Valvular Interstitial(판막 간질)란 무엇입니까?
Valvular Interstitial 판막 간질 - Calcification was earlier believed to be a passive degenerative process, however it is now recognized as an active pathogenic process driven by the cells native to the aortic valve: valvular interstitial (VICs) and endothelial (VECs) cells. [1]석회화는 이전에 수동적 퇴행성 과정으로 여겨졌지만 현재는 대동맥 판막에 고유한 세포인 판막 간질(VIC) 및 내피(VEC) 세포에 의해 구동되는 능동 병원성 과정으로 인식됩니다. [1]
vascular smooth muscle
Further, there are similarities between vascular smooth muscle cells and valvular interstitial cells in terms of their roles in ECM overproduction. [1] Recent studies employing new technologies demonstrate that calcifying extracellular vesicles(EVs)that have specific mineralization-promoting cargos such as tissue nonspecific alkaline phosphatase(TNAP), annexins Ⅱ and Ⅵ, are released from vascular smooth muscle, macrophages, and valvular interstitial cells, and serve as calcifying foci. [2] , vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. [3]또한, 혈관 평활근 세포와 판막 간질 세포 사이에는 ECM 과잉 생산에서의 역할 측면에서 유사점이 있습니다. [1] 신기술을 적용한 최근 연구에서는 조직 비특이적 알칼리성 인산분해효소(TNAP), 아넥신 Ⅱ 및 Ⅵ와 같은 특정 광물화 촉진 화물을 갖는 석회화 세포외 소포(EV)가 혈관 평활근, 대식세포 및 판막 간질 세포 및 석회화 초점 역할을 합니다. [2] nan [3]
maturation occurred predominantly 성숙이 주로 일어났다
Collagen maturation occurred predominantly between 6 and 12 months after implantation, which was accompanied by a progressive switch to a more quiescent phenotype of infiltrating cells with properties of valvular interstitial cells. [1] Collagen maturation occurred predominantly between 6 and 12 months after implantation, which was accompanied by a progressive switch to a more quiescent phenotype of infiltrating cells with properties of valvular interstitial cells. [2] Collagen maturation occurred predominantly between 6 and 12 months after implantation, which was accompanied by a progressive switch to a more quiescent phenotype of infiltrating cells with properties of valvular interstitial cells. [3]콜라겐 성숙은 이식 후 6개월에서 12개월 사이에 주로 발생했으며 판막 간질 세포의 특성을 가진 침윤성 세포의 보다 조용한 표현형으로의 점진적 전환이 동반되었습니다. [1] 콜라겐 성숙은 이식 후 6개월에서 12개월 사이에 주로 발생했으며 판막 간질 세포의 특성을 가진 침윤성 세포의 보다 조용한 표현형으로의 점진적 전환이 동반되었습니다. [2] nan [3]
Human Valvular Interstitial 인간 판막 간질
These results were confirmed in osteogenic medium-induced human valvular interstitial cells. [1] In vitro cultured mouse and human valvular interstitial cells calcified in both OSM and PI conditions, revealing in vitro-ex vivo differences. [2] In a setup using human valvular interstitial cells (VIC) a closed micro-physiological circulation system (MPS) with implemented oxygenator was adopted for culturing in culture-medium oxygen concentrations of 1%, 4%, 13% and 19%, reflecting hypoxic, tissue normoxic, arterial blood and cell incubator situation. [3] Evogliptin administration markedly reduced calcific deposition accompanied by a reduction in proinflammatory cytokine expression in endothelial nitric oxide synthase-deficient mice in vivo, and significantly ameliorated the mineralization of the primary human valvular interstitial cells (VICs), with a reduction in the mRNA expression of bone-associated and fibrosis-related genes in vitro. [4] The limitations of animal models point out the need for in vitro setups investigating human valvular interstitial cells (hVIC). [5] Using transcriptomic approach on human