scholarly journals Serum Response Factor Regulates Expression of Phosphatase and Tensin Homolog Through a MicroRNA Network in Vascular Smooth Muscle Cells

2011 ◽  
Vol 31 (12) ◽  
pp. 2909-2919 ◽  
Author(s):  
Henrick N. Horita ◽  
Peter A. Simpson ◽  
Allison Ostriker ◽  
Seth Furgeson ◽  
Vicki Van Putten ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Serum Response Factor ◽  
Muscle Cells ◽  
Response Factor ◽  
Phosphatase And Tensin Homolog ◽  
Tensin Homolog ◽  
Serum Response

Proliferation of human primary vascular smooth muscle cells depends on serum response factor

2010 ◽  
Vol 89 (2-3) ◽  
pp. 216-224 ◽  
Author(s):  
Daniela Werth ◽  
Gabriele Grassi ◽  
Nina Konjer ◽  
Barbara Dapas ◽  
Rossella Farra ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Serum Response Factor ◽  
Muscle Cells ◽  
Response Factor ◽  
Serum Response

scholarly journals Four isoforms of serum response factor that increase or inhibit smooth-muscle-specific promoter activity

2000 ◽  
Vol 345 (3) ◽  
pp. 445-451 ◽  
Author(s):  
Paul R. KEMP ◽  
James C. METCALFE
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Serum Response Factor ◽  
Muscle Cells ◽  
Dominant Negative ◽  
C2c12 Cells ◽  
Specific Gene ◽  
Response Factor ◽  
Transactivation Domain ◽  
Serum Response

Serum response factor (SRF) is a key transcriptional activator of the c-fos gene and of muscle-specific gene expression. We have identified four forms of the SRF coding sequence, SRF-L (the previously identified form), SRF-M, SRF-S and SRF-I, that are produced by alternative splicing. The new forms of SRF lack regions of the C-terminal transactivation domain by splicing out of exon 5 (SRF-M), exons 4 and 5 (SRF-S) and exons 3, 4 and 5 (SRF-I). SRF-M is expressed at similar levels to SRF-L in differentiated vascular smooth-muscle cells and skeletal-muscle cells, whereas SRF-L is the predominant form in many other tissues. SRF-S expression is restricted to vascular smooth muscle and SRF-I expression is restricted to the embryo. Transfection of SRF-L and SRF-M into C2C12 cells showed that both forms are transactivators of the promoter of the smooth-muscle-specific gene SM22α, whereas SRF-I acted as a dominant negative form of SRF.

Telokin expression in A10 smooth muscle cells requires serum response factor

1997 ◽  
Vol 272 (4) ◽  
pp. C1394-C1404 ◽  
Author(s):  
B. P. Herring ◽  
A. F. Smith
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Transcription Initiation ◽  
Serum Response Factor ◽  
Muscle Cells ◽  
Tata Box ◽  
Luciferase Reporter ◽  
Response Factor ◽  
Specific Expression ◽  
Serum Response

Telokin transcription is initiated from a smooth muscle-specific promoter located in an intron of the smooth muscle myosin light chain kinase gene. We have previously identified a 310-base pair fragment of the promoter that mediates A10 smooth muscle cell-specific expression of telokin. In the current study, telokin-luciferase reporter gene assays in A10 cells and REF52 nonmuscle cells revealed that the promoter region between -81 and +80 contains the regulatory elements required to mediate the in vitro cell specificity of the promoter. Several positive-acting elements, including an E box, myocyte enhancer factor 2 (MEF2)-TATA box, and CArG-serum response element, were identified within this region. Telokin transcription in A10 smooth muscle cells requires all three transcription initiation sites and an AT-rich sequence between -71 and -62 that includes a TATA box. MEF2 interacts with the AT-rich region with low affinity; however, MEF2 binding is not required for transcriptional activity in A10 cells. Binding of serum response factor (SRF) to a CArG element proximal to the TATA sequence is also critical for high levels of transcription in A10 cells. Together these data suggest that an AT-rich motif, acting in concert with SRF and an unusual transcription initiation mechanism, is required for the cell-specific expression of the telokin promoter in A10 smooth muscle cells.

miRNA-181a/b Regulates Phenotypes of Vessel Smooth Muscle Cells Through Serum Response Factor

2017 ◽  
Vol 36 (2) ◽  
pp. 127-135 ◽  
Author(s):  
Xiaoxing Wei ◽  
Xue Hou ◽  
Jianhua Li ◽  
Yongnian Liu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Serum Response Factor ◽  
Muscle Cells ◽  
Response Factor ◽  
Serum Response

scholarly journals Loss of serum response factor induces microRNA-mediated apoptosis in intestinal smooth muscle cells

2015 ◽  
Vol 6 (12) ◽  
pp. e2011-e2011 ◽  
Author(s):  
C Park ◽  
M Y Lee ◽  
O J Slivano ◽  
P J Park ◽  
S Ha ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Serum Response Factor ◽  
Muscle Cells ◽  
Intestinal Smooth Muscle ◽  
Response Factor ◽  
Serum Response

scholarly journals Runx2 Represses Myocardin-Mediated Differentiation and Facilitates Osteogenic Conversion of Vascular Smooth Muscle Cells

2007 ◽  
Vol 28 (3) ◽  
pp. 1147-1160 ◽  
Author(s):  
Toru Tanaka ◽  
Hiroko Sato ◽  
Hiroshi Doi ◽  
Carolina A. Yoshida ◽  
Takehisa Shimizu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Molecular Mechanisms ◽  
Serum Response Factor ◽  
Critical Role ◽  
Muscle Cells ◽  
Tightly Coupled

ABSTRACT Phenotypic plasticity and the switching of vascular smooth muscle cells (SMCs) play a critical role in atherosclerosis. Although Runx2, a key osteogenic transcription factor, is expressed in atherosclerotic plaques, the molecular mechanisms by which Runx2 regulates SMC differentiation remain unclear. Here we demonstrated that Runx2 repressed SMC differentiation induced by myocardin, which acts as a coactivator for serum response factor (SRF). Myocardin-mediated induction of SMC gene expression was enhanced in mouse embryonic fibroblasts derived from Runx2 null mice compared to wild-type mice. Forced expression of Runx2 decreased the expression of SMC genes and promoted osteogenic gene expression, whereas the reduction of Runx2 expression by small interfering RNA enhanced SMC differentiation in human aortic SMCs. Runx2 interacted with SRF and interfered with the formation of the SRF/myocardin ternary complex. Thus, this study provides the first evidence that Runx2 inhibits SRF-dependent transcription, as a corepressor independent of its DNA binding. We propose that Runx2 plays a pivotal role in osteogenic conversion tightly coupled with repression of the SMC phenotype in atherosclerotic lesions.

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