Vascular remodeling is mainly chara

Vascular remodeling is mainly characterized as intima-media thickening and plays a central role in the pathological progression for aortopathy, such as aortic aneurysm.1 Thoracic aortic dissection (TAD) isa life-threatening macro-vascular disease by virtue of its predisposition of rupture. About 40% patients with aortic dissection have notime to reach the hospital and die immediately. In the pathogenesisof TAD, vascular smooth muscle cells (VSMCs) are essential incontraction and synthesis of aortic wall in response to various cellularstimuli, which facilitates vascular remodeling.2–8 With phenotypeswitching, VSMCs alternate from contractile (differentiated) phenotype to synthetic (dedifferentiated) phenotype. DedifferentiatedVSMCs presented elevated viability in proliferation, migration, and synthesis, as well as reduced expression of differentiation markersa-SMA and SM22a.2,9 Pathological phenotype switching is a pivotalfactor contributing to the development of aortic aneurysm and dissection.5,6 Phenotype of VSMCs can be changed by numerous factors,including growth factor, chemotactic factors, cell adhesion molecules,extracellular matrix enzymes, and injury stimuli signal.10 Especially,PDGF promotes the phenotypic switch to synthetic VSMCs and enhances cell proliferation and migration into the neointima after arteryinjury.11 However, the molecular mechanisms underlying the VSMCphenotypic switch and neointima formation still remains unclear.MicroRNA (miRNA), the endogenous 18–24 nucleotide non-codingRNA, is a novel regulator in vascular disease via affecting VSMC functions, including proliferation, apoptosis, differentiation, synthesis,and secretion.12 As an example, miR-143/145 is involved in vascularremodeling via affecting VSMC phenotypic switch,13,14 plasticity,15and matrix synthesis.16 The polymorphism on miR-34b/c signifi-cantly decreased the risk of aneurysm.17 In the present study, we identified miR-134-5p as a key molecule in inhibiting aortic dissectiondevelopment via microarray screening. We further explored theimpact of miR-134-5p on VSMC phenotypic switch and migration.Moreover, the potential molecular mechanism was investigated.Our study provided significant novel insights into the importanceand functional complexities of miRNA for regulation of VSMC functions, vascular remodeling, as well as the development of macrovascular diseases.

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结果 (简体中文) 1: [复制]

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血管重构的主要特征是内膜中层增厚，在主动脉瘤等主动脉病变的病理进展中起着核心作用。1胸主动脉夹层（TAD）由于 具有以下特点而威胁生命它容易破裂。约40％的主动脉夹层患者没有 时间去医院就诊并立即死亡。在 TAD 的发病机制中，血管平滑肌细胞（VSMC）在 主动脉壁的收缩和合成中起着至关重要的 作用，以响应各种细胞刺激，从而促进血管重构[ 2-8]。通过表型转换，VSMC从收缩（分化）表型中替代。类型转换为合成（去分化）表型。去分化 VSMC在增殖，迁移和合成中表现出提高的生存力，并且分化标记物 α-SMA和SM22a的表达降低。 2,9病理表型转换是 促成主动脉瘤和解剖的关键因素。5,6VSMCs的表型可以通过多种因素改变， 包括生长因子，趋化因子，细胞粘附分子， 细胞外基质酶， 10特别地， PDGF促进了表型向合成VSMC的转换，并增强了动脉损伤后细胞的增殖和向新内膜的迁移 。11但是， 仍不清楚VSMC 表型转换和新内膜形成的分子机制。 微小RNA（miRNA）是内源的18-24个核苷酸的非编码 RNA，是一种通过影响VSMC功能（包括增殖，凋亡，分化，合成 和分泌）来调节血管疾病的新型调节剂。12 例如，miR-143 / 145 通过影响VSMC表型转换，13,14可塑性，15 和基质合成参与血管重塑。16miR-34b / c的多态性显 着降低了动脉瘤的发生风险。17在本研究中，我们发现吗？改良的miR-134-5p是 通过微阵列筛选抑制主动脉夹层发展的关键分子。我们进一步探讨了 miR-134-5p对VSMC表型转换和迁移的影响。 此外，研究了潜在的分子机理。 我们的研究 为miRNA在调节VSMC功能，血管重塑以及大血管疾病发展中的重要性和功能复杂性提供了重要的新见解。

