Smooth Muscle-specific α Tropomyosin Is a Marker of Fully Differentiated Smooth Muscle in Lung

Vrhovski, Bernadette; McKay, Karen; Schevzov, Galina; Gunning, Peter W.; Weinberger, Ron P.

doi:10.1369/jhc.4a6504.2005

Cited by 14 publications

(10 citation statements)

References 30 publications

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“…48 In the present study, we found that both TPM1 and SM ␣-actin were abundantly expressed in normal arteries. However, TPM1 protein decreased much more than SM ␣-actin did in ASO arteries, even in arteries with stenosis less than 10%.…”

Section: Wang Et Alsupporting

confidence: 57%

MicroRNA-21 Regulates Vascular Smooth Muscle Cell Function via Targeting Tropomyosin 1 in Arteriosclerosis Obliterans of Lower Extremities

Wang

Chang

et al. 2011

ATVB

134

121

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Objective-The goal of this study was to determine the expression signature and the potential role of microRNAs in human arteries with arteriosclerosis obliterans (ASO). Methods and Results-The expression profiles of microRNAs in human arteries with ASO and in normal control arteries were determined by quantitative reverse transcription-polymerase chain reaction array. Among the 617 detected microRNAs, multiple microRNAs were aberrantly expressed in arteries with ASO. Some of these dysregulated microRNAs were further verified by quantitative reverse transcription-polymerase chain reaction. Among them, microRNA-21 (miR-21) was mainly located in arterial smooth muscle cells (ASMCs) and was increased by more than 7-fold in ASO that was related to hypoxia inducible factor 1-␣. In cultured human ASMCs, cell proliferation and migration were significantly decreased by inhibition of miR-21. 3Ј-Untranslated region luciferase assay confirmed that tropomyosin 1 was a target of miR-21 that was involved in miR-21-mediated cellular effects, such as cell shape modulation. Key Words: atherosclerosis Ⅲ hypoxia Ⅲ peripheral arterial disease Ⅲ vascular muscle Ⅲ microRNA A rteriosclerosis obliterans (ASO) of the lower extremities is a major cause of adult limb loss worldwide. 1-3 Surgery is still the major approach in the treatment of ASO. However, many patients develop restenosis in 1 year after surgery. 1 It is well established that proliferation and migration of arterial smooth muscle cells (ASMCs) are the major cellular events and the major reasons behind ASO formation and posttreatment restenosis. 4 However, the molecular mechanisms involved in regulation of proliferation and migration of ASMCs in ASO remain unclear. Conclusion-The See accompanying articles on pages 1939 and 1941MicroRNAs are a novel class of endogenous, small noncoding RNAs that regulate approximately 30% of the encoding genes of the human genome at the posttranscriptional level by binding the 3Ј-untranslated region (UTR) of their target mRNAs. [5][6][7] The microRNA expression profile in vessels has recently been described by Ji et al 8 Several microRNAs, including microRNA-21 (miR-21), miR-221/222, and miR-145, have been found to modulate ASMC function and be involved in the process of artery stenosis in the rat carotid artery balloon injury model. 8 -10 However, the expression profiles of microRNAs in human arteries with ASO are still unknown.Tissue-specific expression is an important characteristic of microRNA expression. 11 For example, miR-1 is highly expressed in heart, but its expression in artery is low. 8 Such different expression profiles in different tissues suggest that the physiological functions of microRNA in different tissues may be different. 8 Although human ASO and artery stenosis in rat carotid artery injury models share many features, their pathological processes are different. 12,13 Thus, identifying microRNAs in ASO and clarifying their biological functions would be useful for understanding the mechanisms of ASO formation and searc...

