Human adventitial pericytes provide a unique source of anti-calcific cells for cardiac valve engineering: Role of microRNA-132-3p

Jover, Eva; Fagnano, Marco; Cathery, William; Slater, S. D.; Pisanu, Emanuela; Gu, Yan; Avolio, Elisa; Bruno, Vito Domenico; Baz-Lopez, D; Faulkner, Ashton; Carrabba, Michele; Angelini, Gianni; Madeddu, Paolo

doi:10.1016/j.freeradbiomed.2021.01.029

Cited by 7 publications

(4 citation statements)

References 60 publications

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“…Gal‐1 plays a central role in the phenotypic switch of VSMC from contractile to synthetic phenotypes during vascular remodeling 34 . The “metabolic shift” to glycolysis is necessary during physiologic and pathologic osteoblast differentiation to sustain the increased energy requirements of such a demanding transformation 35,58 and to prolong RUNX2 activation 35 . Due to the presence of an unusual number of Cys residues (six), Gal‐1 is highly susceptible to oxidation, being its biological functions regulated by the redox status of the cellular microenviroment 18,22,59,60 .…”

Section: Discussionmentioning

confidence: 99%

Sex‐dependent expression of galectin‐1, a cardioprotective β‐galactoside‐binding lectin, in human calcific aortic stenosis

Jover,

Martín‐Núñez,

Garaikoetxea

et al. 2024

The FASEB Journal

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We aimed to analyze sex‐related differences in galectin‐1 (Gal‐1), a β‐galactoside‐binding lectin, in aortic stenosis (AS) and its association with the inflammatory and fibrocalcific progression of AS. Gal‐1 was determined in serum and aortic valves (AVs) from control and AS donors by western blot and immunohistochemistry. Differences were validated by ELISA and qPCR in AS samples. In vitro experiments were conducted in primary cultured valve interstitial cells (VICs). Serum Gal‐1 was not different neither between control and AS nor between men and women. There was no association between circulating and valvular Gal‐1 levels. The expression of Gal‐1 in stenotic AVs was higher in men than women, even after adjusting for confounding factors, and was associated with inflammation, oxidative stress, extracellular matrix remodeling, fibrosis, and osteogenesis. Gal‐1 (LGALS1) mRNA was enhanced within fibrocalcific areas of stenotic AVs, especially in men. Secretion of Gal‐1 was up‐regulated over a time course of 2, 4, and 8 days in men's calcifying VICs, only peaking at day 4 in women's VICs. In vitro, Gal‐1 was associated with similar mechanisms to those in our clinical cohort. β‐estradiol significantly up‐regulated the activity of an LGALS1 promoter vector and the secretion of Gal‐1, only in women's VICs. Supplementation with rGal‐1 prevented the effects elicited by calcific challenge including the metabolic shift to glycolysis. In conclusion, Gal‐1 is up‐regulated in stenotic AVs and VICs from men in association with inflammation, oxidative stress, matrix remodeling, and osteogenesis. Estrogens can regulate Gal‐1 expression with potential implications in post‐menopause women. Exogenous rGal‐1 can diminish calcific phenotypes in both women and men.

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Section: Discussionmentioning

confidence: 99%

Sex‐dependent expression of galectin‐1, a cardioprotective β‐galactoside‐binding lectin, in human calcific aortic stenosis

Jover,

Martín‐Núñez,

Garaikoetxea

et al. 2024

The FASEB Journal

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“…These exosomes expedite VSMC calcification by delivering miR-21-5p, which, in turn, inhibits cysteine-rich motor neuron 1 (Crim1) ( 67 ). Conversely, adventitial pericytes (APC) counteract calcification by triggering an anti-calcific effect through the upregulation of microRNA-132-3p ( 68 ). Cells constitute the fundamental constituents of tissues, organs, and organisms.…”

Section: Role Of Vascular Cell Senescence In Vascular Calcificationmentioning

confidence: 99%

The functional role of cellular senescence during vascular calcification in chronic kidney disease

Fang,

Zhao,

Huang

et al. 2024

Front. Endocrinol.