valvular interstitial cells (VIC) isolated from fibrocalcific and normal valves, our team has identified an enzyme X downregulated in fibro-calcific VIC. [6] The present study sought to evaluate the presence of the CaSR within human valvular interstitial cells (hVICs), assess the CaSR's functionality, and ascertain its involvement in hVIC calcification. [7]이러한 결과는 골형성 배지로 유도된 인간 판막 간질 세포에서 확인되었다. [1] 시험관 내 배양된 마우스 및 인간 판막 간질 세포는 OSM 및 PI 조건 모두에서 석회화되어 시험관내-생체외 차이를 나타냅니다. [2] nan [3] nan [4] 동물 모델의 한계는 인간 판막 간질 세포(hVIC)를 조사하는 시험관 내 설정의 필요성을 지적합니다. [5] 우리 팀은 섬유 석회성 판막과 정상 판막에서 분리된 인간 판막 간질 세포(VIC)에 대한 전사체 접근 방식을 사용하여 섬유 석회성 VIC에서 하향 조절되는 효소 X를 확인했습니다. [6] nan [7]
Aortic Valvular Interstitial
Aortic valvular interstitial cells (VICs) isolated from patients undergoing valve replacement are commonly used as in vitro models of calcific aortic valve disease (CAVD). [1] However, the mechanism whereby the entry and the presence of blood elements into the valves would have an impact on the biology of aortic valvular interstitial cells (VICs) remains to be deciphered. [2] We tested the hypothesis that RA regulates osteogenic differentiation of human arterial smooth muscle cells and aortic valvular interstitial cells that participate in atherosclerosis and heart valve disease, respectively. [3] Primary aortic valvular interstitial cells (AVICs) were incubated with specific inhibitors and/or siRNA of CCR2 and CCL2 under pro-calcifying medium. [4] RESULTS In cultured human aortic valvular interstitial cells, we found human antigen R enhanced metastasis-associated lung adenocarcinoma transcript 1 stability and thus increased its concentration. [5]판막 교체를 받는 환자로부터 분리된 대동맥 판막 간질 세포(VIC)는 일반적으로 석회화 대동맥 판막 질환(CAVD)의 시험관 내 모델로 사용됩니다. [1] 그러나 혈액 요소가 판막으로 들어가는 메커니즘과 대동맥 판막 간질 세포(VIC)의 생물학에 영향을 미치는 메커니즘은 아직 해독되지 않았습니다. [2] nan [3] nan [4] nan [5]
Porcine Valvular Interstitial 돼지 판막 간질
Model limitations of conventional 2D culture of human or porcine valvular interstitial/endothelial cells (VIC/VECs) isolated from aortic valve tissues but also limited ability of (small) animal models to reflect human (patho)physiological situation in AV position raise the need to establish an in vitro setup using AV tissues. [1] The purpose of this study was to determine whether micromechanical force could induce valve calcification of porcine valvular interstitial cells and to examine the role of integrin αvβ3 in valvular calcification by using a novel method: magnetic twisting cytometry. [2] The TN substrate supported the growth and orientations of seeded porcine valvular interstitial cells (PVICs) and their deposited collagen fibrils. [3] This study compared smooth muscle α-actin (α-SMA), osteopontin (OPN), and suppression of tumorigenicity 2 (ST2) expression between specimens from fibrotic and calcific stages of NR-AS and observed the effects and mechanisms of phenotypic transition of porcine valvular interstitial cells (VICs) in the presence of IL-33. [4] Porcine valvular interstitial cells were cultured in the scaffolds for 14 d to investigate the effect of microfibers prepared with different PCL concentrations on the seeded cells. [5]대동맥 판막 조직에서 분리된 인간 또는 돼지 판막 간질/내피 세포(VIC/VEC)의 기존 2D 배양 모델의 한계뿐 아니라 AV 위치에서 인간(병리) 생리학적 상황을 반영하는 (작은) 동물 모델의 제한된 능력은 다음의 필요성을 높입니다. AV 조직을 사용하여 시험관 내 설정을 설정합니다. [1] 이 연구의 목적은 미세 역학적 힘이 돼지 판막 간질 세포의 판막 석회화를 유도할 수 있는지 여부와 판막 석회화에서 integrin αvβ3의 역할을 새로운 방법인 자기 비틀림 세포계측법을 사용하여 조사하는 것이었습니다. [2] TN 기질은 시드된 돼지 판막 간질 세포(PVIC)와 침착된 콜라겐 섬유소의 성장과 방향을 지원했습니다. [3] 이 연구는 NR-AS의 섬유성 및 석회화 단계의 표본 간의 평활근 α-액틴(α-SMA), 오스테오폰틴(OPN) 및 종양원성 2(ST2) 발현 억제를 비교하고 돼지 표현형 전이의 효과 및 메커니즘을 관찰했습니다. IL-33의 존재하에 판막 간질 세포(VIC). [4] nan [5]
