Mechanical stress alters the expression of calcification-related genes in vascular interstitial and endothelial cells

Rutkovskiy, Arkady; Lund, Maria Louise; Siamansour, Tanja Saman; Reine, Trine M.; Kolset, Svein Olav; Sand, Kristin L.; Ignatieva, Elena; Гордеев, М. Л.; Stensløkken, Kåre‐Olav; Valen, Guro; Vaage, Jarle; Malashicheva, Anna

doi:10.1093/icvts/ivy339

Cited by 19 publications

(14 citation statements)

References 28 publications

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“…VSMCs and MSCs co-cultured with RANKL-expressing ECs or their conditioned medium transdifferentiated into osteoblast-like cells expressing Runx2 and ALP (76). Likewise, fibroblasts co-cultured with mechanically stimulated ECs or the conditioned medium also underwent calcification (77). Furthermore, the conditioned medium from inorganic phosphorus or indoxyl sulfate-induced umbilical vein ECs inhibited expression of osteopontin in MSCs and induced calcification in the presence of IL-8 (78).…”

Section: Vecs and Osteoblast-like Cells In Vascular Calcificationmentioning

confidence: 99%

The Cell Origin and Role of Osteoclastogenesis and Osteoblastogenesis in Vascular Calcification

Jiang

Zhang

et al. 2021

Front. Cardiovasc. Med.

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Arterial calcification refers to the abnormal deposition of calcium salts in the arterial wall, which results in vessel lumen stenosis and vascular remodeling. Studies increasingly show that arterial calcification is a cell mediated, reversible and active regulated process similar to physiological bone mineralization. The osteoblasts and chondrocytes-like cells are present in large numbers in the calcified lesions, and express osteogenic transcription factor and bone matrix proteins that are known to initiate and promote arterial calcification. In addition, osteoclast-like cells have also been detected in calcified arterial walls wherein they possibly inhibit vascular calcification, similar to the catabolic process of bone mineral resorption. Therefore, tilting the balance between osteoblast-like and osteoclast-like cells to the latter maybe a promising therapeutic strategy against vascular calcification. In this review, we have summarized the current findings on the origin and functions of osteoblast-like and osteoclast-like cells in the development and progression of vascular progression, and explored novel therapeutic possibilities.

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Section: Vecs and Osteoblast-like Cells In Vascular Calcificationmentioning

confidence: 99%

The Cell Origin and Role of Osteoclastogenesis and Osteoblastogenesis in Vascular Calcification

Jiang

Zhang

et al. 2021

Front. Cardiovasc. Med.

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“…Under uremic conditions, the kidney releases injury factors into the blood flow, such as WNT inhibitors (Dkk1 or sclerostin) or activin A, which precedes the increase of alkaline phosphatase expression (Fang et al, 2014;Hortells et al, 2017). Heart activity and hemodynamics cause mechanical stress, the expression of Bmp2, and oxidative stress in vascular smooth muscle cells (VSMC) (Rutkovskiy et al, 2019). Reactive oxygen species induce the expression of Runx2 (Chang H. B. et al, 2008), and apoptotic bodies also contribute to MVC (Proudfoot et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

The Thermodynamics of Medial Vascular Calcification

Millán

Lanzer

Sorribas

2021

Front. Cell Dev. Biol.

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Medial vascular calcification (MVC) is a degenerative process that involves the deposition of calcium in the arteries, with a high prevalence in chronic kidney disease (CKD), diabetes, and aging. Calcification is the process of precipitation largely of calcium phosphate, governed by the laws of thermodynamics that should be acknowledged in studies of this disease. Amorphous calcium phosphate (ACP) is the key constituent of early calcifications, mainly composed of Ca2+ and PO43– ions, which over time transform into hydroxyapatite (HAP) crystals. The supersaturation of ACP related to Ca2+ and PO43– activities establishes the risk of MVC, which can be modulated by the presence of promoter and inhibitor biomolecules. According to the thermodynamic parameters, the process of MVC implies: (i) an increase in Ca2+ and PO43– activities (rather than concentrations) exceeding the solubility product at the precipitating sites in the media; (ii) focally impaired equilibrium between promoter and inhibitor biomolecules; and (iii) the progression of HAP crystallization associated with nominal irreversibility of the process, even when the levels of Ca2+ and PO43– ions return to normal. Thus, physical-chemical processes in the media are fundamental to understanding MVC and represent the most critical factor for treatments’ considerations. Any pathogenetical proposal must therefore comply with the laws of thermodynamics and their expression within the medial layer.

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“…59 These data suggest significant roles for Mechanical stress activates ECs and upregulates the expression of BMP2, which further regulates the expression of osteogenic genes in SMCs. 45 MMPs, as mentioned above, may also participate in the interaction through BMP signalling. 59 BMPs can also be loaded into EVs to participate in crosstalk between cells.…”

Section: Ecs Affect Vsmcs Via Mmps In Ckdrelated Vcmentioning

confidence: 99%

“…Cheng et al 39 however, the underlying crosstalk mechanism is unknown. 45 This suggests a potential essential role for ECs in initiating VC. Shear stress (a mechanical force) has corresponding roles in inducing endothelial transdifferentiation.…”

Section: The Role Of Ecs Mediated By High Parathyroid Hormone (Pth)mentioning

confidence: 99%

Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease

et al. 2021

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Chronic kidney disease (CKD) is an extremely serious health problem that causes poor health outcomes and substantial social and economic burdens worldwide. The high cardiovascular morbidity and mortality in the CKD population are mainly caused by extensive and progressive vascular calcification (VC). 1,2 Notably, in CKD patients, severe intimal calcification (known as atherosclerotic calcification and thought to originate from atherosclerosis) and medial calcification (known as Mönckeberg's sclerosis) are both prominent and can occur simultaneously, and both are accelerated with decreasing kidney function. 2,3 However, there are currently no effective treatment measures for VC. Although progress has been made in understanding the pathogenesis of VC, it is still largely assumptive and needs to be clarified. VC was previously regarded as a passive, degenerative disease. With further in-depth research, calcification has been found to be an active and adjustable process, analogous to bone formation, in

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Mechanical stress alters the expression of calcification-related genes in vascular interstitial and endothelial cells

Cited by 19 publications

References 28 publications

The Cell Origin and Role of Osteoclastogenesis and Osteoblastogenesis in Vascular Calcification

The Cell Origin and Role of Osteoclastogenesis and Osteoblastogenesis in Vascular Calcification

The Thermodynamics of Medial Vascular Calcification

Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease

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