Mouse Models of Vascular Diseases by Masataka Sata

By Masataka Sata

This publication is a methodological resource on mice versions of vascular illnesses. masking a number of components, each one bankruptcy is written by way of a pioneering researcher who has built an unique vascular affliction version. Notoriously tricky to breed, each one version is defined intimately and diverse images are supplied with hyperlinks to video clips. Genetically transformed mice are crucial device for learning the pathogenesis of varied illnesses, together with immunological and oncological issues, yet they'd regularly been considered too small for use within the box of heart problems. lately, although, a number of mice versions of vascular ailments were said, and those will make a considerable contribution to easy study on cardiovascular and metabolic disorders.

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Lindner and colleagues were the first to report mechanically induced endothelial denudation model, which involves passage of a flexible guidewire three times in the carotid artery [31]. This procedure completely removes the endothelial cell layer, which results in the recruitment of platelets to the denuded surface and activation of the medial SMCs. Neointimal hyperplasia is typically observed within 2 weeks after the injury. This procedure is the most similar to angioplasty. However, this procedure is a relatively challenging procedure, which leads to difficulty in achieving reproducible results.

1e, contralateral artery) associated with increased flow; and 4) constrictive remodeling (Fig. 1f), characterized by decreased circumference of the injured artery in response to decreased flow, which is also a significant component of human vascular disease. In this injury model, medial vascular smooth muscle cells dedifferentiate, proliferate, and migrate across the internal elastic lamina to comprise the majority of neointimal cells present in the lesion [7]. We performed lineage tracing studies that follow the fate of fully differentiated medial vascular smooth muscle cells expressing smooth muscle myosin heavy chain (SM MHC) [7] to estimate the proportion of neointimal cells derived from differentiated SM MHC-positive cells.

51. Harrison DG. Cellular and molecular mechanisms of endothelial cell dysfunction. J Clin Invest. 1997;100(9):2153–7. 1172/jci119751. 52. Shimokawa H. Primary endothelial dysfunction: atherosclerosis. J Mol Cell Cardiol. 1999;31 (1):23–37. 0841. 53. Huang PL, Huang Z, Mashimo H, Bloch KD, Moskowitz MA, Bevan JA, et al. Hypertension in mice lacking the gene for endothelial nitric oxide synthase. Nature. 1995;377(6546):239–42. 1038/377239a0. 54. Forstermann U, Schmidt HH, Pollock JS, Sheng H, Mitchell JA, Warner TD, et al.

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