valvular interstitial cell 판막 간질 세포
Calcific aortic valve disease (CAVD) is caused by an osteoblastic phenotype switch of valvular interstitial cells (VICs), the predominant cell type in heart valves. [1] Calcific aortic valve stenosis (CAVS) is a heart disease characterized by the progressive fibro-calcific remodeling of the aortic valves, an actively regulated process with the involvement of the reactive oxygen species-mediated differentiation of valvular interstitial cells (VICs) into osteoblast-like cells. [2] We conclude that overactivation of VICs (Valvular interstitial cells) and the imbalance of MMP/TIMP could be important features of the pathomechanism of myxomatous mitral valve degeneration. [3] Methods The level of ferroptosis in tissue and valvular interstitial cells (VICs) was assessed by the contents of 4-HNE, NADPH, ROS, and GSH, lipid peroxidation and mitochondrial morphology. [4] These results were confirmed in osteogenic medium-induced human valvular interstitial cells. [5] In vitro cytocompatibility evaluation results demonstrated that all of the PLCL/SF electrospun scaffolds were cytocompatible and valvular interstitial cells (VICs) cultured on PLCL/SF scaffolds of 80/20 & 70/30 ratios exhibited the best cytocompatibility. [6] In vitro cultured mouse and human valvular interstitial cells calcified in both OSM and PI conditions, revealing in vitro-ex vivo differences. [7] Background: Valvular calcification is central to the pathogenesis and progression of aortic stenosis, with preclinical and observational studies suggesting that bone turnover and osteoblastic differentiation of valvular interstitial cells are important contributory mechanisms. [8] Summary This study focused on characterizing the potential mechanism of valvular toxicity caused by TGFβ receptor inhibitors (TGFβRis) using rat valvular interstitial cells (VICs) to evaluate early biological responses to TGFβR inhibition. [9] Besides the inert structural components of the tissues, collagen fibers are dynamic structures that drive outside-to-inside cell signaling, which informs valvular interstitial cells (VICs) present within the tissue environment. [10] Myxomatous mitral valve degeneration (MMVD) is the most common acquired cardiac disease in canine species, and valvular interstitial cells (VICs) are considered the main responsible for the development of this pathology. [11] Two phenotypes of valvular interstitial cells (VICs), activated VICs and osteoblastic VICs (obVICs), synergistically orchestrate this pathology. [12] In a setup using human valvular interstitial cells (VIC) a closed micro-physiological circulation system (MPS) with implemented oxygenator was adopted for culturing in culture-medium oxygen concentrations of 1%, 4%, 13% and 19%, reflecting hypoxic, tissue normoxic, arterial blood and cell incubator situation. [13] The aim of this study was to better understand the role of the matrix microenvironment in promoting or suppressing calcification, specifically