The pathophysiology of aortic aneurysms (AA) is far from being understood. One reason for this lack of understanding is basic research being constrained to fixated cells or isolated cell cultures, by which cell-to-cell and cell-to-matrix communications are missed. We present a new, in vitro method for extended preservation of aortic wall sections to study pathophysiological processes. Intraoperatively harvested, live aortic specimens were cut into 150 μm sections and cultured. Viability was quantified up to 92 days using immunofluorescence. Cell types were characterized using immunostaining. After 14 days, individual cells of enzymatically digested tissues were examined for cell type and viability. Analysis of AA sections (N = 8) showed a viability of 40% at 7 days and smooth muscle cells, leukocytes, and macrophages were observed. Protocol optimization (N = 4) showed higher stable viability at day 62 and proliferation of new cells at day 92. Digested tissues showed different cell types and a viability up to 75% at day 14. Aortic tissue viability can be preserved until at least 62 days after harvesting. Cultured tissues can be digested into viable single cells for additional techniques. Present protocol provides an appropriate ex vivo setting to discover and study pathways and mechanisms in cultured human aneurysmal aortic tissue.
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http://dx.doi.org/10.1038/s41598-018-26549-4 | DOI Listing |
Circ Heart Fail
January 2025
Aswan Heart Center, Magdi Yacoub Heart Foundation, Egypt (A.M.I., M.R., A. Elsawy, M.H., S.H., W.E., A. Elaithy, A. Elguindy, A. Afifi, Y.A., M.Y.).
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Br J Pharmacol
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Department of Medical Research, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien, Taiwan.
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View Article and Find Full Text PDFIran J Med Sci
December 2024
Department of Medical Physiology, College of Medicine, Zagazig University, Al-Sharquia, Egypt.
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View Article and Find Full Text PDFAtrial remodeling is a major pathophysiological mechanism of atrial fibrillation (AF). Atrial remodeling progresses with aging and background diseases, including hypertension, heart failure, and AF itself. However, its mechanism of action and reversibility have not been completely elucidated.
View Article and Find Full Text PDFJCI Insight
January 2025
Department of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, United States of America.
Aortic dissection or rupture is a major cause of mortality in vascular Ehlers-Danlos Syndrome (vEDS), a connective tissue disorder caused by heterozygous mutations in the COL3A1 gene. C57BL6/J (BL6) mice carrying the Col3a1 G938D/+ mutation recapitulate the vEDS vascular phenotype and die suddenly of aortic rupture/dissection. However, 129S6/SvEvTac (129) mice expressing the same Col3a1 G938D/+ mutation show near-complete life-long protection from vascular rupture.
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