ArticleJournal of vascular surgery2014
Smooth muscle cells from abdominal aortic aneurysms are unique and can independently and synergistically degrade insoluble elastin.
Article in Journal of vascular surgery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 57 citations in OpenAlex.
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- "Attractive" Treatment for Abdominal Aortic Aneurysm Repair: Magnetic Localization of Silk-Iron Packaged Extracellular Vesicles.Journal of functional biomaterials · 2025Article
- Contribution of NLRP3-GSDMD axis to PDGF-BB-induced vascular smooth muscle cell phenotypic transition.American journal of physiology. Cell physiology · 2025Article
- Collagen mimetic peptides as novel therapeutics for vascular disease in the central nervous system.Frontiers in neuroscience · 2025Article
- Stem cell-based therapies for treatment of abdominal aortic aneurysm: development, application, and future potential.npj biomedical innovations · 2025Review
- Olfactory Receptors and Aortic Aneurysm: Review of Disease Pathways.Journal of clinical medicine · 2024Review
- In Vitro Models of Cardiovascular Disease: Embryoid Bodies, Organoids and Everything in Between.Biomedicines · 2024Review
- Serum fetuin-a and risk of thoracic aortic aneurysms: a two-sample mendelian randomization study.Frontiers in endocrinology · 2024Article
- Targeted PERK inhibition with biomimetic nanoclusters confers preventative and interventional benefits to elastase-induced abdominal aortic aneurysms.Bioactive materials · 2023Article
- The mechanism and therapy of aortic aneurysms.Signal transduction and targeted therapy · 2023Review
- The role of vascular smooth muscle cells in the development of aortic aneurysms and dissections.European journal of clinical investigation · 2022Review
- Article
- Article
- Non-coding RNAs Regulate the Pathogenesis of Aortic Dissection.Frontiers in cardiovascular medicine · 2022Review
- Inflammatory Mediators in Atherosclerotic Vascular Remodeling.Frontiers in cardiovascular medicine · 2022Review
- A Review of the Impact of Neutrophils and Neutrophil Extracellular Traps (NETs) on the Development of Aortic Aneurysms in Animal and Human Studies.Medical science monitor : international medical journal of experimental and clinical research · 2021Review
- Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms.Journal of the American Heart Association · 2021Article
- B Cell-Activating Factor Antagonism Attenuates the Growth of Experimental Abdominal Aortic Aneurysm.The American journal of pathology · 2021Article
- Based on bioinformatics analysis lncrna SNHG5 modulates the function of vascular smooth muscle cells through mir-205-5p/SMAD4 in abdominal aortic aneurysm.Immunity, inflammation and disease · 2021Article
- Thymosin β4 protects against aortic aneurysm via endocytic regulation of growth factor signaling.The Journal of clinical investigation · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe purpose of this study was to further elucidate the role of the vascular smooth muscle cells (SMCs) in abdominal aortic aneurysm (AAA) disease. We hypothesized that that AAA SMCs are unique and actively participate in the process of degrading the aortic matrix.
methodsWhole-genome expression profiles of SMCs from AAAs, nondilated abdominal aorta (NAA), and carotid endarterectomy (CEA) were compared. We quantified elastolytic activity by culturing SMCs in [(3)H]elastin-coated plates and measuring solubilized tritium in the media after 7 days. Matrix metalloproteinase (MMP)-2 and MMP-9 production was assessed using real-time polymerase chain reaction, zymography, and Western blotting.
resultsEach SMC type exhibited a unique gene expression pattern. AAA SMCs had greater elastolytic activity than NAA-SMCs (+68%; P < .001) and CEA-SMCs (+45%; P < .001). Zymography showed an increase of active MMP-2 (62 kD) in media from AAA SMCs. AAA SMCs demonstrated twofold greater expression of MMP-2 messenger (m)RNA (P < .05) and 7.3-fold greater MMP-9 expression (P < .01) than NAA-SMCs. Culture with U937 monocytes caused a synergistic increase of elastolysis by AAA SMCs (41%; P < .001) but not NAA-SMCs or CEA-SMCs (P = .99). Coculture with U937 caused a large increase in MMP-9 mRNA in AAA-SMCs and NAA-SMCs (P < .001). MMP-2 mRNA expression was not affected. Western blots of culture media showed a fourfold increase of MMP-9 (92 kD) protein only in AAA-SMCs/U937 but not in NAA-SMCs/U937 (P < .001) and a large increase in active-MMP2 (62 kD), which was less apparent in NAA-SMCs/U937 media (P < .01).
conclusionsAAA-SMCs have a unique gene expression profile and a proelastolytic phenotype that is augmented by macrophages. This may occur by a failure of post-transcriptional control of MMP-9 synthesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.