cDNA cloning and mRNA expression of calponin and SM22 in rat aorta smooth muscle cells

Nishida, Wataru; Kitami, Yutaka; Hiwada, Kunio

doi:10.1016/0378-1119(93)90435-6

Cited by 70 publications

(49 citation statements)

References 21 publications

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“…In addition, we and others (18,46,53) have reported high level sequence identity with the SMC-specific protein SM22␣. To determine whether calponin-h1 was encoded by a single copy gene in the murine genome and whether this gene was part of a multigene family, we hybridized the calponin-h1 cDNA probe to Southern blots containing murine In situ hybridization analyses were performed using radiolabeled calponin-h1 antisense (panels A, C, and E) and sense (panels B, D, and F) riboprobes on adjacent sections of staged murine embryos.…”

Section: Smc Lineage-restricted Expression Of the Calponin-h1supporting

confidence: 54%

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Developmental Pattern of Expression and Genomic Organization of the Calponin-h1 Gene

Samaha¹,

Ip²,

Morrisey

et al. 1996

Journal of Biological Chemistry

104

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Calponin-h1 is a 34-kDa myofibrillar thin filament, actin-binding protein that is expressed exclusively in smooth muscle cells (SMCs) in adult animals. To examine the molecular mechanisms that regulate SMC-specific gene expression, we have examined the temporal, spatial, and cell cycle-regulated patterns of expression of calponin-h1 gene expression and isolated and structurally characterized the murine calponin-h1 gene. Calponin-h1 mRNA is expressed exclusively in SMC-containing tissues in adult animals. During murine embryonic development, calponin-h1 gene expression is (i) detectable in E9.5 embryos in the dorsal aorta, cardiac outflow tract, and tubular heart, (ii) sequentially up-regulated in SMC-containing tissues, and (iii) downregulated to non-detectable levels in the heart during late fetal development. In addition, the gene is expressed in resting rat aortic SMCs, but its expression is rapidly down-regulated when growth-arrested cells reenter phase G 1 of the cell cycle and proliferate. Calponin-h1 is encoded by a 10.7-kilobase single copy gene composed of seven exons, which is part of a multigene family. Transient transfection analyses demonstrated that 1.5 kilobases of calponin-h1 5-flanking sequence is sufficient to program high level transcription of a luciferase reporter gene in cultured primary rat aortic SMCs and the smooth muscle cell line, A7r5. Taken together, these data suggest that the calponin-h1 gene will serve as an excellent model system with which to examine the molecular mechanisms that regulate SMC lineage specification, differentiation, and phenotypic modulation.

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Section: Smc Lineage-restricted Expression Of the Calponin-h1supporting

confidence: 54%

“…8). In addition, single copies of this motif are present in the chicken, rat, and murine SM22␣ proteins (13,18,46,53,56,57), the rat neuronal protein NP25 (58), and the Drosophila muscle protein mp20 (59) (Fig. 8).…”

Section: Fig 5 Southern Blot Analysis Of the Murine Calponin-h1 Genementioning

confidence: 99%

Developmental Pattern of Expression and Genomic Organization of the Calponin-h1 Gene

Samaha¹,

Ip²,

Morrisey

et al. 1996

Journal of Biological Chemistry

104

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“…12,35 It was also originally described as predominantly expressed in smooth muscle cells to bind to actin, suggesting it is involved in cell differentiation and cytoskeletal rearrangement. [9][10][11] Yeo et al Transgelin and colorectal carcinoma L Zhao et al established an experimental model for colitic cancer, and using proteomic analysis to identify proteins involved in colitic cancer suggested that loss of transgelin could be a potential biomarker of repeated colitic-associated colon cancer. Recently, Shields et al 14 characterized transgelin as a gene, the expression of which was abolished by Ras, suggesting that loss of transgelin expression may contribute to transformation by oncogene Ras, and loss of transgelin expression might represent an early event for the tumor progression in breast and colon cancers.…”

Section: Discussionmentioning

confidence: 99%

“…Among them, a remarkable decreased expression of transgelin, a 22 kDa protein also called SM22, WS3-10 and mouse p27, and found abundantly in smooth muscle cells, [9][10][11] was found in colorectal cancer specimens. Transgelin has been shown to bind to and colocalize with F-actin, indicating that it may be involved in cell differentiation by stabilizing the cytoskeleton through actin binding, 12,13 and diminished expression of this protein has been reported in a variety of cell types on transformation [14][15][16] as well as in several human cancers, including lung, renal, prostate and breast cancer.…”

mentioning

confidence: 99%

Transgelin as a suppressor is associated with poor prognosis in colorectal carcinoma patients

et al. 2009

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We performed comparative proteomic analysis of colorectal cancer to investigate potential target proteins correlated with carcinogenesis and prognosis. Among them, transgelin, a 22 kDa protein also called SM22, was identified as a novel tumor suppressor protein, but little is known about this protein in tumors so far. A remarkable reduced expression of transgelin was found in colorectal cancer samples compared with normal colorectal mucosa. The effect of 5-aza-2 0 -deoxycytidine as a demethylation agent would obviously restore the original expression level of transgelin, implicating DNA hypermethylation of transgelin is important in the regulation of transgelin transcription in colorectal cancer. As a control, the investigation at cell line level confirms that transgelin protein comes from epithelium but not mesenchymal cells. Further, immunohistochemical staining for transgelin was performed on paraffin sections of 62 and 126 cases of normal colorectal mucosa and colorectal cancer specimens, respectively. As compared to normal colorectal tissue, we observed a significantly lower transgelin expression in colorectal cancer samples (Po0.001). Survival analysis demonstrated that patients without transgelin expression had shorter overall survival, whereas patients with transgelin expression had better survival (P ¼ 0.006). Multivariate analysis showed that negative transgelin expression was an independent prognostic indicator for patient's survival. Our results suggest that transgelin as a suppressor may serve as important biomarker of malignancy. Loss of transgelin involves gene promoter hypermethylation and is closely associated with poor overall survival in colorectal cancer patients.

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“…12,13 This makes their transcriptional elements inappropriate candidates for driving the expression of heterologous genes in VSMCs. Other potential candidates are the genes encoding VSMC ␣-actin (also known as aortic type ␣-actin), 14 smooth muscle myosin heavy chain, 15 h 1 -calponin, 16 telokin, 17 and SM-22␣ 18,19 each of which represent unique gene products. Of these, the VSMC ␣-actin gene encodes the most abundant protein in mature VSMCs.…”

Section: Introductionmentioning

confidence: 99%

Design of a muscle cell-specific expression vector utilising human vascular smooth muscle α-actin regulatory elements

Chen

et al. 1999

Gene Ther

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cDNA cloning and mRNA expression of calponin and SM22 in rat aorta smooth muscle cells

Cited by 70 publications

References 21 publications

Developmental Pattern of Expression and Genomic Organization of the Calponin-h1 Gene

Developmental Pattern of Expression and Genomic Organization of the Calponin-h1 Gene

Transgelin as a suppressor is associated with poor prognosis in colorectal carcinoma patients

Design of a muscle cell-specific expression vector utilising human vascular smooth muscle α-actin regulatory elements

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