SM22α, a Marker of Adult Smooth Muscle, Is Expressed in Multiple Myogenic Lineages During Embryogenesis

Li, Li; Miano, Joseph M.; Cserjesi, Peter; Olson, Eric N.

doi:10.1161/01.res.78.2.188

Cited by 366 publications

(305 citation statements)

References 45 publications

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“…For example, SM ␣-actin and SM22␣ are expressed as early as E9.5 in the cells surrounding the dorsal aorta, 28 whereas myocardin is not detectable in this tissue until E12.5. 11 Because myocardin transcript is detected in the primitive heart at E9.5, 11 initial induction of these early SMC markers may not require myocardin.…”

Section: Discussionmentioning

confidence: 99%

Forced Expression of Myocardin Is Not Sufficient for Induction of Smooth Muscle Differentiation in Multipotential Embryonic Cells

Yoshida

Kawai-Kowase

Owens

2004

ATVB

103

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Objective-Myocardin, a coactivator of serum response factor, has been shown to be required for expression of multiple CArG-dependent smooth muscle cell (SMC) marker genes. The aim of the present study was to determine whether myocardin alone is sufficient to induce SMC lineage in multipotential stem cells as evidenced by activation of the entire SMC differentiation program. Methods and Results-Overexpression of myocardin induced only a subset of SMC marker genes, including smooth muscle (SM) ␣-actin, SM-myosin heavy chain (MHC), SM22␣, calponin, and desmin in A404 SMC precursor cells, whereas expression of smoothelin-B, aortic carboxypeptidase-like protein, and focal adhesion kinase-related nonkinase, whose promoters lack efficacious CArG elements, was not induced. Similar results were obtained in cultured SMCs, 10T1/2 cells, and embryonic stem cells. Moreover, myocardin inappropriately induced expression of skeletal and cardiac CArG-dependent genes in cultured SMCs. Stable overexpression of dominant-negative myocardin in A404 cells resulted in impaired induction of SM ␣-actin and SM-MHC by all trans-retinoic acid but had no effect on induction of smoothelin-B and aortic carboxypeptidase-like protein expression. Conclusions-Taken together with previous studies, results demonstrate that myocardin is required for the induction of CArG-dependent SMC marker genes but is not sufficient to initiate the complete SMC differentiation program. Key Words: smooth muscle cells Ⅲ transcriptional coactivator Ⅲ serum response factor Ⅲ CArG element S mooth muscle cells (SMCs) play pivotal roles in vascular development and in diseases such as atherosclerosis. Under normal circumstances, differentiated SMCs are highly specialized for their contractile function and express a unique repertoire of contractile proteins, contractile agonist receptors, and signaling molecules to perform this function. 1 The expression levels of most of these SMC-specific/SMCselective proteins reflect the differentiation state of SMCs. 1 Therefore, these proteins are considered as useful markers for studying the control of SMC differentiation. See page 1535There has been considerable progress in elucidation of molecular mechanisms that regulate cell-selective expression of SMC differentiation markers in recent years. For example, expression of most SMC differentiation markers characterized to date, including smooth muscle (SM) ␣-actin, 2 SMmyosin heavy chain (MHC), 3 SM22␣, 4 calponin, 5 and desmin, 6 has been shown to be regulated at the transcriptional level and dependent on multiple CArG elements located within their promoter-enhancer regions. The CArG element has the general sequence motif, CC(A/T-rich) 6 GG and binds the ubiquitously expressed transcription factor, serum response factor (SRF). 7 CArG elements are also required for expression of many growth factor-inducible genes including c-fos and egr-1, 7 and a major challenge has been to identify mechanisms by which CArG-SRF-dependent mechanisms can simultaneously contribute to the apparently dis...

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Section: Discussionmentioning

confidence: 99%

Forced Expression of Myocardin Is Not Sufficient for Induction of Smooth Muscle Differentiation in Multipotential Embryonic Cells

Yoshida

Kawai-Kowase

Owens

2004

ATVB

103

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“…In transgenic mice the 441-bp SM22␣ promoter is active in arterial but not visceral SMCs (29,31). Therefore, the demonstration that the lacZ reporter gene encoded by AdSM22-lacZ was expressed in visceral as well as vascular SMCs was somewhat surprising.…”

Section: Discussionmentioning

confidence: 99%

“…SM22 ␣ is an early marker of the SMC lineage that is expressed at high levels exclusively in visceral and vascular SMCs during postnatal development (28)(29)(30). We have shown that the 441-bp SM22 ␣ promoter activates transcription exclusively in arterial SMCs during postnatal development in transgenic mice (31).…”

Section: Introductionmentioning

confidence: 87%

Transcriptional targeting of replication-defective adenovirus transgene expression to smooth muscle cells in vivo.

Kim¹,

Lin²,

Barr³

et al. 1997

J. Clin. Invest.

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“…However, there is a possibility of contamination by adventitial and interstitial fibroblasts. To rule out this potential confound, we stained isolated cells for SM22α, α-smooth muscle actin (α-SMA), both VSMC markers 7,8 , and vimentin, a fibroblast marker 9 , at passages 1-2 ( Figure 2). We observed no change of these markers through passage 2.…”

Section: Representative Resultsmentioning

confidence: 99%

Isolation of Murine Coronary Vascular Smooth Muscle Cells

Husarek

Zhang

McCallinhart

et al. 2016

JoVE

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While the isolation and culture of vascular smooth muscle cells (VSMCs) from large vessels is well established, we sought to isolate and culture VSMCs from the coronary circulation. Hearts with intact aortic arches were removed and perfused via retrograde Langendorff with digestion solution containing 300 Units/ml of collagenase type II, 0.1 mg/ml soybean trypsin inhibitor and 1 M CaCl 2 . The perfusates were collected at 15 min intervals for 90 min, pelleted by centrifugation, resuspended in plating media, and plated on tissue culture dishes. VSMCs were characterized by presence of SM22α, α-SMA, and vimentin. One of the main advantages of using this technique is the ability to isolate VSMCs from the coronary circulation of mice. Although the small number of cells obtained can limit some of the applications for which the cells can be utilized, isolated coronary VSMCs can be used in a variety of well-established cell culture techniques and assays. Studies investigating VSMCs from genetically modified mice can provide further information about structure-function and signaling processes associated with vascular pathologies. Video LinkThe video component of this article can be found at

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SM22α, a Marker of Adult Smooth Muscle, Is Expressed in Multiple Myogenic Lineages During Embryogenesis

Cited by 366 publications

References 45 publications

Forced Expression of Myocardin Is Not Sufficient for Induction of Smooth Muscle Differentiation in Multipotential Embryonic Cells

Forced Expression of Myocardin Is Not Sufficient for Induction of Smooth Muscle Differentiation in Multipotential Embryonic Cells

Transcriptional targeting of replication-defective adenovirus transgene expression to smooth muscle cells in vivo.

Isolation of Murine Coronary Vascular Smooth Muscle Cells

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