Zinc Ameliorates the Osteogenic Effects of High Glucose in Vascular Smooth Muscle Cells

Henze, Laura A.; Estepa, Misael; Pieske, Burkert; Läng, Florian; Eckardt, Kai‐Uwe; Alesutan, Ioana; Voelkl, Jakob

doi:10.3390/cells10113083

Cited by 17 publications

(10 citation statements)

References 70 publications

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“…The protein concentration was determined by a Bradford assay (Bio-Rad Laboratories, Vienna, Austria). The data were shown normalized to the total protein concentration and to the control group [ 38 , 40 ].…”

Section: Methodsmentioning

confidence: 99%

Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling

et al. 2022

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Medial vascular calcification is common in chronic kidney disease (CKD) and is closely linked to hyperphosphatemia. Vascular smooth muscle cells (VSMCs) can take up pro-calcific properties and actively augment vascular calcification. Various pro-inflammatory mediators are able to promote VSMC calcification. In this study, we investigated the effects and mechanisms of periostin, a matricellular signaling protein, in calcifying human VSMCs and human serum samples. As a result, periostin induced the mRNA expression of pro-calcific markers in VSMCs. Furthermore, periostin augmented the effects of β-glycerophosphate on the expression of pro-calcific markers and aggravated the calcification of VSMCs. A periostin treatment was associated with an increased β-catenin abundance as well as the expression of target genes. The pro-calcific effects of periostin were ameliorated by WNT/β-catenin pathway inhibitors. Moreover, a co-treatment with an integrin αvβ3-blocking antibody blunted the pro-calcific effects of periostin. The silencing of periostin reduced the effects of β-glycerophosphate on the expression of pro-calcific markers and the calcification of VSMCs. Elevated serum periostin levels were observed in hemodialysis patients compared with healthy controls. These observations identified periostin as an augmentative factor in VSMC calcification. The pro-calcific effects of periostin involve integrin αvβ3 and the activation of the WNT/β-catenin pathway. Thus, the inhibition of periostin may be beneficial to reduce the burden of vascular calcification in CKD patients.

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Section: Methodsmentioning

confidence: 99%

Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling

et al. 2022

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“…Zinc supplementation was found to ameliorate phosphate‐mediated osteo‐/chondrogenic transdifferentiation of VSMCs and protect against VC through GPR39–TNFAIP3–NF‐κB axis 293 . This protective effect was also observed in high‐glucose as well as high‐phosphate state 294–296 . Therefore, zinc supplementation may be a promising medicine to hinder the progress of VC in CKD.…”

Section: Potential Therapeutic Strategies Of Vcmentioning

confidence: 97%

“… 293 This protective effect was also observed in high‐glucose as well as high‐phosphate state. 294 , 295 , 296 Therefore, zinc supplementation may be a promising medicine to hinder the progress of VC in CKD.…”

Section: Potential Therapeutic Strategies Of Vcmentioning

confidence: 99%

Vascular calcification: Molecular mechanisms and therapeutic interventions

Pan

Jie

Huang

2023

MedComm

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Vascular calcification (VC) is recognized as a pathological vascular disorder associated with various diseases, such as atherosclerosis, hypertension, aortic valve stenosis, coronary artery disease, diabetes mellitus, as well as chronic kidney disease. Therefore, it is a life‐threatening state for human health. There were several studies targeting mechanisms of VC that revealed the importance of vascular smooth muscle cells transdifferentiating, phosphorous and calcium milieu, as well as matrix vesicles on the progress of VC. However, the underlying molecular mechanisms of VC need to be elucidated. Though there is no acknowledged effective therapeutic strategy to reverse or cure VC clinically, recent evidence has proved that VC is not a passive irreversible comorbidity but an active process regulated by many factors. Some available approaches targeting the underlying molecular mechanism provide promising prospects for the therapy of VC. This review aims to summarize the novel findings on molecular mechanisms and therapeutic interventions of VC, including the role of inflammatory responses, endoplasmic reticulum stress, mitochondrial dysfunction, iron homeostasis, metabolic imbalance, and some related signaling pathways on VC progression. We also conclude some recent studies on controversial interventions in the clinical practice of VC, such as calcium channel blockers, renin–angiotensin system inhibitions, statins, bisphosphonates, denosumab, vitamins, and ion conditioning agents.

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“… 36 , 84 Moreover, zinc has a potentially strong inhibitory effect on vascular calcification by partially regulating the GPR39‐mediated upregulation of TNFAIP3. 85 , 86 The increase in GPR39 expression not only reduces the number of apoptotic macrophages but also inhibits the lipid accumulation of macrophages induced by ox‐LDL to slow down the progression of atherosclerosis. 60 The debate on metal homeostasis has become increasingly intense in recent years, and it has been suggested that disturbances in metal homeostasis are important factors affecting the pathogenesis of androgen insensitivity syndrome.…”

Section: Signaling Pathways Associated With Znr / ...mentioning

confidence: 99%

Signaling pathway mechanisms of neurological diseases induced by G protein‐coupled receptor 39

2023

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Background G protein‐coupled receptor 39 (GPR39) is a transmembrane zinc receptor with two splice variants, which belongs to the G‐protein‐coupled receptor growth hormone‐releasing peptide family. Its expression is induced by zinc, which activates GPR39, and its activation mediates cell proliferation, ion homeostasis, and anti‐inflammatory, antioxidant, and other pathophysiological effects via different signaling pathways. Aims The article reviews the latest literature in this field. In particular, the role of GPR39 in nervous system is discussed. Materials and methods GPR39 can be a promising target in neurological diseases for targeted therapy, which will help doctors overcome the associated problems. Discussion GPR39 is expressed in vivo at several sites. Increasing evidence suggests that GPR39 plays an important role as a neuroprotective agent in vivo and regulates various neurological functions, including neurodegeneration, neuroelectrophysiology, and neurovascular homeostasis. Conclusion This review aims to provide an overview of the functions, signal transduction pathways, and pathophysiological role of GPR39 in neurological diseases and summarize the GPR39 agonists that have been identified in the recent years.

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Zinc Ameliorates the Osteogenic Effects of High Glucose in Vascular Smooth Muscle Cells

Cited by 17 publications

References 70 publications

Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling

Periostin Augments Vascular Smooth Muscle Cell Calcification via β-Catenin Signaling

Vascular calcification: Molecular mechanisms and therapeutic interventions

Signaling pathway mechanisms of neurological diseases induced by G protein‐coupled receptor 39

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