Macrophage galectin-3 enhances intimal translocation of vascular calcification in diabetes mellitus

Sun, Zhen; Li, Lihua; Zhang, Lili; Yan, Jinchuan; Shao, Chen; Bao, Zhang; Liu, Jia; Li, Yalan; Zhou, Mengxue; Hou, Lina; Jing, Lele; Pang, Qiwen; Geng, Ying; Mao, Xiang; Gu, Wen; Wang, Zhongqun

doi:10.1152/ajpheart.00690.2019

Cited by 20 publications

(9 citation statements)

References 74 publications

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“…Similarly, in atherosclerosis, Gal-3 was found to transform VSMCs into osteoblast-like cells, contributing to vascular calcification (22). Upregulation of Gal-3 in macrophages promoted the migration of VSMC-derived extracellular vehicles (EVs) to the intima, inducing diabetic vascular intimal calcification (23).…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 promotes calcification of human aortic valve interstitial cells via the NF-kappa B signaling pathway

Luo

Wang

Liu

et al. 2022

Cardiovasc Diagn Ther

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Background: Calcific aortic valve disease (CAVD) is an active pathobiological process that takes place at the cellular and molecular levels. It involves fibrosis and calcification of aortic valve leaflets, which eventually contributes to heart failure. Galectin-3 (Gal-3), a β-galactoside-binding lectin, is involved in myocardial fibrosis and remodeling. Our study aimed to explore how Gal-3 promoted the osteogenic differentiation of human aortic valve interstitial cells (hVICs) along with elucidating the underlying molecular mechanisms.Methods: To determine the Gal-3 expression in this study, we included the blood samples and aortic valves (AVs) from patients with CAVD (n=20) and normal controls (n=20). The hVICs were stimulated by Osteogenic medium (OM) and were treated with or without recombinant human Gal-3. Calcified transformation of hVICs was assessed by Alizarin Red S staining and osteogenic gene/protein expression.RNA-sequencing was performed for all different treatments to investigate differentially expressed genes (DEGs) along with exploring the enriched pathways for potential molecular targets of Gal-3. The targets were further detected using Western blotting and immunofluorescence staining.Results: Gal-3 levels were found to be significantly increased in CAVD patients. Treatment of valve interstitial cells (VICs) with Gal-3 led to a marked increase in Runx2 and ALP-mRNA/protein expression levels as well as calcification. Gene expression profiles of hVICs cultured with or without Gal-3 revealed 79 upregulated genes and 82 down-regulated genes, which were highly enriched in TNF and NF-κB signaling pathways. Furthermore, Gal-3 could activate the phosphorylation of IκBα and interfere with the translocation of p65 into the cell nucleus of hVICs. However, inhibition of this pathway can suppress the osteogenic differentiation by Gal-3.Conclusions: Gal-3 acts as a positive regulator of osteogenic differentiation by activating the NF-κB signaling pathway in hVICs. Our findings provide novel mechanistic insights into the critical role of Gal-3 in the CAVD progression.

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Section: Discussionmentioning

confidence: 99%

Galectin-3 promotes calcification of human aortic valve interstitial cells via the NF-kappa B signaling pathway

Luo

Wang

Liu

et al. 2022

Cardiovasc Diagn Ther

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“…It is well-known that galectin-3 plays an important role in atherosclerosis development (the dark and bright of calcification). Galectin-3 was not only upregulated in vascular intimal calcification but also induces VSMCs migration and vascular intimal calcification [ 18 , 19 ]. More importantly, galectin-3 day-to-day variation in serum is 3%, and there is no circadian variation of galectin-3 in serum [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Predictive Value of Galectin-3 and Brachial-Ankle Pulse Wave Velocity for Coronary Artery Calcification in Coronary Arteriography Patients

Tian

Ding

Zhang

2022

International Journal of Clinical Practice

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Objectives. To study the predictive value for coronary artery calcification (CAC) of plasma galectin-3 and brachial-ankle pulse wave velocity (BaPWV) in coronary arteriography (CAG) patients. Methods. Patients who received coronary arteriography (CAG) examination were recruited. The level of plasma galectin-3 was measured by the enzyme-linked immunosorbent assay. The arterial stiffness was analyzed by BaPWV and ankle-brachial index (ABI) which were measured using a volume-plethysmographic device. Receiver operating characteristic (ROC) curve was used to analyze the prognostic value of galectin-3 or BaPWV for coronary artery calcification (CAC). Results. The level of galectin-3 and BaPWV was significantly higher in CAC patients compared with that in control ( p < 0.01 ). The level of plasma galectin-3 was positively correlated with BaPWV (r = −0.296, p < 0.01 ) and negatively correlated with ABI (r = −0.296, p < 0.01 ). ROC curve analysis revealed that galectin-3 ≥5.90 ng/ml was the most powerful predictor for CAC with sensitivity of 85.5% and specificity of 83.5%. The area under the curve (AUC) was 0.916. When the level of BaPWV was more than 1909 m/s, the sensitivity and specificity were 61.8% and 69.6%, respectively, for predicting CAC. The AUC was 0.646. Conclusions. The level of plasma galectin-3 increases significantly in CAC patients compared to control, and its level is related to BaPWV and ABI. Galectin-3 and BaPWV can be used to predict CAC, and the diagnosis value (sensitivity and specificity) of galectin-3 for CAC is better than that of BaPWV.

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“…In addition to the direct cell-to-cell approach, immune cells can interfere in exosome-mediated information transport among other cells. In a macrophage/VSMC co-culture system, macrophage galectin-3 regulated the migration of VSMC-derived exosomes and induced diabetic vascular intimal/medial calcification translocation, which may provide a potential method for early intervention in diabetic VC ( 98 ). These findings have extended our knowledge of how exosomes derived from immune cells regulate immune responses during VC.…”

Section: Exosome-mediated Crosstalk In the Vascular Wall Microenviron...mentioning

confidence: 99%

Cellular Crosstalk in the Vascular Wall Microenvironment: The Role of Exosomes in Vascular Calcification

Shan

Lin

et al. 2022

Front. Cardiovasc. Med.

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Vascular calcification is prevalent in aging, diabetes, chronic kidney disease, cardiovascular disease, and certain genetic disorders. However, the pathogenesis of vascular calcification is not well-understood. It has been progressively recognized that vascular calcification depends on the bidirectional interactions between vascular cells and their microenvironment. Exosomes are an essential bridge to mediate crosstalk between cells and organisms, and thus they have attracted increased research attention in recent years. Accumulating evidence has indicated that exosomes play an important role in cardiovascular disease, especially in vascular calcification. In this review, we introduce vascular biology and focus on the crosstalk between the different vessel layers and how their interplay controls the process of vascular calcification.

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Macrophage galectin-3 enhances intimal translocation of vascular calcification in diabetes mellitus

Cited by 20 publications

References 74 publications

Galectin-3 promotes calcification of human aortic valve interstitial cells via the NF-kappa B signaling pathway

Galectin-3 promotes calcification of human aortic valve interstitial cells via the NF-kappa B signaling pathway

Predictive Value of Galectin-3 and Brachial-Ankle Pulse Wave Velocity for Coronary Artery Calcification in Coronary Arteriography Patients

Cellular Crosstalk in the Vascular Wall Microenvironment: The Role of Exosomes in Vascular Calcification

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