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戈勒姆-斯托特病患者成骨细胞中失调的 microRNA。

Dysregulated miRNAs in bone cells of patients with Gorham-Stout disease.

机构信息

Bone Physiopathology Research Unit, Genetics and Rare Diseases Research Division, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.

Rare Diseases and Medical Genetics Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.

出版信息

FASEB J. 2021 Mar;35(3):e21424. doi: 10.1096/fj.202001904RR.

Abstract

Gorham-Stout disease (GSD) is a very rare disease characterized by increased bone erosion with angiomatous proliferation. The mechanisms underlying this disorder have not been deeply investigated. Due to its rarity, no guidelines are currently available for treatment and management of GSD. We recently evaluated the cellular alterations of the bone remodeling in patients showing that osteoclast precursors displayed increased ability to differentiate into osteoclasts and that affected osteoclasts resorb bone more actively than control cells. Moreover, osteoblasts isolated from a patient showed a defective ability to form mineralized nodules. In this paper, we investigated the molecular pathways involved in the cellular defects of GSD bone cells. For this study, we recruited nine patients and performed miRNome analysis of bone cells. Between the 178 miRNAs robustly expressed in GSD osteoclasts, significant modulation of three miRNAs (miR-1246, miR-1-3p, and miR-137-3p) involved in the regulation of osteoclast formation and activity or in the angiomatous proliferation was found in patients' cells. Interestingly, miR-1246 was also up-regulated in serum exosomes from patients. Analysis of miRNAs from patient osteoblasts suggested alteration of miR-204a-5p, miR-615-3p and miR-378a-3p regulating osteoblast function and differentiation. The resulting miRNA pattern may help to understand better the mechanisms involved in GSD and to identify new potential therapeutic targets for this rare disease.

摘要

戈勒姆-斯托特病(GSD)是一种非常罕见的疾病,其特征是骨骼侵蚀伴血管性增生。这种疾病的发病机制尚未得到深入研究。由于其罕见性,目前尚无针对 GSD 的治疗和管理指南。我们最近评估了表现出这种疾病的患者的骨骼重塑细胞变化,结果表明破骨细胞前体具有更强的分化为破骨细胞的能力,受影响的破骨细胞比对照细胞更积极地吸收骨骼。此外,从一名患者中分离出的成骨细胞表现出形成矿化结节的能力缺陷。在本文中,我们研究了 GSD 骨细胞的细胞缺陷所涉及的分子途径。为此,我们招募了九名患者,并对骨细胞进行了 miRNome 分析。在 GSD 破骨细胞中表达丰富的 178 个 miRNA 中,发现三种 miRNA(miR-1246、miR-1-3p 和 miR-137-3p)的表达存在显著调节,这些 miRNA 参与破骨细胞的形成和活性或血管性增生的调节。有趣的是,miR-1246 也在上皮细胞来源的细胞外囊泡中上调。对患者成骨细胞的 miRNA 分析表明,miR-204a-5p、miR-615-3p 和 miR-378a-3p 的表达发生改变,这些 miRNA 参与成骨细胞的功能和分化。所得 miRNA 模式可能有助于更好地理解 GSD 涉及的机制,并确定这种罕见疾病的新潜在治疗靶点。

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