scholarly journals Inhibition of tendon cell migration by dexamethasone is correlated with reduced alpha-smooth muscle actin gene expression: A potential mechanism of delayed tendon healing

2003 ◽  
Vol 21 (2) ◽  
pp. 265-271 ◽  
Author(s):  
Wen-Chung Tsai ◽  
Fuk-Tan Tang ◽  
May-Kuen Wong ◽  
Jong-Hwei S. Pang
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Actin ◽  
Tendon Healing ◽  
Actin Gene ◽  
Muscle Actin ◽  
Potential Mechanism ◽  
Alpha Smooth Muscle Actin ◽  
Muscle Actin Gene

scholarly journals A 29-nucleotide DNA segment containing an evolutionarily conserved motif is required in cis for cell-type-restricted repression of the chicken alpha-smooth muscle actin gene core promoter.

1988 ◽  
Vol 8 (1) ◽  
pp. 241-250 ◽  
Author(s):  
S L Carroll ◽  
D J Bergsma ◽  
R J Schwartz
Keyword(s):  
Smooth Muscle ◽  
Core Promoter ◽  
Smooth Muscle Actin ◽  
Gene Promoter ◽  
Actin Gene ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Actin Genes ◽  
Muscle Actin Gene ◽  
Ccaat Box

A series of 5' deletion mutations of the upstream flanking sequences of the chicken alpha-smooth muscle (aortic) actin gene was prepared and inserted into the chloramphenicol acetyltransferase expression vector pSV0CAT. Deletion recombinants were transfected into fibroblasts, which actively express the alpha-smooth muscle actin gene, and primary myoblast cultures, which accumulate much lower quantities of alpha-smooth muscle actin mRNAs. The first 122 nucleotides of 5'-flanking DNA were found to contain a "core" promoter capable of accurately directing high levels of transcription in both fibroblasts and myotubes. The activity of this core promoter is modulated in fibroblasts by a "governor" element(s) located at least in part between nucleotides -257 and -123. This region contains sequences potentially conserved between mammalian and avian alpha-smooth muscle actin genes as well as one of a pair of 16-base-pair inverted CCAAT box-associated repeats which are conserved among all chordate muscle actin genes examined to date. A smaller DNA segment (-151 to -123) containing these upstream CCAAT box-associated repeats was sufficient to suppress expression of the core promoter in muscle cultures, suggesting that the upstream CCAAT box-associated repeats play a negative role in the alpha-smooth muscle actin gene promoter.

A 29-nucleotide DNA segment containing an evolutionarily conserved motif is required in cis for cell-type-restricted repression of the chicken alpha-smooth muscle actin gene core promoter

1988 ◽  
Vol 8 (1) ◽  
pp. 241-250
Author(s):  
S L Carroll ◽  
D J Bergsma ◽  
R J Schwartz
Keyword(s):  
Smooth Muscle ◽  
Core Promoter ◽  
Smooth Muscle Actin ◽  
Gene Promoter ◽  
Actin Gene ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Actin Genes ◽  
Muscle Actin Gene ◽  
Ccaat Box

A series of 5' deletion mutations of the upstream flanking sequences of the chicken alpha-smooth muscle (aortic) actin gene was prepared and inserted into the chloramphenicol acetyltransferase expression vector pSV0CAT. Deletion recombinants were transfected into fibroblasts, which actively express the alpha-smooth muscle actin gene, and primary myoblast cultures, which accumulate much lower quantities of alpha-smooth muscle actin mRNAs. The first 122 nucleotides of 5'-flanking DNA were found to contain a "core" promoter capable of accurately directing high levels of transcription in both fibroblasts and myotubes. The activity of this core promoter is modulated in fibroblasts by a "governor" element(s) located at least in part between nucleotides -257 and -123. This region contains sequences potentially conserved between mammalian and avian alpha-smooth muscle actin genes as well as one of a pair of 16-base-pair inverted CCAAT box-associated repeats which are conserved among all chordate muscle actin genes examined to date. A smaller DNA segment (-151 to -123) containing these upstream CCAAT box-associated repeats was sufficient to suppress expression of the core promoter in muscle cultures, suggesting that the upstream CCAAT box-associated repeats play a negative role in the alpha-smooth muscle actin gene promoter.

Chromosomal mapping of the human smooth muscle actin gene (enteric type, ACTA3) to 2p13.1 and molecular nature of the HindIII polymorphism

Genomics ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 720-723 ◽  
Author(s):  
Hisao Ueyama ◽  
Johji Inazawa ◽  
Hoyoku Nishino ◽  
Deng Han-Xiang ◽  
Yukiko Ochiai ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Chromosomal Mapping ◽  
Actin Gene ◽  
Muscle Actin ◽  
Muscle Actin Gene ◽  
Hindiii Polymorphism ◽  
Molecular Nature

scholarly journals p21/waf1 and Smooth-Muscle Actin α Expression in Stromal Fibroblasts of Oral Cancers

2010 ◽  
Vol 33 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Ioulia Chatzistamou ◽  
Nikolina Dioufa ◽  
George Trimis ◽  
Alexandra Sklavounou ◽  
Christos Kittas ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Smooth Muscle Actin ◽  
Myoepithelial Cells ◽  
Mrna Levels ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Stromal Fibroblasts ◽  
Oral Cancers ◽  
Malignant Lesions

Background: Concerted alterations between stromal fibroblasts and neoplastic cells underline the carcinogenic process. Activation of alpha-smooth muscle actin (SMA) expression, a cytoskeleton protein normally expressed only in myoepithelial cells, is considered a landmark for the activation of stromal fibroblasts with little however being known regarding the mechanism governing the expression of SMA in the stroma.Methods: We have evaluated by immunohistochemistry the expression of SMA in the stroma of oral malignant and pre-malignant lesions, in association with the expression of p53 and p21 tumor suppressors that were shown previously to be deregulated and/or mutated in stromal fibroblasts of various cancers. The effects of p21 knockdown in SMA expression and cell migration and the mRNA levels of endogenous p21 in fibroblasts co-cultured with cancer cells were also assessed.Results: We found that both p21 and SMA expression was elevated in the stroma, but not the epithelium, of malignant as compared to pre-malignant lesions. We also noted that the expression of both was positively correlated, implying that SMA expression may be regulated by p21. Consistently with this notion we found that siRNA-mediated p21 suppression resulted in the reduction of SMA levels and also inhibited cell migration.Conclusion: Our results show that p21 deregulation is associated with the activation of stromal fibroblasts of oral cancers by a mechanism that involves the stimulation of SMA expression.

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