scholarly journals Vascular Smooth Muscle α-Actin Gene Transcription during Myofibroblast Differentiation Requires Sp1/3 Protein Binding Proximal to the MCAT Enhancer

2002 ◽  
Vol 277 (39) ◽  
pp. 36433-36442 ◽  
Author(s):  
John G. Cogan ◽  
Sukanya V. Subramanian ◽  
John A. Polikandriotis ◽  
Robert J. Kelm ◽  
Arthur R. Strauch
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Protein Binding ◽  
Gene Transcription ◽  
Actin Gene ◽  
Myofibroblast Differentiation

scholarly journals YB-1 Coordinates Vascular Smooth Muscle α-Actin Gene Activation by Transforming Growth Factor β1 and Thrombin during Differentiation of Human Pulmonary Myofibroblasts

2005 ◽  
Vol 16 (10) ◽  
pp. 4931-4940 ◽  
Author(s):  
Aiwen Zhang ◽  
Xiaoying Liu ◽  
John G. Cogan ◽  
Matthew D. Fuerst ◽  
John A. Polikandriotis ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Gene Transcription ◽  
Transforming Growth Factor ◽  
Human Fibroblasts ◽  
Transforming Growth Factor Β1 ◽  
Translational Efficiency ◽  
Myofibroblast Differentiation ◽  
Early Protein

Profibrotic regulatory mechanisms for tissue repair after traumatic injury have developed under strong evolutionary pressure to rapidly stanch blood loss and close open wounds. We have examined the roles played by two profibrotic mediators, transforming growth factor β1 (TGFβ1) and thrombin, in directing expression of the vascular smooth muscle α-actin (SMαA) gene, an important determinant of myofibroblast differentiation and early protein marker for stromal cell response to tissue injury. TGFβ1 is a well known transcriptional activator of the SMαA gene in myofibroblasts. In contrast, thrombin independently elevates SMαA expression in human pulmonary myofibroblasts at the posttranscriptional level. A common feature of SMαA up-regulation mediated by thrombin and TGFβ1 is the involvement of the cold shock domain protein YB-1, a potent repressor of SMαA gene transcription in human fibroblasts that also binds mRNA and regulates translational efficiency. YB-1 dissociates from SMαA enhancer DNA in the presence of TGFβ1 or its Smad 2, 3, and 4 coregulatory mediators. Thrombin does not effect SMαA gene transcription but rather displaces YB-1 from SMαA exon 3 coding sequences previously shown to be required for mRNA translational silencing. The release of YB-1 from promoter DNA coupled with its ability to bind RNA and shuttle between the nucleus and cytoplasm is suggestive of a regulatory loop for coordinating SMαA gene output in human pulmonary myofibroblasts at both the transcriptional and translational levels. This loop may help restrict organ-destructive remodeling due to excessive myofibroblast differentiation.

scholarly journals Sequential activation of alpha-actin genes during avian cardiogenesis: vascular smooth muscle alpha-actin gene transcripts mark the onset of cardiomyocyte differentiation.

1988 ◽  
Vol 107 (6) ◽  
pp. 2575-2586 ◽  
Author(s):  
D L Ruzicka ◽  
R J Schwartz
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cardiac Cells ◽  
Actin Gene ◽  
Heart Tube ◽  
Specific Expression ◽  
Actin Genes ◽  
Beta Actin ◽  
Smooth Muscle Alpha Actin ◽  
Alpha Actin

The expression of cytoplasmic beta-actin and cardiac, skeletal, and smooth muscle alpha-actins during early avian cardiogenesis was analyzed by in situ hybridization with mRNA-specific single-stranded DNA probes. The cytoplasmic beta-actin gene was ubiquitously expressed in the early chicken embryo. In contrast, the alpha-actin genes were sequentially activated in avian cardiac tissue during the early stages of heart tube formation. The accumulation of large quantities of smooth muscle alpha-actin transcripts in epimyocardial cells preceded the expression of the sarcomeric alpha-actin genes. The accumulation of skeletal alpha-actin mRNAs in the developing heart lagged behind that of cardiac alpha-actin by several embryonic stages. At Hamburger-Hamilton stage 12, the smooth muscle alpha-actin gene was selectively down-regulated in the heart such that only the conus, which subsequently participates in the formation of the vascular trunks, continued to express this gene. This modulation in smooth muscle alpha-actin gene expression correlated with the beginning of coexpression of sarcomeric alpha-actin transcripts in the epimyocardium and the onset of circulation in the embryo. The specific expression of the vascular smooth muscle alpha-actin gene marks the onset of differentiation of cardiac cells and represents the first demonstration of coexpression of both smooth muscle and striated alpha-actin genes within myogenic cells.

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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