Characterization of the phenotype of smooth muscle cells in human fetal aorta on the basis of ultrastructure, immunofluorescence, and the composition of cytoskeletal and cytocontractile proteins

Nikkari, Seppo T.; Rantala, Immo; Pystynen, P; Nikkari, T.

doi:10.1016/0021-9150(88)90188-8

Cited by 24 publications

(10 citation statements)

References 21 publications

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“…As development progresses, embryonic VSMCs gain the characteristics of mature smooth muscle cells; they possess a heterochromatic nucleus, decreased synthetic organelles, and are filled with myofilaments. These descriptions of chicken vessel ultrastructure are similar to observations of mammalian VSMC development [25, 26, 27]. …”

Section: Primordial Vsmcssupporting

confidence: 62%

Developmental Biology of the Vascular Smooth Muscle Cell: Building a Multilayered Vessel Wall

Hungerford

Little²

1999

J Vasc Res

256

183

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The assembly of the vessel wall from its cellular and extracellular matrix components is a critical process in the development and maturation of the cardiovascular system. However, fundamental questions concerning the origin of vessel wall cells and the mechanisms that regulate their development and differentiation remain unanswered. The initial step of vessel wall morphogenesis is formation of a primary vascular network, comprised of nascent endothelial cell tubes, via the processes of vasculogenesis and angiogenesis. Subsequently, primordial vascular smooth muscle cells (VSMCs) are recruited to the endothelium to form a multilayered vessel wall. During the course of development and maturation, the VSMC plays diverse roles: it is a biosynthetic, proliferative, and contractile component of the vessel wall. Although the field of vascular development has blossomed in the past decade, the molecules and mechanisms that regulate this developmental pathway are not well defined. The focus of this review is on those facets of VSMC development important for transforming a nascent endothelial tube into a multilayered structure. We discuss the primordial VSMC with particular attention to its purported origins, the components of the extracellular milieu that contribute to its development, and the contribution of embryonic hemodynamics to vessel wall assembly.

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Section: Primordial Vsmcssupporting

confidence: 62%

Developmental Biology of the Vascular Smooth Muscle Cell: Building a Multilayered Vessel Wall

Hungerford

Little²

1999

J Vasc Res

256

183

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“…This pattern closely resembles the one in developing SM tissue [112,113,116,154,163,208] (table 1) and the maturational profile of SMCs in atherosclerotic lesions [3,12,57,58,112,115,156] or in the arterial wall of balloon-catheterized animals [81,133] (see below).…”

Section: Markers Of Vascular Sm C Differentiation In Vivo and In Vitromentioning

confidence: 80%

“…It is interesting to note that up to the early postnatal phase of development, SMCs are confined to the media layer and the intact intima is not detectable yet [2,70,154,171]. The intima layer appears later in development, especially in humans [70], and might be considered as an adaptive response to modified biochemical, metabolic, and mechanical conditions acting on a specific genetic set up.…”

Section: Structural and Functional Orgnization Of Vascular Sm Cs Durimentioning

confidence: 99%

“…This indicates that the earlier developmental stages are crucial in establishing a balanced interaction between the differ ent cell types involved in vasculogenesis [47,126,184,185], In very early stages of development, locally re cruited [27,136,184] mesenchymal cells, lacking SM-specific structural attributes [27,75,99,132,153], move into the region surrounding small endothelial tubes. Later on these cells assume some structural characteristics of SMCs and incorporate in the wall as cellular layers [2,116,136,154]. SMC proliferation and differentiation occurring in the formation of the arterial wall appear to be controlled by locally activated autocrine/paracrine mech anisms present in cells of the growing arterial wall which might contribute to the maturation process [184], Structural maturation proceeds in such a way that SMC lose their ability to proliferate [33,77], their fibroblast-like appearance, and become filled with myofila ments [60,153,198], The physiological hypertrophy of SMC [23,24] which takes place at this time is accompa nied by a progressive accumulation of cells with a tetraploid nuclear content [160].…”

Section: Structural and Functional Orgnization Of Vascular Sm Cs Durimentioning

confidence: 99%

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Myosin Isoform Expression in Smooth Muscle Cells during Physiological and Pathological Vascular Remodeling

et al. 1994

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There is substantial evidence indicating that the study of cytoskeletal and cytocontractile protein composition in vascular smooth muscle cells (SMCs) can be valuable in tracing structural changes during vascular remodeling. Recent nucleic acid and protein investigations suggest that myosin can be used as a new specific marker for the identification of SMC phenotypes in some pathological conditions affecting the vascular wall. In view of this new information, it would seem timely to review the structural bases of myosin isoform expression in the vascular smooth muscle system as well as the factors involved in its regulation. A puzzling feature has arisen in recent studies on this topic: the presence of non-muscle myosin variants in SMCs during physiological and pathological vascular remodeling. In the response to injury caused by mechanical, chemical and hormonal factors in animals, characterized by proliferation and migration of vascular SMCs from the media to the intima, there is a partial or complete recapitulation of a myosin isoform pattern pertinent to developing vascular smooth muscle tissue. Analysis of myosin isoform content in the vascular wall also demonstrates that: (1) changes in SMC composition may occur independent of medial SMC migration into intima, and (2) the presence of fetal-type SMCs in the neointima is not necessarily related to specific positional changes of medial SMCs.

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“…At the same time, we also found that in the young age group, 2 cases (cases 1 and 4) were negative for c~-actin. Nevertheless, this observation is potentially important because in the fetal aorta, smooth muscle a-actin increases and smooth muscle ]3-actin decreases with gestational age [14]. This change is interpreted as a differentiation phenomenon in which smooth muscle cells gradually transform from the synthetic state (smooth muscle /3-actin positive) to the contractile state (smooth muscle a-actin positive).…”

Section: Commentmentioning

confidence: 99%

Hypoplastic aortic arch morphology pertinent to growth after surgical correction of aortic coarctation

Machii¹,

Becker²

1997

The Annals of Thoracic Surgery

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Characterization of the phenotype of smooth muscle cells in human fetal aorta on the basis of ultrastructure, immunofluorescence, and the composition of cytoskeletal and cytocontractile proteins

Cited by 24 publications

References 21 publications

Developmental Biology of the Vascular Smooth Muscle Cell: Building a Multilayered Vessel Wall

Developmental Biology of the Vascular Smooth Muscle Cell: Building a Multilayered Vessel Wall

Myosin Isoform Expression in Smooth Muscle Cells during Physiological and Pathological Vascular Remodeling

Hypoplastic aortic arch morphology pertinent to growth after surgical correction of aortic coarctation

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