MicroRNA-34a modulates vascular calcification

Badi, Ileana; Mancinelli, Luigi; Polizzotto, Andrea; Zeni, Filippo; Ferri, Debora; Burba, Ilaria; Brambilla, Francesca; Saccu, Claudio; Bianchi, Marco E.; Capogrossi, M. C.; Pompilio, Giulio; Raucci, Angela

doi:10.1016/j.vph.2017.12.040

Cited by 3 publications

(6 citation statements)

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“…Specifically, miR-34a has been associated to frailty, aging, and diabetes (Figure 1) (Boon et al, 2013;Chakraborty et al, 2014;Rippo et al, 2014;Badi et al, 2018;Thounaojam and Bartoli, 2019;Kukreti and Amuthavalli, 2020;Ni et al, 2020;Manakanatas et al, 2022) and is generally considered a bona fide biomarker of cellular and vascular senescence (Badi et al, 2015;Park et al, 2020;Manakanatas et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

Functional role of miR-34a in diabetes and frailty

et al. 2022

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Emerging evidence has shown that microRNAs (miRNAs) play critical role in the pathogenesis of several disorders. In the present minireview, we focus our attention on the functional role of a specific miRNA, namely miR-34a, in the pathophysiology of frailty and diabetes mellitus. Based on the current literature, we speculate that this miRNA may serve as a potential biomarker of frailty in diabetic older adults. Additionally, its actions on oxidative stress might represent a druggable target to obtain new potentials treatments.

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Section: Introductionmentioning

confidence: 99%

Functional role of miR-34a in diabetes and frailty

et al. 2022

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“…In order to induce hyperphosphataemia-mediated calcification, HASMCs (5 × 10 4 ) were cultured in a medium containing a high concentration of inorganic phosphate (Pi; DMEM supplemented with 15% FBS, 5 mM of phosphate, 10 mM of sodium pyruvate, and 50 µg/mL of ascorbic acid) for 0 to 7 days (Days 0, 3, 5, and 7) [7,10]. Cells were first seeded in SmGM-2 Basal Medium (#CC-3182, Lonza, Basel, Switzerland) for 6 h, and, after their adhesion, the medium was changed to a high Pi medium.…”

Section: Calcification Assaysmentioning

confidence: 99%

“…Fifteen-week-old male C57BL6/J mice (Charles River Laboratories International, Inc.) were used to obtain aortic rings. For in vivo calcification experiments, ten-week-old male WT mice were treated with either 500,000 IU/kg/day Vitamin D (Cholecalciferol, #C1357, Sigma-Aldrich, St. Louis, MO, USA) or a mock solution (1% (v/v) Ethanol, 7% (v/v) Kolliphor ® EL, and 3.75% (w/v) Dextrose (all from Sigma-Aldrich)) administered subcutaneously for three consecutive days and sacrificed seven days after the first injection [7,10]. Animals were anaesthetized with an intraperitoneal injection of ketamine (100 mg/kg) and perfused with PBS.…”

Section: Animal Experimentsmentioning

confidence: 99%

“…We also assessed if the activation of the JAK-STAT pathway is associated with VC in vivo using a mouse model of medial VC induced by an overdose of Vitamin D (Vit D; [7,10]). Calcification of the aortas was measured using means of Von Kossa staining (Figure 4A).…”

Section: The Jak-stat Pathway Is Activated During Hasmc Calcification...mentioning

confidence: 99%

“…The VSMC osteogenic switch is characterised by the loss of α-smooth muscle actin (α-SMA) and smooth muscle protein 22α (SM22α) contractile proteins and the expression of specific osteogenic factors, Runt-related transcription factor 2 (RUNX2) and sex-determining region Y-box9 (SOX9) that, in turn, modulate genes involved in bone development and metabolism, including alkaline phosphatase (ALP), osteopontin (OPN), osteocalcin, and bone morphogenic protein 2 (BMP-2) [3]. Recent evidence indicates that senescent VSMCs express bone-related proteins and are more prone to calcification [6][7][8][9]. Moreover, senescent VSMCs are characterised by the release of senescence-associated secretory phenotype (SASP) factors consisting of inflammatory molecules, growth factors, and extracellular matrix components that, by promoting senescence of nearby cells, facilitate the osteo/chondrogenic switch and VC [6,8,10].…”

Section: Introductionmentioning

confidence: 99%

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High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification

Macrì,

Vigorito,

Castiglione

et al. 2023

Biomolecules

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Vascular calcification (VC) is an age-related complication characterised by calcium-phosphate deposition in the arterial wall driven by the osteogenic transformation of vascular smooth muscle cells (VSMCs). The JAK-STAT pathway is an emerging target in inflammation. Considering the relationship between VC and inflammation, we investigated the role of JAK-STAT signalling during VSMC calcification. Human aortic smooth muscle cells (HASMCs) were cultured in high-inorganic phosphate (Pi) medium for up to 7 days; calcium deposition was determined via Alizarin staining and colorimetric assay. Inflammatory factor secretion was evaluated via ELISA and JAK-STAT members’ activation using Western blot or immunohistochemistry on HASMCs or calcified aortas of Vitamin D-treated C57BL6/J mice, respectively. The JAK-STAT pathway was blocked by JAK Inhibitor I and Von Kossa staining was used for calcium deposits in murine aortic rings. During Pi-induced calcification, HASMCs released IL-6, IL-8, and MCP-1 and activated JAK1-JAK3 proteins and STAT1. Phospho-STAT1 was detected in murine calcified aortas. Blocking of the JAK-STAT cascade reduced HASMC proliferation and pro-inflammatory factor expression and release while increasing calcium deposition and osteogenic transcription factor RUNX2 expression. Consistently, JAK-STAT pathway inhibition exacerbates mouse aortic ring calcification ex vivo. Intriguingly, our results suggest an alternative link between VSMC inflammation and VC.

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The emerging role of cell senescence in atherosclerosis

Zheng

Wang

et al. 2020

Clinical Chemistry and Laboratory Medicine (CCLM)

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Cell senescence is a fundamental mechanism of aging and appears to play vital roles in the onset and prognosis of cardiovascular disease, fibrotic pulmonary disease, liver disease and tumor. Moreover, an increasing body of evidence shows that cell senescence plays an indispensable role in the formation and development of atherosclerosis. Multiple senescent cell types are associated with atherosclerosis, senescent human vascular endothelial cells participated in atherosclerosis via regulating the level of endothelin-1 (ET-1), nitric oxide (NO), angiotensin II and monocyte chemoattractant protein-1 (MCP-1), senescent human vascular smooth muscle cells-mediated plaque instability and vascular calcification via regulating the expression level of BMP-2, OPN, Runx-2 and inflammatory molecules, and senescent macrophages impaired cholesterol efflux and promoted the development of senescent-related cardiovascular diseases. This review summarizes the characteristics of cell senescence and updates the molecular mechanisms underlying cell senescence. Moreover, we also discuss the recent advances on the molecular mechanisms that can potentially regulate the development and progression of atherosclerosis.

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MicroRNA-34a modulates vascular calcification

Cited by 3 publications

References 0 publications

Functional role of miR-34a in diabetes and frailty

Functional role of miR-34a in diabetes and frailty

High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification

The emerging role of cell senescence in atherosclerosis

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