Alteration of Type I Collagen in the Radial Artery of Patients With End-Stage Renal Disease

Bai, Yaling; Zhang, Junxia; Xu, Jinyi; Cui, Liwen; Zhang, Huiran; Zhang, Shenglei

doi:10.1097/maj.0000000000000408

Cited by 13 publications

(7 citation statements)

References 32 publications

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“…Furthermore, the increasing phosphate concentration in vitro results in upregulation of Runx2 expression and downregulation of smooth muscle-specific gene expression (10). Furthermore, Runx2 has been shown to be expressed in the calcified vascular lesion of CKD patients (33). Thus, Runx2 has been regarded as the earliest and most specific osteogenic marker of differentiation for the promoting calcification.…”

Section: Discussionmentioning

confidence: 99%

Menaquinone‑4 modulates the expression levels of calcification‑associated factors to inhibit calcification of rat aortic vascular smooth muscle cells in a dose‑dependent manner

Cui

Zhang

et al. 2018

Exp Ther Med

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Vascular calcification (VC) caused by chronic kidney disease (CKD)-mineral and bone disorder is a common complication of CKD. Recent studies have demonstrated that menaquinone-4 (MK-4) is negativly associated with VC in patients with CKD. Furthermore, we have previously shown that runt-related transcription factor 2 (Runx2) is important in the phenotypic transformation process of rat vascular smooth muscle cells (VSMCs), which is the key step for the development of VC. The present study investigated the influence of MK-4 on the phenotypic transformation process of rat VSMCs in order to illustrate its role in the process of VC. Calcification assays were perfomed to access the calcified degree of rat VSMCs. Additionally, the genes and proteins related to phenotypic transformation were measured by reverse transcription-polymerase chain reaction and western blotting methods. It was revealed that calcium deposition in the cells was evidently increased with an addition of β-glycerophosphate (β-GP) and could be completely prevented by co-incubation with MK-4 in a dose-dependent manner. Furthermore, the expression of Runx2 in the β-GP-induced VSMCs was inhibited by MK-4. It was also revealed that the expression of SMAD1 and bone morphogenetic protein (BMP)-2 were decreased in the β-GP-induced VSMCs treated with MK-4 in a dose-dependent manner; however, the expression of SMAD7 was increased in the β-GP-induced VSMCs treated with MK-4 in a dose-dependent manner. These observations suggest that MK-4 reduces mineralization by regulating the BMP-2 signaling pathway in order to attenuate the expression of Runx2.

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Section: Discussionmentioning

confidence: 99%

Menaquinone‑4 modulates the expression levels of calcification‑associated factors to inhibit calcification of rat aortic vascular smooth muscle cells in a dose‑dependent manner

Cui

Zhang

et al. 2018

Exp Ther Med

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“…In 10 studies (10 of 63 studies), stiffness was assessed locally (termed "single-point" onward) by measuring local vessel diameter and distension by ultrasound or MRI and estimating the corresponding local pulse pressure driving the cyclic distension (9,28,64,80,81,87,113,125,138,143). Conventionally, pressure-diameter or pressure-area data are used to calculate local distensibility (DC) or compliance (CC) coefficients, which are linear approximations over the observed diastolic/systolic range.…”