with respect to the role that valvular interstitial cells (VICs) play in CAVD. [14] Most research regarding CAVD is based on experiments using two-dimensional (2D) cell culture or artificially created three-dimensional (3D) environments of valvular interstitial cells (VICs). [15] canine valvular interstitial cells (VICs), valvular endothelial cells (VECs) and human umbilical vein endothelial cells (HUVECs) were used in this study. [16] An imbalance of pro- and anti-angiogenic factors is thought to play a role in driving this disease process, and valvular interstitial cells (VICs) may act as a significant source of these factors. [17] CAVD is considered to be an actively regulated disease process, mainly controlled by valvular interstitial cells (VICs). [18] Evogliptin administration markedly reduced calcific deposition accompanied by a reduction in proinflammatory cytokine expression in endothelial nitric oxide synthase-deficient mice in vivo, and significantly ameliorated the mineralization of the primary human valvular interstitial cells (VICs), with a reduction in the mRNA expression of bone-associated and fibrosis-related genes in vitro. [19] Bioreactor cultivation led to shrinking and thickening of the valve leaflets compared to native leaflets while gross morphology and the presence of valvular interstitial cells were preserved. [20] Osteogenesis differentiation of valvular interstitial cells (VICs) is the key process of CAVD. [21] Pro‐inflammatory cytokines play critical roles in regulating valvular interstitial cell (VIC) phenotypic changes that can cause heart valve fibrosis and calcification. [22] The purpose of this study was to determine whether micromechanical force could induce valve calcification of porcine valvular interstitial cells and to examine the role of integrin αvβ3 in valvular calcification by using a novel method: magnetic twisting cytometry. [23] Collagen maturation occurred predominantly between 6 and 12 months after implantation, which was accompanied by a progressive switch to a more quiescent phenotype of infiltrating cells with properties of valvular interstitial cells. [24] The ECM structure is maintained by valvular interstitial cells (VICs), which reside within the leaflets. [25] Collagen maturation occurred predominantly between 6 and 12 months after implantation, which was accompanied by a progressive switch to a more quiescent phenotype of infiltrating cells with properties of valvular interstitial cells. [26] Mitral valve fibrosis is mediated by valvular interstitial cells (VICs), which reside in the valve leaflets and often differentiate into myofibroblast-like cells during disease conditions. [27] Cryosections of MVs from patients with IMR displayed activated valvular interstitial cells (aVICs) and double positive CD31+ αSMA+ cells, a hallmark of EndMT. [28] Extracellular phosphates promote a phenotypic shift in vascular smooth muscle and valvular interstitial cells towards an osteoblast gene expression pattern, which provokes the active phase of mineralization. [29] Collagen maturation occurred predominantly between 6 and 12 months after implantation, which was accompanied by a progressive switch to a more quiescent phenotype of infiltrating cells with properties of valvular interstitial cells. [30] We demonstrate