (Proteoglycans)
RN  - 0 (chondroitin sulfate proteoglycan 4)
RN  - 0 (platelet-derived growth factor A)
RN  - EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor alpha)
RN  - EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
SB  - IM
MH  - Animals
MH  - Antigens/analysis/genetics/*physiology
MH  - Aorta
MH  - Calcium-Calmodulin-Dependent Protein Kinases/*metabolism
MH  - Cell Division/drug effects
MH  - Cell Movement/drug effects
MH  - Genomic Library
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Mitogen-Activated Protein Kinase 1
MH  - Muscle, Smooth, Vascular/cytology/drug effects/*physiology
MH  - Optic Nerve/physiology
MH  - Phosphorylation
MH  - Platelet-Derived Growth Factor/*pharmacology
MH  - Proteoglycans/analysis/genetics/*physiology
MH  - Receptor, Platelet-Derived Growth Factor alpha
MH  - Receptors, Platelet-Derived Growth Factor/drug effects/*physiology
MH  - Stem Cells/physiology
EDAT- 1999/02/26 00:00
MHDA- 1999/02/26 00:01
CRDT- 1999/02/26 00:00
PHST- 1999/02/26 00:00 [pubmed]
PHST- 1999/02/26 00:01 [medline]
PHST- 1999/02/26 00:00 [entrez]
PST - ppublish
SO  - J Cell Sci. 1999 Mar;112 ( Pt 6):905-15.