Elastin

Parks, William C.; Pierce, Richard A.; Lee, Katherine A.; Mecham, Robert P.

doi:10.1016/s1569-2558(08)60201-5

Cited by 66 publications

(35 citation statements)

References 155 publications

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“…By 175 days of gestation, tropoelastin mRNA was detectable, and relative steady-state mRNA levels increased about &fold by the end of gestation. This pattern of tropoelastin expression in elastic cartilage is similar to that observed in other elastic tissues (Parks et al, 1993).…”

Section: Developmental Expression Of Elastin In Elastic Cartilagesupporting

confidence: 85%

“…Alternatively, cytokines or other effector molecules released by a differentiating population and acting in a paracrine or autocrine fashion would reach a critical local concentration more rapidly in cells at a high density. Various cytokines stimulate elastin production (Parks et al, 1993), and, in fact, medium conditioned by activated vascular smooth muscle cells contains a soluble activity that induces tropoelastin expression in committed fetal ligament fibroblasts . In addition, but not mutually exclusive of the above mechanisms, increased density of mesenchymal cells in developing cartilage and in micromass culture may facilitate the formation of cel1:cell contacts.…”

Section: Discussionmentioning

confidence: 99%

“…Differentiation of pre-elastogenic cells in developing tissues is associated with cessation of proliferation and enhanced matrix production (Parks et al, 198813;Parks et al, 1993), and recent in vivo studies of developing pulmonary arteries demonstrated ~~~ ~ ~~ Fig. 7.…”

Section: Discussionmentioning

confidence: 99%

“…Elastic fibers are assembled extracellularly and are comprised of two distinct components. The most abundant of these is elastin, which is an enzymatically crosslinked product of soluble tropoelastin monomers (Parks et al, 1993). Microfibrils, which make up about 10% of the mass of elastic fibers and are comprised of glycoproteins, such as fibrillin 15 and MAGP (Sakai et al, 1986;Gibson et al, 1991), form 10 to 12 nm fibers that provide a scaffold upon which tropoelastin is deposited and crosslinked into the growing elastic fiber (Ross et al, 1977;Mecham and Heuser, 1990a,b).…”

Section: Introductionmentioning

confidence: 99%

“…In most mammalian tissues, the bulk of elastogenesis occurs during late fetal and early neonatal periods, and by maturity production is complete and synthesis of new tropoelastin ceases (Parks et al, 1993). Because of the extreme durability and extended half-life of elastin, fiber function and tissue integrity are not compromised by this limited production (Rucker and Dubick, 1984;Shapiro et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

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Increased mesenchymal cell density accompanies induction of tropoelastin expression in developing elastic tissue

Lee

Pierce

Mecham

et al. 1994

Developmental Dynamics

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We studied the differentiation of elastin-producing fetal bovine chondrocytes to understand the regulatory processes associated with induction of elastin expression. Analysis of auricular elastic cartilage development in vivo indicated that differentiation of the prechondrogenic blastema to an elastogenic phenotype was preceded and accompanied by condensation of the mesenchymal cells. In addition, induction of elastin production was temporally and spatially linked to expression of type I1 collagen and proteoglycans. We assessed the influence of cell density on the induction of tropoelastin expression in pre-elastogenic cells from developing ear buds, Tropoelastin expression was induced in prechondrogenic mesenchymal cells only if the cells were maintained at a high cellular density. In addition, high density culture upregulated tropoelastin expression in fully differentiated chondrocytes. Together these data suggest that high cell density facilitates celkcell interactions that affect cell proliferation and influence tropoelastin expression.

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Section: Developmental Expression Of Elastin In Elastic Cartilagesupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Increased mesenchymal cell density accompanies induction of tropoelastin expression in developing elastic tissue

Lee

Pierce

Mecham

et al. 1994

Developmental Dynamics

Self Cite

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Altered bladder function in transgenic mice expressing rat elastin

et al. 1999

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The elasticity of tissues subjected to repeated deformation is provided by the presence of elastic fibers in the extracellular matrix (ECM). The most abundant component of elastic fibers is elastin, whose soluble precursor is tropoelastin. To establish the role elastin plays in the bladder, this study describes the biosynthetic, histologic, and physiologic consequences of expression of an isoform of rat tropoelastin in transgenic mouse bladder. The polymerase chain reaction (PCR) was used to determine expression of a rat tropoelastin minigene in transgenic mice. Histochemical methods were used to demonstrate changes in elastic fibers in frozen sections of bladder. Cystometric analysis was carried out in transgenic and non‐transgenic mice, prior to and after 3 weeks of partial outlet obstruction. The PCR assay demonstrated that bladder tissue of transgenic mice expressed rat tropoelastin mRNA, whereas non‐transgenes did not. Increased deposition of elastic fibers was demonstrated with the Verhoeff‐van Gieson stain. Bladders of transgenic animals were more compliant than bladders of their non‐transgenic littermates. Partial outlet obstruction resulted in increased bladder volume and more compliant bladders in non‐transgenic mice. In contrast, the bladder volume and compliance in transgenes was almost unchanged by obstruction. This study demonstrates that normal elastic fiber assembly is prerequisite for the compliant properties of the bladder wall. Moreover, the response of the bladder to obstruction is critically influenced by elastin synthesis. Neurourol. Urodynam. 18:55–68, 1999. © 1999 Wiley‐Liss, Inc.

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