PMID- 10347091
OWN - NLM
STAT- MEDLINE
DCOM- 19990623
LR  - 20190706
IS  - 0009-7330 (Print)
IS  - 0009-7330 (Linking)
VI  - 84
IP  - 10
DP  - 1999 May 28
TI  - EVEC, a novel epidermal growth factor-like repeat-containing protein upregulated 
      in embryonic and diseased adult vasculature.
PG  - 1166-76
AB  - A hallmark of vascular lesions is the phenotypic modulation of vascular smooth
      muscle cells (VSMCs) from a quiescent, contractile state to a more primitive,
      proliferative phenotype with a more fetal pattern of gene expression. Using
      subtraction hybridization to identify genes that may regulate this transition, we
      cloned a novel gene named EVEC, an acronym for its expression in the embryonic
      vasculature and the presence of Ca2+ binding epidermal growth factor-like repeats
      contained in the predicted protein structure. Although these repeats are
      characteristic of the extracellular matrix proteins, fibrillin, fibulin, and the 
      latent transforming growth factor-beta binding proteins, EVEC most closely
      resembles the H411 and T16/S1-5 gene products, the latter of which are believed
      to regulate DNA synthesis in quiescent fibroblasts. Using in situ hybridization, 
      we demonstrated that EVEC is expressed predominantly in the VSMCs of developing
      arteries in E11.5 through E16.5 mouse embryos. Lower levels of expression are
      also observed in endothelial cells, perichondrium, intestine, and mesenchyme of
      the face and kidney. EVEC mRNA expression is dramatically downregulated in adult 
      arteries, except in the uterus, where cyclic angiogenesis continues; however,
      EVEC expression is reactivated in 2 independent rodent models of vascular injury.
      EVEC mRNA is observed in cellular elements of atherosclerotic plaques of LDL
      receptor-deficient, human apolipoprotein B transgenic mice and in VSMCs of the
      media and neointima of balloon-injured rat carotid arteries. These data suggest
      that EVEC may play an important role in the regulation of vascular growth and
      maturation during development and in lesions of injured vessels.
FAU - Kowal, R C
AU  - Kowal RC
AD  - Department of Internal Medicine, University of Texas Southwestern Medical Center,
      Dallas, Texas 75235-9148, USA.
FAU - Richardson, J A
AU  - Richardson JA
FAU - Miano, J M
AU  - Miano JM
FAU - Olson, E N
AU  - Olson EN
LA  - eng
SI  - GENBANK/AF137350
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circ Res
JT  - Circulation research
JID - 0047103
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (FBLN5 protein, human)
RN  - 0 (Fbln5 protein, mouse)
RN  - 0 (Fbln5 protein, rat)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
RN  - 62229-50-9 (Epidermal Growth Factor)
RN  - 9007-58-3 (Elastin)
SB  - IM
CIN - Circ Res. 1999 May 28;84(10):1234-5. PMID: 10347098
MH  - Age Factors
MH  - Animals
MH  - Arteriosclerosis/genetics/metabolism
MH  - Blotting, Northern
MH  - COS Cells
MH  - Cells, Cultured
MH  - Cloning, Molecular
MH  - Cytoplasmic Granules/metabolism
MH  - Elastin/analysis
MH  - Epidermal Growth Factor/*genetics/metabolism
MH  - *Extracellular Matrix Proteins
MH  - Fetus/chemistry/physiology
MH  - *Gene Expression Regulation, Developmental
MH  - In Situ Hybridization
MH  - Mice
MH  - Microsomes/chemistry/metabolism
MH  - Molecular Sequence Data
MH  - Muscle, Smooth, Vascular/*chemistry/cytology/physiology
MH  - Phenotype
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - *Recombinant Proteins
MH  - Repetitive Sequences, Nucleic Acid
MH  - Sequence Homology, Amino Acid
MH  - Tunica Intima/chemistry/cytology/physiology
MH  - Up-Regulation/physiology
EDAT- 1999/05/29 00:00
MHDA- 1999/05/29 00:01
CRDT- 1999/05/29 00:00
PHST- 1999/05/29 00:00 [pubmed]
PHST- 1999/05/29 00:01 [medline]
PHST- 1999/05/29 00:00 [entrez]
AID - 10.1161/01.res.84.10.1166 [doi]
PST - ppublish
SO  - Circ Res. 1999 May 28;84(10):1166-76. doi: 10.1161/01.res.84.10.1166.