Similarities and Differences in Smooth Muscle α-Actin Induction by TGF-β in Smooth Muscle Versus Non–Smooth Muscle Cells

Hautmann, Martina B.; Adam, Paul J.; Owens, Gary K.

doi:10.1161/01.atv.19.9.2049

Cited by 107 publications

(97 citation statements)

References 44 publications

(67 reference statements)

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“…On the other hand, previous reports show that TGF-b1 up-regulates the expression of early SM cell differentiation markers such as SM a-actin and SM 22a in non-SM cells. 40 In the present study, a small fraction of ADSCs treated with TGF-b1 expressed SM aactin (Figure 8), which is consistent with a previous report. 30 In summary, TGF-b1 promoted the cardiomyogenic differentiation of rat ADSCs in vitro.…”

Section: Discussionsupporting

confidence: 93%

In vitro cardiomyogenic differentiation of adipose‐derived stromal cells using transforming growth factor‐β1

Gwak

Bhang

Yang

et al. 2009

Cell Biochemistry & Function

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Transplanting stem cells differentiated towards a cardiac lineage can regenerate cardiac muscle tissues to treat myocardial infarction. In this study, we tested the hypothesis that transforming growth factor-b1 (TGF-b1) induces cardiomyogenic differentiation of adiposederived stromal cells (ADSCs) in vitro. Rat ADSCs were cultured with TGF-b1 (10 ng ml À1 ) for 2 weeks in vitro. ADSCs cultured without TGF-b1 served as a control. The mRNA expression of cardiac-specific gene was induced by TGF-b1, while the control culture did not show cardiac-specific gene expression. Immunocytochemical analyses showed that a small fraction of ADSCs cultured with TGF-b1 for 2 weeks stained positively for cardiac myosin heavy chain (MHC) and a-sarcomeric actin. Flow cytometric analyses showed that the proportion of cells expressing cardiac MHC increased with TGF-b1. However, no mesenchymal differentiation (e.g., osteogenic and adipogenic differentiation) was detected other than cardiomyogenic differentiation. These results showed that TGF-b1 induce ADSC cardiomyogenic differentiation in vitro, which could be useful for myocardial infarction stem cell therapy.

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Section: Discussionsupporting

confidence: 93%

In vitro cardiomyogenic differentiation of adipose‐derived stromal cells using transforming growth factor‐β1

Gwak

Bhang

Yang

et al. 2009

Cell Biochemistry & Function

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“…Interestingly, the promoters of multiple other SMC differentiation marker genes, including SM22␣ and SM myosin heavy chain, were also found to contain similar TCE regions (11). We also demonstrated that the TCE is essential for TGF-␤-induced ␣-SM actin expression in non-SMCs (24), consistent with the observations that TGF-␤ can induce SMC differentiation marker genes in a variety of mesenchyme-derived cells.…”

supporting

confidence: 86%

“…In summary, there is clear evidence of the involvement of TGF-␤ in the regulation of SMC differentiation in vivo and that TGF-␤ can stimulate expression of the SMC differentiation marker gene ␣-SM actin in a variety of mesenchymal cells in culture through a TCE-dependent mechanism (11,24). However, as yet, there is a lack of evidence demonstrating a role for the TCE in the regulation of SMC differentiation marker gene expression in vivo, and the trans-acting factors that regulate TCE activity have not been identified.…”

mentioning

confidence: 99%

Positive- and Negative-acting Krüppel-like Transcription Factors Bind a Transforming Growth Factor β Control Element Required for Expression of the Smooth Muscle Cell Differentiation Marker SM22α in Vivo

Adam¹,

Regan

Hautmann

et al. 2000

Journal of Biological Chemistry

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232

240

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Transforming growth factor ␤ (TGF-␤) is implicated in the regulation of smooth muscle cell (SMC) differentiation. We previously identified a novel TGF-␤ control element (TCE) in the promoters of SMC differentiation marker genes, including ␣-smooth muscle actin and SM22␣. In this study, the importance of the TCE in regulation of SM22␣ gene expression in vivo was investigated by mutating it within the context of a mouse SM22␣ promoter-lacZ transgenic construct. Mutation of the TCE completely abolished SM22␣ promoter activity in arterial SMCs as well as in developing heart and skeletal muscle. To identify the transcription factor(s) binding to the TCE, we performed yeast one-hybrid cloning analysis and identified gut-enriched Krü ppellike factor (GKLF). However, cotransfection studies in cultured cells showed that GKLF repressed the TGF-␤-dependent increases in SM22␣ and ␣-smooth muscle actin promoter activities. Furthermore, GKLF was not highly expressed in differentiated SMCs in vivo, and TGF-␤ down-regulated GKLF expression in dedifferentiated cultured SMCs. In contrast, overexpression of a related factor (BTEB2) transactivated SM22␣ promoter activity. Thus, our findings suggest a reciprocal role for related Krü ppel-like transcription factors in the regulation of SMC differentiation through a TCE-dependent mechanism.