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Section: Wang Et Alsupporting

confidence: 57%

MicroRNA-21 Regulates Vascular Smooth Muscle Cell Function via Targeting Tropomyosin 1 in Arteriosclerosis Obliterans of Lower Extremities

Wang

Chang

et al. 2011

ATVB

134

121

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“…The precise identity of the cells in the bronchioles, micro-vasculature and alveolar septae of the lungs that may express the α-T-sensitive cytoskeleton gene cluster remain to be more fully characterized. Previous studies have shown that the expression of these genes is restricted to smooth muscle cells [59][60][61]. In addition, members of the actin and myosin families are also expressed in endothelial cells [62] which make up to 50% of the cells in lung parenchyma.…”

Section: Cellular Localization Of Proteins Encoded By Selected α-T Sementioning

confidence: 99%

Genome wide responses of murine lungs to dietary α-tocopherol

Oommen

Vasu

Leonard

et al. 2007

Free Radical Research

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Abstractα-tocopherol (α-T) may affect biological processes by modulating mRNA concentrations. This study screened the responses of ~15,000 lung mRNAs to dietary α-T in mice. The lung was chosen as the target organ because it is subjected to cyclical variations in oxidant and inflammatory stressors and α-T has been implicated in their modulations. The analysis identified ~400 mRNAs sensitive to α-T status of lungs determined by dietary α-T. The female lung transcriptome appears to be more sensitive to the α-T status than that of the male lungs. Here, we focus on the induction of 13 cytoskeleton genes by dietary α-T because they were similarly induced in the male and the female lungs. Their inductions were confirmed by quantitative-real-time-polymerase chain reaction (qRT-PCR). Immunohistochemical analyses of three of the encoded proteins suggest that they are expressed in lung vasculature and alveolar regions. The data suggest that the lung α-T status may modulate cytoarchitecture of lungs.

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“…This does not absolutely prove that there is only ␣-smooth Tm in the Tm6 band, but it does unambiguously show that the ␣-smooth Tm migrates at the position of Tm6. A complete characterization of the ␣/2a antibody is published separately (Vrhovski et al 2005) because this is the first time that such an antibody has become available. The conclusion reached from the Vrhovski et al data is that both Western blots and immunohistochemistry on human and mouse lung with the ␣-smooth Tm antibody (␣/2a) showed an identical profile and tissue colocalization with ␣-smooth actin.…”

Section: Expression Profile Of Tm Isoforms In Mouse Tissuesmentioning

confidence: 99%

Tissue-specific Tropomyosin Isoform Composition

Schevzov¹,

Vrhovski²,

Bryce³

et al. 2005

J Histochem Cytochem.

Self Cite

106

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S U M M A R Y Four distinct genes encode tropomyosin (Tm) proteins, integral components of the actin microfilament system. In non-muscle cells, over 40 Tm isoforms are derived using alternative splicing. Distinct populations of actin filaments characterized by the composition of these Tm isoforms are found differentially sorted within cells (Gunning et al. 1998b). We hypothesized that these distinct intracellular compartments defined by the association of Tm isoforms may allow for independent regulation of microfilament function. Consequently, to understand the molecular mechanisms that give rise to these different microfilaments and their regulation, a cohort of fully characterized isoform-specific Tm antibodies was required. The characterization protocol initially involved testing the specificity of the antibodies on bacterially produced Tm proteins. We then confirmed that these Tm antibodies can be used to probe the expression and subcellular localization of different Tm isoforms by Western blot analysis, immunofluorescence staining of cells in culture, and immunohistochemistry of paraffin wax-embedded mouse tissues. These Tm antibodies, therefore, have the capacity to monitor specific actin filament populations in a range of experimental systems.

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Smooth Muscle-specific α Tropomyosin Is a Marker of Fully Differentiated Smooth Muscle in Lung

Cited by 14 publications

References 30 publications

MicroRNA-21 Regulates Vascular Smooth Muscle Cell Function via Targeting Tropomyosin 1 in Arteriosclerosis Obliterans of Lower Extremities

MicroRNA-21 Regulates Vascular Smooth Muscle Cell Function via Targeting Tropomyosin 1 in Arteriosclerosis Obliterans of Lower Extremities

Genome wide responses of murine lungs to dietary α-tocopherol

Tissue-specific Tropomyosin Isoform Composition

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