evidence for rather chondrogenic features of valvular interstitial cells by histological staining and immunodetection of SOX-9, aggrecan, and type 2a1 collagen. [31] The limitations of animal models point out the need for in vitro setups investigating human valvular interstitial cells (hVIC). [32] Valvular endothelium mediates valvular homeostasis and controls valvular interstitial cell phenotype transformation. [33] However, studies employing valvular interstitial cells (VICs) to examine effects of TGF-β1 on calcification provide contradictory results. [34] Hydrogel properties were determined, and valvular interstitial cell functions like phenotype, proliferation, migration, mRNA expression of extracellular matrix (ECM) molecules, ECM deposition, and tissue fusion were characterized by histochemical stainings and RT‐qPCR. [35] Transcatheter aortic valve replacement alters a patient’s serum proteome, reversing valvular interstitial cell and cardiac myofibroblast activation. [36] AS is characterized by the differenciation of valvular interstitial cells (VICs) into osteoblastic cells, leading to valvular calcification. [37] To confirm the mechanism, coexpression of β‐catenin, TIEG1, and LEF1 in valve cells in vitro, led to the coactivation of the TOPFLASH reporter, which was further confirmed by the observation that TIEG1 and β‐catenin colocalize with one another in the nucleus of valvular interstitial cells (VICs) following stimulation with transforming growth factor‐β treatment, an established activator of TIEG1. [38] Aortic valvular interstitial cells (VICs) isolated from patients undergoing valve replacement are commonly used as in vitro models of calcific aortic valve disease (CAVD). [39] In vitro studies investigated the effects of Lp(a) and OxPL on valvular interstitial cells. [40] The presence of adipocytes in the prolapsed valve could be considered to arise from the proliferation of pluripotent valvular interstitial cells. [41] Expression analysis using a lacZ reporter and single-cell RNA sequencing highlight Adamts19 as a novel marker for valvular interstitial cells; inference of gene regulatory networks in valvular interstitial cells positions Adamts19 in a highly discriminatory network driven by the transcription factor lymphoid enhancer-binding factor 1 downstream of the Wnt signaling pathway. [42] Further, there are similarities between vascular smooth muscle cells and valvular interstitial cells in terms of their roles in ECM overproduction. [43] Using transcriptomic approach on human valvular interstitial cells (VIC) isolated from fibrocalcific and normal valves, our team has identified an enzyme X downregulated in fibro-calcific VIC. [44] A 3D, laminar, filter paper-based cell culture system that was previously established as a method of analyzing valvular interstitial cell migration and protein expression was adapted here for studying the impact of specific extracellular matrix proteins on cellular viability and calcification proclivity. [45] Hence, we hypothesized that classical key factors of type 2 diabetes, hyperinsulinemia and hyperglycemia, may affect signaling, metabolism and degenerative processes of valvular interstitial cells (VIC), the main cell type of heart valves. [46] However, the mechanism whereby the entry and the presence of blood elements