ArticleAtherosclerosis2014
Osteoglycin deficiency does not affect atherosclerosis in mice.
Article in Atherosclerosis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Exploring the role of osteoglycin in type 2 diabetes: implications for insulin resistance and vascular pathophysiology.American journal of physiology. Endocrinology and metabolism · 2023Article
- Osteoglycin as a Potential Biomarker of Mild Kidney Function Impairment in Type 2 Diabetes Patients.Journal of clinical medicine · 2021Article
- Low Levels of Plasma Osteoglycin in Patients with Complex Coronary Lesions.Journal of atherosclerosis and thrombosis · 2018Article
- Association of SLRPs with carotid artery atherosclerosis in essential hypertensive patients.Journal of human hypertension · 2018Article
- Serum Mimecan Is Associated With Arterial Stiffness in Hypertensive Patients.Journal of the American Heart Association · 2015Article
- Regulation of hyaluronan synthesis in vascular diseases and diabetes.Journal of diabetes research · 2015Review
- Vascular proteoglycans and atherosclerosis: not over yet.Atherosclerosis · 2014Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe small leucine-rich proteoglycan Osteoglycin/Mimecan (OGN) is a component of the extracellular matrix, where it regulates collagen fibrillogenesis and cytokine availability. OGN is abundant in normal vessels and in atherosclerotic and restenotic lesions of rat, rabbit and human arteries. Osteoglycin-null mice show alterations in the thickness of collagen fibers of the cornea and the skin. In this work, we inspect the possible involvement of OGN in the atherosclerosis progression using a double knockout mouse model.
methodsIn order to examine the progression of atherosclerosis in the absence of OGN, we developed double Apoe and Ogn knockout mice and performed a comparative histomorphological and immunofluorescence study of the atherosclerotic lesions of Apoe(-/-)Ogn(-/-) and Apoe(-/-)Ogn(+/+) mice.
resultsWe demonstrate the presence of Ogn transcript in the aorta of wildtype mice, its absence in Ogn(-/-) mice, and the normal histomorphology of arteries of Ogn(-/-) mice. The composition of the extracellular matrix and also the cellular content and distribution were similar in atherosclerotic lesions of Apoe(-/-)Ogn(-/-) and Apoe(-/-)Ogn(+/+) mice. Quantification of the lesion size revealed no significant differences between double and single knockout mice. The incidence, size and distribution of calcium deposits were similar in both groups of mice.
conclusionsThe lack of the proteoglycan OGN does not affect the progression of atherosclerosis in mice. Possible causes for the absence of phenotype in the Apoe/Ogn double mutants are discussed.
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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.