Chick tropoelastin isoforms. From the gene to the extracellular matrix.

Pollock, Joanne; Baule, Valerie J.; Rich, Celeste B.; Ginsburg, Claudia; Curtiss, Sandra W.; Foster, Jeffrey S.

doi:10.1016/s0021-9258(19)39650-4

Cited by 26 publications

(1 citation statement)

References 26 publications

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“…Elastin is only present in vertebrate animals, and there is extensive homology among human, chick, bovine, and rat species at the nucleic and amino acid levels (191). During an organism's lifespan, elastin gene expression and protein synthesis occur within a narrow timeframe initiating late in embryonic development and terminating in adolescence with essentially no de novo elastin production throughout adult life of the animal (15,26,34,119,133,142,145,163). The narrow timeframe of elastin expression and synthesis is unusual for an ECM component, as generally ECM production is dynamic throughout the organism's lifespan.…”

Section: Elastin Characterizationmentioning

confidence: 99%

Elastin, arterial mechanics, and cardiovascular disease

Cocciolone

Hawes

Staiculescu

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

230

161

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Large, elastic arteries are composed of cells and a specialized extracellular matrix that provides reversible elasticity and strength. Elastin is the matrix protein responsible for this reversible elasticity that reduces the workload on the heart and dampens pulsatile flow in distal arteries. Here, we summarize the elastin protein biochemistry, self-association behavior, cross-linking process, and multistep elastic fiber assembly that provide large arteries with their unique mechanical properties. We present measures of passive arterial mechanics that depend on elastic fiber amounts and integrity such as the Windkessel effect, structural and material stiffness, and energy storage. We discuss supravalvular aortic stenosis and autosomal dominant cutis laxa-1, which are genetic disorders caused by mutations in the elastin gene. We present mouse models of supravalvular aortic stenosis, autosomal dominant cutis laxa-1, and graded elastin amounts that have been invaluable for understanding the role of elastin in arterial mechanics and cardiovascular disease. We summarize acquired diseases associated with elastic fiber defects, including hypertension and arterial stiffness, diabetes, obesity, atherosclerosis, calcification, and aneurysms and dissections. We mention animal models that have helped delineate the role of elastic fiber defects in these acquired diseases. We briefly summarize challenges and recent advances in generating functional elastic fibers in tissue-engineered arteries. We conclude with suggestions for future research and opportunities for therapeutic intervention in genetic and acquired elastinopathies.

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Section: Elastin Characterizationmentioning

confidence: 99%

Elastin, arterial mechanics, and cardiovascular disease

Cocciolone

Hawes

Staiculescu

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

230

161

View full text Add to dashboard Cite

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Elastogenesis in the developing chick lung is transcriptionally regulated

et al. 1998

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The overall goals of this study were to establish the level at which elastin gene expression is regulated during chick lung embryogenesis and to identify the temporal and spatial relationships among elastogenesis, smooth muscle cell differentiation, and cell proliferation. A comparison of lung elastin mRNA and transcriptional levels during embryogenesis shows that elastin expression is developmentally regulated at the transcriptional level. The increase in elastogenic activity occurs during the late stages of lung embryogenesis and coincides with terminal maturation of the tertiary bronchi. In situ hybridization analysis demonstrates that the increase in elastin mRNA expression is confined to the tertiary bronchial respiratory subunits, connective tissue septa, and supporting vasculature of the lung parenchyma. Immunohistochemical localization of smooth muscle cell α‐actin and tropoelastin suggests that α‐actin–immunoreactive cells of the lung parenchyma are a major contributor to the increase in elastin expression during embryogenesis. This observation is also reflected by Northern blot analysis, which demonstrates a temporal coincidence in the increase of both α‐actin and elastin mRNA levels. Histone mRNA expression, which was used as an index of cellular proliferation, reveals a level and spatial pattern inversely related to that of the elastin transcript. Tissue transfections of chick lungs isolated from 18‐day embryos with various elastin gene deletion/reporter constructs illustrate that the elastin promoter is not promiscuous within a tissue environment and that sequences spanning the −500 to +2 region are capable of directing promoter activity spatially comparable to the endogenous elastin gene. Dev. Dyn. 1998;213:170–181. © 1998 Wiley‐Liss, Inc.

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Elastin and the Lung

Davidson

1992

Biochemistry of Pulmonary Emphysema

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Chick tropoelastin isoforms. From the gene to the extracellular matrix.

Cited by 26 publications

References 26 publications

Elastin, arterial mechanics, and cardiovascular disease

Elastin, arterial mechanics, and cardiovascular disease

Elastogenesis in the developing chick lung is transcriptionally regulated

Elastin and the Lung

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