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Vascular calcification (VC) has emerged as a key predictor of cardiovascular events in patients with chronic kidney disease (CKD). In recent years, an expanding body of research has put forth the concept of accelerated vascular aging among CKD patients, highlighting the significance of vascular cells senescence in the process of VC. Within the milieu of uremia, senescent vascular endothelial cells (VECs) release extracellular microvesicles (MV) that promote vascular smooth muscle cells (VSMCs) senescence, thereby triggering the subsequent osteogenic phenotypic switch and ultimately contributing to the VC process. In addition, senescent vascular progenitor or stem cells with diminished ability to differentiate into VECs and VSMCS, compromise the repair of vascular integrity, on the other hand, release a cascade of molecules associated with senescence, collectively known as the senescence-associated secretory phenotype (SASP), perpetuating the senescence phenomenon. Furthermore, SASP triggers the recruitment of monocytes and macrophages, as well as adjacent VECs and VSMCs into a pro-adhesive and pro-inflammatory senescent state. This pro-inflammatory microenvironment niche not only impacts the functionality of immune cells but also influences the differentiation of myeloid immune cells, thereby amplifying the reduced ability to effectively clear senescent cells of senescent macrophages, promoted calcification of VSMCs. The objective of this paper is to provide a comprehensive review of the contribution of vascular cell senescence to the emergence and advancement of VC. Gaining a comprehensive understanding of the involvement of cellular senescence within the vessel wall is pivotal, especially when it comes to its intersection with VC. This knowledge is essential for advancing groundbreaking anti-aging therapies, aiming to effectively mitigate cardiovascular diseases.

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“…Jover et al first reported that miR-132 was constitutively expressed by adventitial pericytes (APCs) and upregulated following high phosphate stimulation, playing a key role in the human APCs resistance to calcification through downregulating several target genes relevant to osteogenic differentiation. Treatment of swine cardiac valves with APCs-derived conditioned medium conferred them with resistance to high phosphate-induced osteogenesis, with this effect being negated when using the medium of miR-132-silenced APCs ( Jover et al, 2021 ).…”

Section: Mir-132-based Therapeutic Potential In Cardiovascular Diseasementioning

confidence: 99%

Advances in miR-132-Based Biomarker and Therapeutic Potential in the Cardiovascular System

Chen

et al. 2021

Front. Pharmacol.

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Atherosclerotic cardiovascular disease and subsequent heart failure threaten global health and impose a huge economic burden on society. MicroRNA-132 (miR-132), a regulatory RNA ubiquitously expressed in the cardiovascular system, is up-or down-regulated in the plasma under various cardiac conditions and may serve as a potential diagnostic or prognostic biomarker. More importantly, miR-132 in the myocardium has been demonstrated to be a master regulator in many pathological processes of ischemic or nonischemic heart failure in the past decade, such as myocardial hypertrophy, fibrosis, apoptosis, angiogenesis, calcium handling, neuroendocrine activation, and oxidative stress, through downregulating target mRNA expression. Preclinical and clinical phase 1b studies have suggested antisense oligonucleotide targeting miR-132 may be a potential therapeutic approach for ischemic or nonischemic heart failure in the future. This review aims to summarize recent advances in the physiological and pathological functions of miR-132 and its possible diagnostic and therapeutic potential in cardiovascular disease.

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Human adventitial pericytes provide a unique source of anti-calcific cells for cardiac valve engineering: Role of microRNA-132-3p

Cited by 7 publications

References 60 publications

Sex‐dependent expression of galectin‐1, a cardioprotective β‐galactoside‐binding lectin, in human calcific aortic stenosis

Sex‐dependent expression of galectin‐1, a cardioprotective β‐galactoside‐binding lectin, in human calcific aortic stenosis

The functional role of cellular senescence during vascular calcification in chronic kidney disease

Advances in miR-132-Based Biomarker and Therapeutic Potential in the Cardiovascular System

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