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结果 (简体中文) 2:[复制]

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Vascular remodeling is mainly characterized as intima-media thickening and plays a central role in the pathological progression for aortopathy, such as aortic aneurysm.1 Thoracic aortic dissection (TAD) is a life-threatening macro-vascular disease by virtue of its predisposition of rupture. About 40% patients with aortic dissection have no time to reach the hospital and die immediately. In the pathogenesis of TAD, vascular smooth muscle cells (VSMCs) are essential in contraction and synthesis of aortic wall in response to various cellular stimuli, which facilitates vascular remodeling.2–8 With phenotype switching, VSMCs alternate from contractile (differentiated) phenotype to synthetic (dedifferentiated) phenotype. Dedifferentiated VSMCs presented elevated viability in proliferation, migration, and synthesis, as well as reduced expression of differentiation markers a-SMA and SM22a. 2,9 Pathological phenotype switching is a pivotal factor contributing to the development of aortic aneurysm and dissection.5,6 Phenotype of VSMCs can be changed by numerous factors, including growth factor, chemotactic factors, cell adhesion molecules, extracellular matrix enzymes, and injury stimuli signal.10 Especially, PDGF promotes the phenotypic switch to synthetic VSMCs and enhances cell proliferation and migration into the neointima after artery injury.11 However, the molecular mechanisms underlying the VSMC phenotypic switch and neointima formation still remains unclear. MicroRNA (miRNA), the endogenous 18–24 nucleotide non-coding RNA, is a novel regulator in vascular disease via affecting VSMC functions, including proliferation, apoptosis, differentiation, synthesis, and secretion.12 As an example, miR-143/145 is involved in vascular remodeling via affecting VSMC phenotypic switch,13,14 plasticity,15 and matrix synthesis.16 The polymorphism on miR-34b/c signifi- cantly decreased the risk of aneurysm.17 In the present study, we identified miR-134-5p as a key molecule in inhibiting aortic dissection development via microarray screening. We further explored the impact of miR-134-5p on VSMC phenotypic switch and migration. Moreover, the potential molecular mechanism was investigated. Our study provided significant novel insights into the importance and functional complexities of miRNA for regulation of VSMC functions, vascular remodeling, as well as the development of macrovascular diseases.

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结果 (简体中文) 3:[复制]

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血管重构以内膜-中层增厚为主要特征，在主动脉瘤等主动脉瘤的病理过程中起重要作用 因易破裂而危及生命的大血管疾病。大约40%的主动脉夹层患者没有 是时候去医院了，马上就死了。在发病机制中 在TAD中，血管平滑肌细胞是必需的 主动脉壁对多种细胞的收缩和合成反应 刺激，促进血管重构。2-8有表型 转换时，血管平滑肌细胞从收缩（分化）表型向合成（去分化）表型交替。去分化 血管平滑肌细胞在增殖、迁移和合成方面表现出较高的活性，同时分化标记物的表达减少 a-SMA和SM22a。 2,9病理表型转换是关键 血管平滑肌细胞的表型可由多种因素改变， 包括生长因子，趋化因子，细胞粘附分子， 细胞外基质酶和损伤刺激信号， PDGF促进血管内皮细胞表型向合成血管平滑肌细胞的转化，促进血管内皮细胞增殖和迁移 然而，血管平滑肌细胞潜在的分子机制 表型转换和新生内膜的形成仍不清楚。 MicroRNA（miRNA），内源性18-24核苷酸非编码 RNA是一种通过影响血管平滑肌细胞增殖、凋亡、分化、合成等功能而在血管疾病中发挥作用的新型调节因子， 例如miR-143/145参与血管 通过影响血管平滑肌细胞表型开关进行重塑，13,14可塑性，15 miR-34b/c多态性与基质合成有关- 在本研究中，我们确定miR-134-5p是抑制主动脉夹层的关键分子 通过微阵列筛选开发。我们进一步探讨了 miR-134-5p对血管平滑肌细胞表型转换和迁移的影响。 并对其潜在的分子机理进行了探讨。 我们的研究为这种重要性提供了新的见解 miRNA在调节血管平滑肌细胞功能、血管重塑以及大血管疾病发展方面的功能复杂性。

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