into the valves would have an impact on the biology of aortic valvular interstitial cells (VICs) remains to be deciphered. [47] However, studies using valvular interstitial cells (VICs) to examine effects of TGFβ1 on calcification provide contradictory results. [48] We tested the hypothesis that RA regulates osteogenic differentiation of human arterial smooth muscle cells and aortic valvular interstitial cells that participate in atherosclerosis and heart valve disease, respectively. [49] In subsequent experiments, we demonstrated a therapeutic potential of miRNA regulation during calcification in cardiac valvular interstitial cells. [50]석회성 대동맥 판막 질환(CAVD)은 심장 판막의 주요 세포 유형인 판막 간질 세포(VIC)의 골아세포 표현형 스위치에 의해 발생합니다. [1] 석회화 대동맥 판막 협착증(CAVS)은 대동맥 판막의 점진적 섬유 석회화 리모델링을 특징으로 하는 심장 질환으로, 활성 산소 종에 의해 매개되는 판막 간질 세포(VIC)가 조골 세포와 유사하게 분화하는 능동적으로 조절되는 과정입니다. 세포. [2] 우리는 VICs(Valvular interstitial cells)의 과활성화와 MMP/TIMP의 불균형이 점액종성 승모판 변성의 병리 기전의 중요한 특징이 될 수 있다고 결론지었습니다. [3] 방법 조직 및 판막 간질 세포(VIC)의 ferroptosis 수준은 4-HNE, NADPH, ROS 및 GSH의 함량, 지질 과산화 및 미토콘드리아 형태로 평가되었습니다. [4] 이러한 결과는 골형성 배지로 유도된 인간 판막 간질 세포에서 확인되었다. [5] 시험관 내 세포 적합성 평가 결과 모든 PLCL/SF 전기방사 지지체는 세포 적합성이며 80/20 및 70/30 비율의 PLCL/SF 지지체에서 배양된 판막 간질 세포(VIC)가 최고의 세포 적합성을 나타냈다. [6] 시험관 내 배양된 마우스 및 인간 판막 간질 세포는 OSM 및 PI 조건 모두에서 석회화되어 시험관내-생체외 차이를 나타냅니다. [7] 배경: 판막 석회화는 대동맥판 협착증의 발병 및 진행의 핵심이며, 전임상 및 관찰 연구에 따르면 판막 간질 세포의 골 전환 및 조골 분화가 중요한 기여 기전임을 시사합니다. [8] nan [9] nan [10] 점액종성 승모판 변성(MMVD)은 송곳니 종에서 가장 흔한 후천성 심장 질환이며 판막 간질 세포(VIC)가 이 병리의 발병에 대한 주요 책임으로 간주됩니다. [11] 판막 간질 세포(VIC)의 두 가지 표현형, 활성화된 VIC 및 골아세포 VIC(obVIC)는 이 병리를 상승적으로 조정합니다. [12] nan [13] 이 연구의 목적은 특히 CAVD에서 판막 간질 세포(VIC)의 역할과 관련하여 석회화를 촉진하거나 억제하는 매트릭스 미세 환경의 역할을 더 잘 이해하는 것이었습니다. [14] CAVD에 관한 대부분의 연구는 판막 간질 세포(VIC)의 2차원(2D) 세포 배양 또는 인공적으로 생성된 3차원(3D) 환경을 사용한 실험을 기반으로 합니다. [15] nan [16] 혈관신생 촉진 인자와 항혈관신생 인자의 불균형이 이 질병의 진행을 촉진하는 역할을 하는 것으로 생각되며, 판막 간질 세포(VIC)가 이러한 인자의 중요한 원인으로 작용할 수 있습니다. [17] CAVD는 주로 판막 간질 세포(VIC)에 의해 조절되는 능동적으로 조절되는 질병 과정으로 간주됩니다. [18] nan [19] 생물 반응기 배양은 전체 형태와 판막 간질 세포의 존재가 보존되는 동안 천연 소엽과 비교하여 판막 소엽의 수축 및 비후를 초래했습니다. [20] 판막 간질 세포(VIC)의 골형성 분화는 CAVD의 핵심 과정입니다. [21] nan [22] 이 연구의 목적은 미세 역학적 힘이 돼지 판막 간질 세포의 판막 석회화를 유도할 수 있는지 여부와 판막 석회화에서 integrin αvβ3의 역할을 새로운 방법인 자기 비틀림 세포계측법을 사용하여 조사하는 것이었습니다. [23] 콜라겐 성숙은 이식 후 6개월에서 12개월 사이에 주로 발생했으며 판막 간질 세포의 특성을 가진 침윤성 세포의 보다 조용한 표현형으로의 점진적 전환이 동반되었습니다. [24] ECM 구조는 소엽 내에 있는 판막 간질 세포(VIC)에 의해 유지됩니다. [25] 콜라겐 성숙은 이식 후 6개월에서 12개월 사이에 주로 발생했으며 판막 간질 세포의 특성을 가진 침윤성 세포의 보다 조용한 표현형으로의 점진적 전환이 동반되었습니다. [26] 승모판 섬유증은 판막 간질 세포(VIC)에 의해 매개되며, 이 세포는 판막 소엽에 상주하고 질병 상태 동안 종종 근섬유아세포 유사 세포로 분화합니다. [27] nan [28] 세포외 인산염은 혈관 평활근 및 판막 간질 세포에서 조골 세포 유전자 발현 패턴을 향한 표현형 이동을 촉진하여 활성 단계의 광물화를 유발합니다. [29] nan [30] 우리는 SOX-9, aggrecan 및 type 2a1 콜라겐의 조직학적 염색 및 면역 검출에 의해 판막 간질 세포의 오히려 연골 형성 특징에 대한 증거를 입증합니다. [31] 동물 모델의 한계는 인간 판막 간질 세포(hVIC)를 조사하는 시험관 내 설정의 필요성을 지적합니다. [32] nan [33] nan [34] nan [35] nan [36] nan [37] nan [38] 판막 교체를 받는 환자로부터 분리된 대동맥 판막 간질 세포(VIC)는 일반적으로 석회화 대동맥 판막 질환(CAVD)의 시험관 내 모델로 사용됩니다. [39] nan [40] nan [41] nan [42] 또한, 혈관 평활근 세포와 판막 간질 세포 사이에는 ECM 과잉 생산에서의 역할 측면에서 유사점이 있습니다. [43] 우리 팀은 섬유 석회성 판막과 정상 판막에서 분리된 인간 판막 간질 세포(VIC)에 대한 전사체 접근 방식을 사용하여 섬유 석회성 VIC에서 하향 조절되는 효소 X를 확인했습니다. [44] nan [45] nan [46] 그러나 혈액 요소가 판막으로 들어가는 메커니즘과 대동맥 판막 간질 세포(VIC)의 생물학에 영향을 미치는 메커니즘은 아직 해독되지 않았습니다. [47] nan [48] nan [49] nan [50]