PMID- 16461377
OWN - NLM
STAT- MEDLINE
DCOM- 20060801
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 291
IP  - 1
DP  - 2006 Jul
TI  - Ca2+ source-dependent transcription of CRE-containing genes in vascular smooth 
      muscle.
PG  - H97-105
AB  - Altered Ca2+ handling has immediate physiological and long-term genomic effects 
      on vascular smooth muscle function. Previously we showed that Ca2+ entry through 
      voltage-dependent Ca2+ channels (VDCCs) or store-operated Ca2+ channels (SOCCs) 
      results in phosphorylation of the Ca2+/cAMP response element (CRE)-binding 
      protein in cerebral arteries. Here, oligonucleotide array analysis was used to 
      determine gene transcription profiles resulting from these two Ca2+ entry 
      pathways in human cerebrovascular smooth muscle cell cultures. Results were 
      confirmed and expanded using quantitative RT-PCR, Western blot, and 
      immunofluorescence. A distinct, yet overlapping, set of CRE-regulated genes was 
      induced by VDCC activation using K+ membrane depolarization vs. SOCC activation 
      by thapsigargin (TG). Membrane depolarization selectively induced a sustained 
      increase in early growth response-1 (Egr-1) mRNA and protein, which were 
      inhibited by the VDCC blocker nimodipine and the SOCC inhibitor 
      2-aminoethoxydiphenylborate (2-APB). TG selectively induced a sustained increase 
      in MAPK phosphatase-1 (MKP-1) mRNA and protein, and these effects were decreased 
      by 2-APB, but not by nimodipine. The physiological agonist ANG II also stimulated 
      expression of Egr-1 and MKP-1. Coadministration of 2-APB prevented expression of 
      Egr-1 and MKP-1, whereas nimodipine blocked only Egr-1 expression. TG and ANG II 
      induced phosphorylation of ERK, which was sensitive to 2-APB and was selectively 
      required for CRE-binding protein phosphorylation. Our findings thus indicate that 
      Ca2+ entry through VDCCs and store-operated Ca2+ entry can differentially 
      regulate CRE-containing genes in vascular smooth muscle and also imply that 
      agonist-induced signals involved in modulation of gene transcription can be 
      controlled by multiple sources of Ca2+.
FAU - Pulver-Kaste, Renee A
AU  - Pulver-Kaste RA
AD  - Department of Pharmacology, Division of Neurological Surgery, University of 
      Vermont, Burlington, VT 05405, USA.
FAU - Barlow, Christy A
AU  - Barlow CA
FAU - Bond, Jeffery
AU  - Bond J
FAU - Watson, Anjanette
AU  - Watson A
FAU - Penar, Paul L
AU  - Penar PL
FAU - Tranmer, Bruce
AU  - Tranmer B
FAU - Lounsbury, Karen M
AU  - Lounsbury KM
LA  - eng
GR  - 1-P20-RR-16462/RR/NCRR NIH HHS/United States
GR  - R01-HL-67351/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20060203
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Calcium Channels, L-Type)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channels, L-Type/*physiology
MH  - Calcium Signaling/*physiology
MH  - Cells, Cultured
MH  - Cyclic AMP Response Element-Binding Protein/*physiology
MH  - Humans
MH  - Muscle, Smooth, Vascular/*physiology
MH  - Myocytes, Smooth Muscle/*physiology
MH  - Rats
MH  - Transcription, Genetic/*physiology
EDAT- 2006/02/08 09:00
MHDA- 2006/08/02 09:00
CRDT- 2006/02/08 09:00
PHST- 2006/02/08 09:00 [pubmed]
PHST- 2006/08/02 09:00 [medline]
PHST- 2006/02/08 09:00 [entrez]
AID - 00753.2005 [pii]
AID - 10.1152/ajpheart.00753.2005 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2006 Jul;291(1):H97-105. doi: 
      10.1152/ajpheart.00753.2005. Epub 2006 Feb 3.