◀ Back to IGF1
IGF1 — SMC3
Text-mined interactions from Literome
Myllärniemi et al., Cardiovasc Drugs Ther 1999
:
Administration of the PDGF-R tyrosine kinase inhibitor in vivo, tested and found to inhibit the proliferation of
SMC induced by PDGF-AA and PDGF-BB, but not by
IGF-1 , EGF, or bFGF, resulted in a 60 % reduction in the absolute number and percentage of BrdU + cells after the second balloon injury to pre existing neointima, but had no significant effect on proliferation after the first injury
Ling et al., Mol Endocrinol 2003
:
These results define a mechanism by which ligand occupancy of alphaVbeta3 regulates the
SMC response to
IGF-I
Resch et al., Endocrinology 2006
(Carotid Artery Injuries...) :
In this study, we used mice with targeted disruption of the pregnancy associated plasma protein-A gene ( PAPP-A-/- ) and wild-type ( WT ) littermates to test the hypotheses that PAPP-A, a metalloproteinase that cleaves inhibitory IGF binding protein (IGFBP)-4, regulates vascular
SMC responses to
IGF-I in vitro and is critical for the development of vascular neointima after injury in vivo
Maile et al., Exp Diabetes Res 2010
(Hyperglycemia) :
Furthermore we determined that TSP-1 also enhanced phosphorylation of the beta3 subunit of the alphaVbeta3 integrin, another molecular event that we have shown are critical for
SMC response to
IGF-I in high glucose
Bale et al., Am J Physiol Endocrinol Metab 2013
(Carotid Artery Injuries) :
In this study, we used transgenic mice that constitutively express human PAPP-A in arterial smooth muscle to test the hypothesis that overexpression of PAPP-A enhances vascular
smooth muscle cell ( SMC ) response to
IGF-I in vivo
Dempsey et al., J Cell Physiol 1990
:
This study investigates the potential proliferative
effects of
IGF-I on
SMC cultured from the pulmonary arteries ( PA ) of neonatal calves
Gong et al., J Biol Chem 1995
:
Epidermal growth factor (EGF) or
insulin-like growth factor I (IGF-I) alone
had little effect on
SMC ScR activity
Tamaroglio et al., Exp Cell Res 1994
:
IGF-I enhances
SMC and FN mRNA levels, implying that acquisition of additional FN mRNA units accounts for the increase in FN levels
Yamamoto et al., Exp Cell Res 1994
:
We examined the
effects of platelet derived growth factor ( PDGF ),
insulin-like growth factor-I (IGF-I) , and epidermal growth factor (EGF) on the regulation of
SMC grown on type I collagen coated dishes in serum-free primary culture
Duan et al., J Biol Chem 1996
:
Previous studies have shown that porcine aortic smooth muscle cells ( SMCs ) secrete two insulin-like growth factor binding proteins ( IGFBP ), IGFBP-2 and -4, and that these IGFBPs modulate
IGF-I stimulated
SMC proliferation and migration
Wang et al., Endocrinology 1998
:
Although we can not exclude that the effects of IGFBP-4 may be IGF independent, these data suggest that IGFBP-4 is a functional antagonist of
IGF-I action on
SMC in vivo
Clemmons et al., Mol Cell Endocrinol 1998
:
This event results in a potentiation of
IGF-I action on fibroblasts and
smooth muscle cells ( SMC )