scholarly journals Ca2+ can control vascular smooth-muscle thin filaments without caldesmon phosphorylation

1986 ◽  
Vol 237 (2) ◽  
pp. 605-607 ◽  
Author(s):  
S B Marston
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Binding Protein ◽  
Direct Interaction ◽  
Half Time ◽  
Thin Filaments

The Ca2+-dependent regulation of the activation of myosin MgATPase by vascular-smooth-muscle thin filaments involves caldesmon. This effect may be due to the direct interaction of caldesmon with a Ca2+-binding protein such as calmodulin or phosphorylation of caldesmon by a Ca2+-dependent kinase. I have found that Ca2+ switches on aorta thin filaments in less than 10 s, whereas the caldesmon in the thin filaments is phosphorylated only slowly (half-time greater than 10 min) and the maximum phosphorylation is very low (1 molecule per 7 molecules of caldesmon). I conclude that the phosphorylation of caldesmon hypothesis is untenable.

scholarly journals FXR1 Is an IL-19-Responsive RNA-Binding Protein that Destabilizes Pro-inflammatory Transcripts in Vascular Smooth Muscle Cells

Cell Reports ◽  
2018 ◽  
Vol 24 (5) ◽  
pp. 1176-1189 ◽  
Author(s):  
Allison B. Herman ◽  
Christine N. Vrakas ◽  
Mitali Ray ◽  
Sheri E. Kelemen ◽  
Michael J. Sweredoski ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Muscle Cells

scholarly journals lncRNA-SNHG14 Promotes Atherosclerosis by Regulating RORα Expression through Sponge miR-19a-3p

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Baoliang Zhu ◽  
Jing Liu ◽  
Ying Zhao ◽  
Jing Yan
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Direct Interaction ◽  
Muscle Cells ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Regulatory Relationship ◽  
Vsmc Proliferation

Coronary heart disease (CHD) is the most common cardiovascular disease with high prevalence, disability, and mortality. The balance between proliferation and apoptosis of vascular smooth muscle cells (VSMCs) plays a key role in the initiation of atherosclerosis. In this study, we found a significant decrease in the expression of lncRNA-SNHG14 in atherosclerotic plaque tissues of ApoE-/- mice. Overexpression of lncRNA-SNHG14 can inhibit VSMC proliferation while promoting apoptosis. There is a potential reciprocal regulatory relationship between lncRNASNHG14 and miR-19a-3p, which inhibit each other’s expression in vascular smooth muscle cells. In addition, the luciferase reporter gene analysis results showed that there was a direct interaction between miR-19a-3p and the 3′UTR of RORα. The results of qRT-PCR showed that the level of RORα mRNA was significantly increased in the aortas treated with miR-19a-3p and SNHG14 compared with that treated with miR-19a-3p alone. In conclusion, we demonstrated that lncRNA-SNHG14 regulates the apoptosis/proliferation balance of VSMCs in atherosclerosis.

scholarly journals Apoptosis Induced by Inhibition of Cyclic AMP Response Element–Binding Protein in Vascular Smooth Muscle Cells

Circulation ◽  
2003 ◽  
Vol 108 (10) ◽  
pp. 1246-1252 ◽  
Author(s):  
Tomotake Tokunou ◽  
Rei Shibata ◽  
Hisashi Kai ◽  
Toshihiro Ichiki ◽  
Takashi Morisaki ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cyclic Amp ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Binding Protein ◽  
Muscle Cells ◽  
Response Element ◽  
Element Binding Protein ◽  
Cyclic Amp Response Element

Ca2+ source-dependent transcription of CRE-containing genes in vascular smooth muscle

2006 ◽  
Vol 291 (1) ◽  
pp. H97-H105 ◽  
Author(s):  
Renee A. Pulver-Kaste ◽  
Christy A. Barlow ◽  
Jeffery Bond ◽  
Anjanette Watson ◽  
Paul L. Penar ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Gene Transcription ◽  
Binding Protein ◽  
Cerebral Arteries ◽  
Membrane Depolarization ◽  
Oligonucleotide Array ◽  
Ang Ii ◽  
Multiple Sources ◽  
Sustained Increase

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+.

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