Aortic intimal thickening and myosin isoform expression in hyperthyroid rabbits.

Giuriato, Luca; Borrione, Anna; Zanellato, Anna Maria Cecilia; Tonello, Marta; Scatena, Marta; Scannapieco, Gianluigi; Pauletto, Paolo; Sartore, Saverio

doi:10.1161/01.atv.11.5.1376

Cited by 18 publications

(17 citation statements)

References 54 publications

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“…A number of factors may be involved in determining the individual and species-spe cific variability in atherogenesis sensitivity: duration of diet [12.20-22] and diet composition [23], lipid metabo lism specificities [9,10], structural and functional integri ty of endothelium [24] , lipid oxidation levels [25], the transformation of cholesterol to bile acids [26], extent of thrombus formation [6], degree of leukocyte infiltration [27], hormonal status [19,28], preexistence of a 'natural intima' [6] and aging [29][30][31]. In addition, due to the het erogeneous genetic background, individual differences in the rate at which the disease develops and progresses can also be demonstrated within a given species [32].…”

Section: Discussionmentioning

confidence: 99%

“…Bromo-Deoxyuridine Incorporation DNA synthesis in aortic SM cells was evaluated by bromo-deoxyuridine (BrdU) incorporation studies, following the procedure of Giuriato et al [19]. Twenty-four and 12 h before sacrifice, the rats were injected intraperitoneally with BrdU, 30 mg body weight.…”

Section: Immunofluorescencementioning

confidence: 99%

“…Twenty-four and 12 h before sacrifice, the rats were injected intraperitoneally with BrdU, 30 mg body weight. High (intestine) and low (myocardium) replicating tissues from BrdUtreated animals were included in the tests to validate the experiments [19], The indirect immunoperoxidase method and 3-amino-9-ethylcarbazole detecting system (positive nuclei appeared red) were used to reveal the BrdU-incorporating nuclei in the aortic tissues. Unrcacting nuclei were visualized by Mayer's hematoxylin counterstaining (nuclei appeared blue-violet).…”

Section: Immunofluorescencementioning

confidence: 99%

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Atherosclerosis Resistance in Rats Correlates with Lack of Expansion of an Immature Smooth Muscle Cell Population

Amore

Chiavegato²,

Paulon³

et al. 1996

J Vasc Res

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In this study we asked whether the well-known atherosclerosis resistance of rats might be reduced with aging. Two groups of young, adult and aged Wistar rats, one of which was kept on a standard, low-cholesterol (CT) diet, and the other one was fed a 2% CT diet for 2 months were enrolled. Potential modifications in the phenotypic profile of aortic smooth muscle (SM) were assessed by SDS-gel electrophoresis, Western blotting and immunofluorescence procedures using a panel of monoclonal antibodies to myosin isoforms, cytoskeletal and extracellular matrix proteins. With development and aging, the expression of 196-kD non-muscle-type myosin heavy-chain isoform (MyHC), the EIIIA fibronectin variant and keratins was downregulated, whereas that of the 204- and 200-kD SM-type MyHC isoforms, SM-type α-actin and desmin did not change. The levels of hypercholesterolemia achieved in this model did not substantially modify the distribution of the downregulated markers, except for the subendothelial grouping of immature SM cells in aged rats. Morphometric measurements indicated a slight increase of medial cross-sectional area accompanied by a decrease in total SM cell number, both with aging and with hypercholesterolemia. In no circumstance was the presence of atherosclerotic lesions histologically detectable. Bromo-deoxyuridine (BrdU) incorporation analysis revealed a marked age-dependent decline in DNA synthesis and the formation of binucleated cells in aged aortas. This pattern was not influenced by hypercholesterolemia, except in aged rats where BrdU-positive SM cells are almost doubled. Our data indicate that aging and hypercholesterolemia cannot affect the phenotypic stability of rat SM cells and confirm that the change from a fully differentiated to an immature state is a general prerequisite to allow the development of atherosclerotic lesions in mammalian species.

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Section: Discussionmentioning

confidence: 99%

Section: Immunofluorescencementioning

confidence: 99%

Section: Immunofluorescencementioning

confidence: 99%

See 1 more Smart Citation

Atherosclerosis Resistance in Rats Correlates with Lack of Expansion of an Immature Smooth Muscle Cell Population

Amore

Chiavegato²,

Paulon³

et al. 1996

J Vasc Res

View full text Add to dashboard Cite

show abstract

“…The angioplasty catheter was then removed and the surgical wound closed. Animals were sacrificed 48 h after injury and the carotids were reacted for immunocytochemistry as reported by Giuriato et al [65]. Positive cells appear dark.…”

Section: Endothelial Lesionmentioning

confidence: 99%

“…3) [67] accompanied by intimal thickening formation ( fig. 5) [65] and the accumulation of an almost pure population of SMCs showing a fetal phenotype (table 5). Insulin infu sion has a similar effect on the aortic media without any evidence of myosin isoforms switching towards the fetal SMC phenotype (table 5).…”

Section: Hormonesmentioning

confidence: 99%

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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Rabbit ductus arteriosus during development: Anatomical structure and smooth muscle cell composition

et al. 1993

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The anatomical structure as well as the smooth muscle cell (SMC1) composition of the ductus arteriosus (DA) were studied in rabbits ranging in age from 29 days of gestation to 20 days after birth. Computer-assisted, three-dimensional reconstructions of hematoxylin-eosin stained serial cryosections from ductus arteriosus-aorta (DA-AO) junctures revealed that DA in animals near term is separated from the aorta by a "septumlike" structure that is continuous with the aortic wall. Two days after birth, obliteration of DA is almost complete, and a small "pocketlike" cavity appears in the pre-existing site in which DA merged into the aorta. This small cavity in the aortic arch was still evident in the large majority of animals examined even 20 days after birth, as also demonstrated by scanning electron microscopy. At this time period DA consisted of a central, fibrotic region surrounded by several layers of SMC (the ligamentum arteriosum, LA) and ended within the aortic media just above the small cavity, forming a round "scar." Vascular SMC composition of DA during closure was examined by means of indirect and double immunofluorescence procedures, using a panel of monoclonal antibodies against some cytoskeletal and cytocontractile proteins (vimentin, desmin, smooth muscle (SM), and nonmuscle (NM) myosin isoforms). "Intimal cushions" were particularly evident from 5 hr after birth and were found to be desmin-negative, homogenously reactive for vimentin and NM myosin, and heterogeneously stained with anti-SM myosin antibody. In SMC subjacent to the "intimal cushions," distribution of vimentin and SM myosin was homogeneous, whereas the one of desmin and NM myosin content was heterogeneous. The cytoskeletal and cytocontractile protein content displayed by SMC during the closure of DA is similar to that of "intimal thickening" found in some pathological conditions of the arterial wall in adult rabbits. Completation of DA closure (day 2) was accompanied by the disappearance of cellular heterogeneity in myosin isoform distribution in both the "intimal cushions" and the underlying media. These results give new insights into: (1) the structure of DA-AO juncture, which can be relevant to the physiology of blood circulation in the fetus, and (2) the phenotypic similarity of vascular SMC populations involved in the formation of "intimal cushions" and "intimal thickening."

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Aortic intimal thickening and myosin isoform expression in hyperthyroid rabbits.

Cited by 18 publications

References 54 publications

Atherosclerosis Resistance in Rats Correlates with Lack of Expansion of an Immature Smooth Muscle Cell Population

Atherosclerosis Resistance in Rats Correlates with Lack of Expansion of an Immature Smooth Muscle Cell Population

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

Rabbit ductus arteriosus during development: Anatomical structure and smooth muscle cell composition

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