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“…Strong evidence for a functional relationship between Tgf␤ expression and function is provided by promoter analysis of smooth muscle cell-related genes. The expression of smooth muscle alpha actin (SM ␣-actin) and smooth muscle myosin heavy chain (SM-MHC) are two examples of this phenomenon (Hautmann et al, 1999). Tgf␤1 is expressed in the endothelium of the arteries and veins throughout the time period studied (this report; Akhurst et al, 1990).…”

Section: Arterial Vessel Wallmentioning

confidence: 81%

Expression patterns of Tgfβ1–3 associate with myocardialisation of the outflow tract and the development of the epicardium and the fibrous heart skeleton

Molin

Bartram

Heiden

et al. 2003

Developmental Dynamics

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Transforming growth factor-beta (Tgf␤) is essential for normal embryogenesis. The cardiac phenotypes obtained after knockout of each of the three mammalian isoforms suggest different roles during morphogenesis. We studied cardiovascular expression of Tgf␤1-3 in parallel tissue sections of normal mouse embryos from 9.5 to 15.5 days post coitum (dpc) by using radioactive in situ hybridisation. The Tgf␤ isoforms are differentially expressed in unique and in overlapping patterns during cardiovascular development. In the vessels, Tgf␤1 is found in the intima, whereas Tgf␤2 and -␤3 are mainly present in the media and adventitia of the great arteries. Tgf␤1 is present in the endocardium at all stages examined. The Tgf␤2 signal in the endocardium of the atrioventricular canal and outflow tract (9.5 dpc) shifts during epithelial-mesenchymal transformation toward the mesenchymal cushions (10.5-11.5 dpc) after which it exhibits a marked spatiotemporal expression pattern as the cushion differentiation progresses (11.5-15.5 dpc). The myocardium underlying the endocardial cushions and the atrial muscular septum are intensely positive for Tgf␤2 at early stages (9.5-11.5 dpc) and expression decreases at 12.5 days. In contrast to earlier reports, we find marked overlap of Tgf␤2 and -␤3 expression. Tgf␤3 expression shows a characteristic distribution in the mesenchymal cushions, suggesting a role in cushion differentiation, possibly additional to Tgf␤2. From 14.5 dpc onward, a strong Tgf␤3 signal is found in the fibrous septum primum of the atrium and in the fibrous skeleton of the heart. Special attention was paid to the proepicardial organ and its derivatives. The proepicardial organ strongly expresses Tgf␤2 as early as 9.5 days, and all isoforms are present in the epicardium from 12.5 dpc onward. The spatiotemporal cardiovascular expression of Tgf␤1-3 supports both specific and complementary functions during cardiovascular development that might explain functional redundancy between the Tgf␤-isoforms. The information provided favors novel roles of Tgf␤1-3 in epicardial development, of Tgf␤2 in myocardialisation, and of Tgf␤3 in differentiation of the fibrous structures of the heart. Developmental Dynamics 227: 431-444, 2003.

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Similarities and Differences in Smooth Muscle α-Actin Induction by TGF-β in Smooth Muscle Versus Non–Smooth Muscle Cells

Cited by 107 publications

References 44 publications

In vitro cardiomyogenic differentiation of adipose‐derived stromal cells using transforming growth factor‐β1

In vitro cardiomyogenic differentiation of adipose‐derived stromal cells using transforming growth factor‐β1

Positive- and Negative-acting Krüppel-like Transcription Factors Bind a Transforming Growth Factor β Control Element Required for Expression of the Smooth Muscle Cell Differentiation Marker SM22α in Vivo

Expression patterns of Tgfβ1–3 associate with myocardialisation of the outflow tract and the development of the epicardium and the fibrous heart skeleton

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