Stephens Elizabeth H, Nguyen Tom C, Blazejewski Jack G, Vekilov Dragoslava P, Connell Jennifer P, Itoh Akinobu, Ingels Neil B, Miller D Craig, Grande-Allen K Jane
Department of Bioengineering, Rice University, PO Box 1892, MS142, Houston, TX, 77251-1892, USA.
Department of Cardiothoracic Surgery, Columbia University School of Medicine, New York, NY, USA.
Heart Vessels. 2016 Jul;31(7):1186-95. doi: 10.1007/s00380-015-0768-8. Epub 2015 Nov 12.
The details of valvular leaflet healing following valvuloplasty and leaflet perforation from endocarditis are poorly understood. In this study, the synthesis and turnover of valvular extracellular matrix due to healing of a critical sized wound was investigated. Twenty-nine sheep were randomized to either CTRL (n = 11) or HOLE (n = 18), in which a 2.8-4.8 mm diameter hole was punched in the posterior mitral leaflet. After 12 weeks, posterior leaflets were harvested and histologically stained to localize extracellular matrix components. Immunohistochemistry was also performed to assess matrix components and markers of matrix turnover. A semi-quantitative grading scale was used to quantify differences between HOLE and CTRL. After 12 weeks, the hole diameter was reduced by 71.3 ± 1.4 % (p < 0.001). Areas of remodeling surrounding the hole contained more activated cells, greater expression of proteoglycans, and markers of matrix turnover (prolyl 4-hydroxylase, metalloproteases, and lysyl oxidase, each p ≤ 0.025), along with fibrin accumulation. Two distinct remodeling regions were evident surrounding the hole, one directly bordering the hole rich in versican and hyaluronan and a second adjacent region with abundant collagen and elastic fiber turnover. The remodeling also caused reduced delineation between valve layers (p = 0.002), more diffuse staining of matrix components and markers of matrix turnover (p < 0.001), and disruption of the collagenous fibrosa. In conclusion, acute valve injury elicited distinct, heterogeneous alterations in valvular matrix composition and structure, resulting in partial wound closure. Because these changes could also affect leaflet mechanics and valve function, it will be important to determine their impact on healing wounds.
瓣膜成形术后瓣叶愈合以及心内膜炎导致的瓣叶穿孔的细节目前尚不清楚。在本研究中,我们调查了因临界尺寸伤口愈合导致的瓣膜细胞外基质的合成与更新。将29只绵羊随机分为对照组(n = 11)和打孔组(n = 18),在打孔组中,于二尖瓣后叶上打一个直径2.8 - 4.8毫米的孔。12周后,采集后叶并进行组织学染色以定位细胞外基质成分。还进行了免疫组织化学分析以评估基质成分和基质更新标志物。使用半定量分级量表来量化打孔组和对照组之间的差异。12周后,孔直径缩小了71.3 ± 1.4%(p < 0.001)。孔周围的重塑区域含有更多活化细胞、蛋白聚糖表达增加以及基质更新标志物(脯氨酰4 - 羟化酶、金属蛋白酶和赖氨酰氧化酶,各p ≤ 0.025),同时伴有纤维蛋白积聚。孔周围有两个明显的重塑区域,一个直接与富含多功能蛋白聚糖和透明质酸的孔相邻,另一个相邻区域有丰富的胶原蛋白和弹性纤维更新。重塑还导致瓣膜各层之间的界限不清(p = 0.002)、基质成分和基质更新标志物的染色更弥散(p < 0.001)以及胶原纤维层的破坏。总之,急性瓣膜损伤引发了瓣膜基质组成和结构的明显异质性改变,导致伤口部分愈合。由于这些变化也可能影响瓣叶力学和瓣膜功能,确定它们对愈合伤口的影响将很重要。