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骨形态发生蛋白2(BMP2)在马退行性悬韧带腱炎的发病机制中起作用吗?

Does BMP2 play a role in the pathogenesis of equine degenerative suspensory ligament desmitis?

作者信息

Young Madeline, Moshood Olaniyi, Zhang Jian, Sarbacher Carolyn A, Mueller P O Eric, Halper Jaroslava

机构信息

Department of Pathology, College of Veterinary Medicine, The University of Georgia, Athens, GA, 30602, USA.

Department of Large Animal Medicine, College of Veterinary Medicine, The University of Georgia, Athens, GA, 30602, USA.

出版信息

BMC Res Notes. 2018 Sep 18;11(1):672. doi: 10.1186/s13104-018-3776-9.

Abstract

OBJECTIVE

Horses afflicted with degenerative suspensory ligament desmitis (DSLD) suffer from progressive leg pain and lameness without history of trauma. DSLD is a systemic disorder caused by abnormal accumulation of proteoglycans in many connective tissues. One proteoglycan found in higher quantities in DSLD is decorin. The accumulated decorin has an abnormally glycosylated glycosaminoglycan chain in DSLD. In addition to acellular accumulations of proteoglycans foci of active fibroblasts/tenoblasts were observed in some tendons and suspensory ligaments (SLs) from DSLD cases We have hypothesized that this represents an early event in DSLD and that production of chondrogenic growth factors, such as BMP2, and/or enzyme participating in glycosylation of glycosaminoglycans is a major factor in initiation and progression of DSLD.

RESULTS

Using immunohistochemistry we have identified BMP2 in these cellular foci, indicating association with proteoglycan production, but not in other cells in the tendon and SLs. In contrast, very little staining for TGFβ and dermatan sulfate epimerase, an enzyme involved in glycosylation of glycosaminoglycan chains, was observed in these foci and other cells in both control and DSLD-affected tendons and SLs. Our data support our hypothesis that chondrogenic growth factors may be responsible, at least in part for progression of DSLD in horses.

摘要

目的

患有退行性悬韧带腱炎(DSLD)的马匹会遭受渐进性腿部疼痛和跛行,且无外伤史。DSLD是一种由蛋白聚糖在许多结缔组织中异常积聚引起的全身性疾病。在DSLD中发现含量较高的一种蛋白聚糖是核心蛋白聚糖。在DSLD中,积聚的核心蛋白聚糖具有异常糖基化的糖胺聚糖链。除了蛋白聚糖的无细胞积聚外,在一些来自DSLD病例的肌腱和悬韧带(SLs)中还观察到活跃的成纤维细胞/成腱细胞灶。我们推测这代表了DSLD中的一个早期事件,并且软骨生成生长因子(如骨形态发生蛋白2,BMP2)的产生和/或参与糖胺聚糖糖基化的酶是DSLD发生和发展的主要因素。

结果

使用免疫组织化学方法,我们在这些细胞灶中鉴定出了BMP2,表明其与蛋白聚糖的产生有关,但在肌腱和悬韧带的其他细胞中未发现。相比之下,在对照和受DSLD影响的肌腱及悬韧带的这些病灶和其他细胞中,观察到转化生长因子β(TGFβ)和参与糖胺聚糖链糖基化的酶硫酸皮肤素表异构酶的染色非常少。我们的数据支持了我们的假设,即软骨生成生长因子可能至少部分地导致了马匹DSLD的进展。

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