Lu C-C, Liu M-M, Culshaw G, French A, Corcoran B
Royal (Dick) School of Veterinary Studies and The Roslin Institute, The University of Edinburgh, Easterbush, Roslin, Mid-Lothian, Scotland, EH25 9RG, UK.
School of Veterinary Medicine, The University of Glasgow, Garscube Campus, Bearsden Road, Glasgow, Scotland, G61 1QH, UK.
J Vet Cardiol. 2016 Jun;18(2):100-9. doi: 10.1016/j.jvc.2015.12.003. Epub 2016 Feb 6.
The aim of this study was to determine if there are differences in cellular changes in Cavalier King Charles spaniel (CKCS) myxomatous mitral valves compared to non-CKCS dogs.
Cavalier King Charles spaniels (n = 6) and age-matched mixed breed (n = 6) with severe myxomatous mitral valve disease (MMVD), and normal mixed breed (n = 4) dogs.
Immunohistochemistry staining and qualitative and quantitative analysis of mitral valves sections, examining for the presence of CD11c and CD45, vimentin, alpha smooth muscle actin (α-SMA) and embryonic smooth muscle myosin heavy chain (Smemb), von Willebrand factor and CD31 and Ki-67.
Vimentin positive cell numbers were increased in the MMVD dogs and distributed throughout the valve with greatest density close to the endothelium. There were no significant differences in cell marker expression for the two diseased groups, but cell numbers were significantly increased compared to controls for α-SMA (CKCS only) and Smemb (CKCS and mixed breed: p < 0.05). Alpha smooth muscle actin+ cells were primarily located at the valve edge, with Smemb+ cells similarly located, but also present throughout the valve stroma. A small number of cells close to the valve edge co-expressed α-SMA and Smemb. Endothelial von Willebrand factor expression was identified in all valves, with evidence of disrupted endothelium in the diseased, but was also found in diseased valve stroma. There was no staining for CD11c, CD45 or CD31 in any valve. Ki-67+ cells formed linear clusters at the leaflet tip and were sparsely distributed throughout both myxomatous valve groups.
The cellular changes notes with advanced stage MMVD appear similar for CKCS when compared to mixed breed dogs.
本研究的目的是确定与非骑士查理王小猎犬相比,骑士查理王小猎犬(CKCS)的黏液瘤样二尖瓣的细胞变化是否存在差异。
患有严重黏液瘤样二尖瓣疾病(MMVD)的骑士查理王小猎犬(n = 6)和年龄匹配的混种犬(n = 6),以及正常混种犬(n = 4)。
对二尖瓣切片进行免疫组织化学染色以及定性和定量分析,检测CD11c、CD45、波形蛋白、α平滑肌肌动蛋白(α-SMA)、胚胎平滑肌肌球蛋白重链(Smemb)、血管性血友病因子、CD31和Ki-67的表达情况。
波形蛋白阳性细胞数量在患有MMVD的犬中增加,且分布于整个瓣膜,在内皮附近密度最高。两个患病组的细胞标志物表达无显著差异,但与对照组相比,α-SMA(仅CKCS)和Smemb(CKCS和混种犬:p < 0.05)的细胞数量显著增加。α平滑肌肌动蛋白阳性细胞主要位于瓣膜边缘,Smemb阳性细胞也位于类似位置,但在整个瓣膜基质中也有分布。靠近瓣膜边缘的少数细胞同时表达α-SMA和Smemb。在所有瓣膜中均检测到内皮血管性血友病因子表达,患病瓣膜存在内皮破坏的证据,但在患病瓣膜基质中也有发现。所有瓣膜均未检测到CD11c、CD45或CD31染色。Ki-67阳性细胞在小叶尖端形成线性簇,在两个黏液瘤样瓣膜组中均稀疏分布。
与混种犬相比,CKCS晚期MMVD的细胞变化相似。