scholarly journals Dynamic Interplay of Smooth Muscle α-Actin Gene-Regulatory Proteins Reflects the Biological Complexity of Myofibroblast Differentiation

Biology ◽  
2013 ◽  
Vol 2 (2) ◽  
pp. 555-586 ◽  
Author(s):  
Arthur Strauch ◽  
Seethalakshmi Hariharan
Keyword(s):  
Smooth Muscle ◽  
Regulatory Proteins ◽  
Actin Gene ◽  
Myofibroblast Differentiation ◽  
Biological Complexity ◽  
Gene Regulatory ◽  
Dynamic Interplay

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 Induction of Vascular Smooth Muscle α-Actin Gene Transcription in Transforming Growth Factor β1-Activated Myofibroblasts Mediated by Dynamic Interplay between the Pur Repressor Proteins and Sp1/Smad Coactivators

2004 ◽  
Vol 15 (10) ◽  
pp. 4532-4543 ◽  
Author(s):  
Sukanya V. Subramanian ◽  
John A. Polikandriotis ◽  
Robert J. Kelm ◽  
Jason J. David ◽  
Charles G. Orosz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Myofibroblast Differentiation ◽  
Repressor Proteins ◽  
Smad Protein ◽  
Transcriptional Activator Protein ◽  
Dynamic Interplay

The mouse vascular smooth muscle α-actin (SMA) gene enhancer is activated in fibroblasts by transforming growth factor β1 (TGFβ1), a potent mediator of myofibroblast differentiation and wound healing. The SMA enhancer contains tandem sites for the Sp1 transcriptional activator protein and Purα and β repressor proteins. We have examined dynamic interplay between these divergent proteins to identify checkpoints for possible control of myofibroblast differentiation during chronic inflammatory disease. A novel element in the SMA enhancer named SPUR was responsible for both basal and TGFβ1-dependent transcriptional activation in fibroblasts and capable of binding Sp1 and Pur proteins. A novel Sp1:Pur:SPUR complex was dissociated when SMA enhancer activity was increased by TGFβ1 or Smad protein overexpression. Physical association of Pur proteins with Smad2/3 was observed as was binding of Smads to an upstream enhancer region that undergoes DNA duplex unwinding in TGFβ1-activated myofibroblasts. Purβ repression of the SMA enhancer could not be relieved by TGFβ1, whereas repression mediated by Purα was partially rescued by TGFβ1 or overexpression of Smad proteins. Interplay between Pur repressor isoforms and Sp1 and Smad coactivators may regulate SMA enhancer output in TGFβ1-activated myofibroblasts during episodes of wound repair and tissue remodeling.

Bending of DNA by gene-regulatory proteins: construction and use of a DNA bending vector

Gene ◽  
1989 ◽  
Vol 85 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Jin Kim ◽  
Christian Zwieb ◽  
Carl Wu ◽  
Sankar Adhya
Keyword(s):  
Dna Bending ◽  
Regulatory Proteins ◽  
Gene Regulatory

scholarly journals Characterization of bacterial artificial chromosome transgenic mice expressing mCherry fluorescent protein substituted for the murine smooth muscle α-actin gene

genesis ◽  
2010 ◽  
Vol 48 (7) ◽  
pp. 457-463 ◽  
Author(s):  
John J. Armstrong ◽  
Irina V. Larina ◽  
Mary E. Dickinson ◽  
Warren E. Zimmer ◽  
Karen K. Hirschi
Keyword(s):  
Smooth Muscle ◽  
Bacterial Artificial Chromosome ◽  
Transgenic Mice ◽  
Fluorescent Protein ◽  
Artificial Chromosome ◽  
Actin Gene

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.

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