Section: Content Analysis Of Selected Papersmentioning

confidence: 99%

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

Reesink

Spronck

2019

American Journal of Physiology-Heart and Circulatory Physiology

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Clinical assessment of arterial stiffness relies on noninvasive measurements of regional pulse wave velocity or local distensibility. However, arterial stiffness measures do not discriminate underlying changes in arterial wall constituent properties (e.g., in collagen, elastin, or smooth muscle), which is highly relevant for development and monitoring of treatment. In arterial stiffness in recent clinical-epidemiological studies, we systematically review clinical-epidemiological studies (2012–) that interpreted arterial stiffness changes in terms of changes in arterial wall constituent properties (63 studies included of 514 studies found). Most studies that did so were association studies (52 of 63 studies) providing limited causal evidence. Intervention studies (11 of 63 studies) addressed changes in arterial stiffness through the modulation of extracellular matrix integrity (5 of 11 studies) or smooth muscle tone (6 of 11 studies). A handful of studies (3 of 63 studies) used mathematical modeling to discriminate between extracellular matrix components. Overall, there exists a notable gap in the mechanistic interpretation of stiffness findings. In constitutive model-based interpretation, we first introduce constitutive-based modeling and use it to illustrate the relationship between constituent properties and stiffness measurements (“forward” approach). We then review all literature on modeling approaches for the constitutive interpretation of clinical arterial stiffness data (“inverse” approach), which are aimed at estimation of constitutive properties from arterial stiffness measurements to benefit treatment development and monitoring. Importantly, any modeling approach requires a tradeoff between model complexity and measurable data. Therefore, the feasibility of changing in vivo the biaxial mechanics and/or vascular smooth muscle tone should be explored. The effectiveness of modeling approaches should be confirmed using uncertainty quantification and sensitivity analysis. Taken together, constitutive modeling can significantly improve clinical interpretation of arterial stiffness findings.

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“…Similarly, a previous study indicated that exposure to elevated phosphorus levels results in the upregulation of Runx2 expression and ALP activity ( 18 ). Runx2 is a notable transcription factor in the process of VSMC osteo-/chondrogenic transdifferentiation, which induces the expression of major bone matrix components, including type I collagen ( 5 ), osteocalcin ( 19 ) and OPN ( 20 ). Runx2 can be transcribed from the distal P1 promoter or the P2 promoter, resulting in the expression of two different subtypes (Runx2 I and II), which can be expressed in ossified and cartilage cells; both subtypes exhibit similar features in chondrocytes and osteoblasts.…”

Section: Discussionmentioning

confidence: 99%

“…A potentially life-threatening cardiovascular factor in patients with CKD is the presence of vascular calcification, which exists in up to 47-83% of patients with CKD (2)(3)(4). Vascular calcification in patients with CKD can be broadly divided into two types: Intimal calcification and medial calcification, with the latter observed more commonly (5). A previous study has suggested that the mechanism of vascular calcification is a cell-mediated, highly regulated process similar to osteogenesis (6).…”

Section: Introductionmentioning

confidence: 99%

microRNA‑103a regulates the calcification of vascular smooth muscle cells by targeting runt‑related transcription factor 2 in high phosphorus conditions

Bai

et al. 2021

Exp Ther Med

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Vascular calcification, such as atherosclerosis, is a serious complication of chronic kidney disease that is characterized by tunica media calcification, and has gained increasing attention from researchers. The commonly observed association between vascular calcification and osteoporosis suggests a link between bone and vascular disorders. As microRNAs (miRNAs) have a wide range of gene regulation functions, such as cell proliferation, apoptosis, stress and transdifferentiation, the current study aimed to determine whether miRNAs play a vital role in the calcification and osteoblastic differentiation of rat thoracic aorta vascular smooth muscle cells (VSMCs). Gene expression analysis was performed on seven miRNAs (miR-29a, -30b, -103a, -125b, -133a, -143 and -211) that maybe potentially involved in the differentiation of smooth muscle cells into osteoblastic cells. The results showed that the levels of miR-29a, -30b, -103a, -125b and -143 were markedly reduced in the VSMC calcification model, particularly miR-103a, whereas runt-related transcription factor 2 (RUNX2) expression was increased. Furthermore, it was found that the expression of RUNX2 was significantly decreased following the upregulation of miR-103a, and that the expression of RUNX2 was significantly increased by downregulating miR-103a in VSMCs. Therefore, it was concluded that miR-103a plays a notable role in the transdifferentiation of the VSMCs in high phosphorus-induced calcification by targeting the regulation of RUNX2, and may therefore constitute a new target for the diagnosis and treatment of vascular calcification.

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Alteration of Type I Collagen in the Radial Artery of Patients With End-Stage Renal Disease

Cited by 13 publications

References 32 publications

Menaquinone‑4 modulates the expression levels of calcification‑associated factors to inhibit calcification of rat aortic vascular smooth muscle cells in a dose‑dependent manner

Menaquinone‑4 modulates the expression levels of calcification‑associated factors to inhibit calcification of rat aortic vascular smooth muscle cells in a dose‑dependent manner

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

microRNA‑103a regulates the calcification of vascular smooth muscle cells by targeting runt‑related transcription factor 2 in high phosphorus conditions

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