MicroRNAs as pharmacological targets in endothelial cell function and dysfunction

Chamorro-Jorganes, Aránzazu; Araldi, Elisa; Suárez, Yajaira

doi:10.1016/j.phrs.2013.04.002

Cited by 92 publications

(67 citation statements)

References 227 publications

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“…The ability to detect miR200 in blood is consistent with previous reports that miRNAs are present in the circulation (reviewed in Kato et al, 2013; Epstein, 2014). Indeed, circulating miRNAs have been suggested to originate from several sources relevant to our studies including inflammatory foci (Kong et al, 2010), endothelial cells (Chamorro-Jorganes et al, 2013), or mononuclear cells and platelets (Hunter et al, 2008). …”

Section: Resultsmentioning

confidence: 99%

Preserved DNA Damage Checkpoint Pathway Protects against Complications in Long-Standing Type 1 Diabetes

et al. 2015

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SUMMARY The mechanisms underlying the development of complications in type 1 diabetes (T1D) are poorly understood. Disease modeling of induced pluripotent stem cells (iPSCs) from patients with longstanding T1D(disease duration ≥ 50 years) with severe (Medalist +C) or absent to mild complications (Medalist −C) revealed impaired growth, reprogramming, and differentiation in Medalist +C. Genomics and proteomics analyses suggested differential regulation of DNA damage checkpoint proteins favoring protection from cellular apoptosis in Medalist −C. In silico analyses showed altered expression patterns of DNA damage checkpoint factors among the Medalist groups to be targets of miR200, whose expression was significantly elevated in Medalist +C serum. Notably, neurons differentiated from Medalist +C iPSCs exhibited enhanced susceptibility to genotoxic stress that worsened upon miR200 overexpression. Furthermore, knockdown of miR200 in Medalist +C fibroblasts and iPSCs rescued checkpoint protein expression and reduced DNA damage. We propose miR200-regulated DNA damage checkpoint pathway as a potential therapeutic target for treating complications of diabetes.

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Section: Resultsmentioning

confidence: 99%

Preserved DNA Damage Checkpoint Pathway Protects against Complications in Long-Standing Type 1 Diabetes

et al. 2015

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“…Perturbations in EC function are associated with the activation of signaling pathways and changes in gene expression. The role of several miRNAs in controlling EC function and vascular homeostasis has been reviewed elsewhere (Boon et al, 2012; Chamorro-Jorganes et al, 2013; Fish, 2012; Hartmann and Thum, 2011). In this section, we will focus on the role of miR-181 family members in controlling EC specification, function, and vascular inflammation.…”

Section: Role Of Mir-181 Family Members In Endothelial Cellsmentioning

confidence: 99%

Role of miR-181 family in regulating vascular inflammation and immunity

Sun

Sit

Feinberg

2014

Trends in Cardiovascular Medicine

146

125

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The microRNA family, miR-181, plays diverse roles in regulating key aspects of cellular growth, development, and activation. Accumulating evidence supports a central role for the miR-181 family in vascular inflammation by controlling critical signaling pathways, such as downstream NF-κB signaling, and targets relevant to endothelial cell activation and immune cell homeostasis. This review examines the current knowledge of the miR-181 family’s role in key cell types that critically control cardiovascular inflammation under pathological and physiological stimuli.

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“…Flow-regulated miRNAs and their roles in vascular remodeling were also reviewed recently [11, 12]. Increasing evidence suggests that miRNAs are involved in the regulation of EC function, cytokine responsiveness, and vascular inflammation [13]. This review summarizes our current understanding of endothelial miRNAs as critical regulators of EC activation, vascular inflammation, and the initiation of atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Endothelial MicroRNAs and Atherosclerosis

Sun

Belkin

Feinberg

2013

Curr Atheroscler Rep

119

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The vascular endothelium, a thin layer of endothelial cells (ECs) that line the inner surface of blood vessels, is a critical interface between blood and all tissues. EC activation, dysfunction, and vascular inflammation occur when the endothelium is exposed to various insults such as proinflammatory cytokines, oxidative stress, hypertension, hyperglycemia, aging, and shear stress. These insults lead to the pathogenesis of a range of disease states, including atherosclerosis. Several signaling pathways, especially nuclear factor κB mediated signaling, play crucial roles in these pathophysiological processes. Recently, microRNAs (miRNAs) have emerged as important regulators of EC function by fine-tuning gene expression. In this review, we discuss how miRNAs regulate EC function and vascular inflammation in response to a variety of pathophysiologic stimuli. An understanding of the role of miRNAs in EC activation and dysfunction may provide novel targets and therapeutic opportunities for controlling atherosclerosis and other chronic inflammatory disease states.

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MicroRNAs as pharmacological targets in endothelial cell function and dysfunction

Cited by 92 publications

References 227 publications

Preserved DNA Damage Checkpoint Pathway Protects against Complications in Long-Standing Type 1 Diabetes

Preserved DNA Damage Checkpoint Pathway Protects against Complications in Long-Standing Type 1 Diabetes

Role of miR-181 family in regulating vascular inflammation and immunity

Endothelial MicroRNAs and Atherosclerosis

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