Mechanisms of elastin calcification and its prevention with aluminum chloride pretreatment
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Elastin calcification occurs in bioprosthetic heart valve implants. The authors have developed a rat subdermal model to study purified elastin calcification. Purified elastin implants undergo severe calcification within 21 day period and it is found to be poorly crystallin hydroxyapatite by X-ray analysis. Aluminum chloride pretreatment of elastin inhibits its calcification due to the strong binding of aluminum ions to elastin leading to the alteration in elastin structures.Elastin calcification occurs in bioprosthetic heart valve implants. The authors have developed a rat subdermal model to study purified elastin calcification. Purified elastin implants undergo severe calcification within 21 day period and it is found to be poorly crystallin hydroxyapatite by X-ray analysis. Aluminum chloride pretreatment of elastin inhibits its calcification due to the strong binding of aluminum ions to elastin leading to the alteration in elastin structures.
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Matrix (chemical analysis)
Fibrillin
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ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTElastin mRNA levels and insoluble elastin accumulation in neonatal rat smooth muscle cell culturesLeesa M. Barone, B. Leslie Wolfe, Barbara Faris, and Carl FranzblauCite this: Biochemistry 1988, 27, 9, 3175–3182Publication Date (Print):May 3, 1988Publication History Published online1 May 2002Published inissue 3 May 1988https://pubs.acs.org/doi/10.1021/bi00409a008https://doi.org/10.1021/bi00409a008research-articleACS PublicationsRequest reuse permissionsArticle Views59Altmetric-Citations18LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Tropoelastin
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Thoracic aorta
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Abstract —The elastin content in the thoracic aorta of male Brown-Norway (BN) rats is 31.4±1.2% (dry weight), whereas that of male LOU rats is 37.2±1.0%. A similar difference in the elastin content of the thoracic aorta is also observed in female animals. Furthermore, in the thoracic aorta of young, growing rats as well as in cultured aortic smooth muscle cells, the steady-state level of elastin mRNA is significantly lower in the BN than in the LOU strain. These results suggested that 1 or more genes control the elastin mRNA level and the elastin content in the aortas of BN and LOU rats. A possible relationship between a polymorphism in the elastin gene and the elastin content of the aorta was tested. For this purpose, the aortic elastin content was measured in F 1 and F 2 generations bred from LOU and BN rats and was compared with that of the F 0 (parental) generation. A polymorphic marker located in intron 25 of the elastin gene has been used to genotype the F 2 rats. The degree of genetic determination of aortic elastin content was estimated to be 73% in the F 2 cohort, but the elastin locus accounts for only 3.9% of the total variance in aortic elastin content. Other genes are thus responsible for the major part of the observed interstrain difference by regulating the transcription of the gene, the stability of elastin mRNA, and/or posttranslational events.
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Abstract We have previously studied the process of calcification in bioprosthetic porcine heart valves crosslinked with glutaraldehyde. Observations using light microscopy had indicated that calcification of elastic fibers occurs in implanted heart valves, in addition to calcification associated with collagen fibers. To determine the contribution of elastin to the process of calcification, small pieces of rabbit aorta were crosslinked with 0.2% glutaraldehyde, rinsed in buffer, and implanted subcutaneously in young adult male rats. Cross‐linked jugular vein implants were included as controls. After an implantation period of 1 month or longer, we observed many areas of calcification in the aortic media associated with elastin and fewer such areas associated with collagen. The elastin‐rich aortic tissues accumulated more calcium than venous tissues. Calcium deposits appeared similar in both allogeneic and xenogeneic implants. Calcified areas viewed under the electron microscope included intercellular nonfibrous material. Calcified areas involved predominantly the outer layers of elastic fibers. Calcific deposits included needle‐ like crystals of hydroxyapatite but often consisted of an amorphous flocculant material surrounded by crystals. The close spatial relationship of hydroxyapatite crystals and elastic membranes seen in this study may be relevant to the initiation of dystrophic calcification in glutaraldehyde cross‐linked aortic grafts. © 1992 John Wiley & Sons, Inc.
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The relative levels of elastin-specific mRNA were used as a measure of tropoelastin expression in uteri from pregnant Sprague-Dawley rats. The levels of elastin-specific mRNA were also correlated with values for net tropoelastin production and net deposition of mature, crosslinked elastin. The total content of uterine elastin increased throughout gestation, reaching maximal levels at Day 19 of gestation, which were three times those of nongravid tissue. Following involution, the elastin content decreased rapidly to near baseline values by 5 days postpartum. The content of soluble elastin, estimated using an enzyme-linked immunosorbent assay, paralleled in part the increase in elastin deposition and elastin mRNA levels. Uterine elastin metabolism appears to be unlike that in other elastic tissues, e.g., lung and large blood vessels. In most elastin containing tissues, the protein is synthesized during discrete developmental periods and is not readily degraded. However, uterine elastin is continuously expressed, and appears to be in a continual cycle of degradation and replacement.
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Desmosine
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The presence of elastin layers in the aortic walls of twelve human fetuses was confirmed with scanning electron microscope pictures after hot alkali treatment and histochemical examination. In addition, the number of elastin layers in aortic walls of 5 different segments were compared in fetuses of varying ages. Aldehyde fuchsin stained slides of elastin ascending aortas showed a range between 27 and 55 layers of elastin in fetuses of 8 weeks to 32 weeks. However, in the lower abdominal aortas, elastin layers decreased from 28 to only 3 layers for fetuses of the same age. Furthermore, as elastin layers decreased from ascending aorta to abdominal aorta with the progression of fetal life, similar changes in the elastin lamellae were observed. These results suggest that while aortas grow rapidly in length, the medial elastin thickens slowly, perhaps due to slow development of hydrodynamic forces and pressures. Also the adventitial elastin appears to lose out gradually along the length from ascending aorta to abdominal aorta.
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Elastic fiber
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Background— Elastin calcification is a widespread feature of vascular pathology, and circumstantial evidence exists for a correlation between elastin degradation and calcification. We hypothesized that matrix metalloproteinase (MMP)–mediated vascular remodeling plays a significant role in elastin calcification. Methods and Results— In the present studies, we determined that short-term periadventitial treatment of the rat abdominal aorta with low concentrations of calcium chloride (CaCl 2 ) induced chronic degeneration and calcification of vascular elastic fibers in the absence of aneurysm formation and inflammatory reactions. Furthermore, the rate of progression of calcification depended on the application method and concentration of CaCl 2 applied periarterially. Initial calcium deposits, associated mainly with elastic fibers, were persistently accompanied by elastin degradation, disorganization of aortic extracellular matrix, and moderate levels of vascular cell apoptosis. Application of aluminum ions (known inhibitors of elastin degradation) before the CaCl 2 -mediated injury significantly reduced elastin calcification and abolished both extracellular matrix degradation and apoptosis. We also found that MMP-knockout mice were resistant to CaCl 2 -mediated aortic injury and did not develop elastin degeneration and calcification. Conclusion— Collectively, these data strongly indicate a correlation between MMP-mediated elastin degradation and vascular calcification.
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