Shasti Mark, Jacquet Robin, McClellan Phillip, Yang Julianne, Matsushima Seika, Isogai Noritaka, Murthy Ananth, Landis William J
Department of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH, United States.
Department of Polymer Science, University of Akron, Akron, OH, United States.
Int J Pediatr Otorhinolaryngol. 2014 Mar;78(3):416-22. doi: 10.1016/j.ijporl.2013.11.028. Epub 2013 Dec 1.
Microtia is a congenital partial or total loss of the external ear with current treatment approaches involving autologous construction from costal cartilage. Alternatively, tissue engineering provides possible use of normal or microtia auricular chondrocytes harvested from patients. This study investigated effects in vitro of basic fibroblast growth factor (FGF-2) and osteogenic protein 1 (OP-1) on human pediatric normal and microtia auricular chondrocytes and their potential proliferation and differentiation for cellular expansion. A working hypothesis was that FGF-2 promotes proliferation and OP-1 maintains an auricular phenotype of these cells.
Two patients, one undergoing otoplasty and one an ear construction, yielded normal and microtia auricular chondrocytes, respectively. The two donor sets of isolated chondrocytes were equally divided into four experimental cell groups. These were controls without added growth factors and cells supplemented with FGF-2, OP-1 or FGF-2/OP-1 combined. Cells were cultured 3, 5, 7, and 10 days (3 replicates/time point), counted and assayed by RT-qPCR to determine elastin and types II and III collagen gene expression.
Compared to control counterparts, normal and microtia chondrocytes with OP-1 alone were similar in numbers and varied in elastin and types II and III collagen expression over all culture times. Compared to respective controls and chondrocyte groups with OP-1 alone, normal and microtia cell groups with FGF-2 had statistically significant (p<0.05) enhanced proliferation and statistically significant (p<0.05) decreased elastin and types II and III collagen expression over 10 days of culture.
FGF-2 effects on normal and microtia chondrocytes support its use for increasing cell numbers while OP-1 maintains a chondrocyte phenotype, otherwise marked by increasing type III collagen expression and cellular dedifferentiation to fibroblasts in culture.
小耳畸形是一种先天性的外耳部分或全部缺失,目前的治疗方法包括用肋软骨进行自体构建。另外,组织工程提供了使用从患者身上获取的正常或小耳畸形耳软骨细胞的可能性。本研究调查了碱性成纤维细胞生长因子(FGF-2)和成骨蛋白1(OP-1)对人小儿正常和小耳畸形耳软骨细胞的体外作用,以及它们在细胞扩增方面的潜在增殖和分化情况。一个工作假设是FGF-2促进增殖,而OP-1维持这些细胞的耳软骨表型。
两名患者,一名接受耳整形手术,一名进行耳部构建,分别产生了正常和小耳畸形耳软骨细胞。这两组分离的软骨细胞供体被平均分为四个实验细胞组。这些组分别是不添加生长因子的对照组以及添加FGF-2、OP-1或FGF-2/OP-1组合的细胞组。细胞培养3、5、7和10天(每个时间点3个重复),进行计数并通过RT-qPCR检测,以确定弹性蛋白以及II型和III型胶原蛋白基因的表达。
与对照细胞相比,单独使用OP-1的正常和小耳畸形软骨细胞数量相似,在所有培养时间内弹性蛋白以及II型和III型胶原蛋白的表达有所不同。与各自的对照组和单独使用OP-1的软骨细胞组相比,添加FGF-2的正常和小耳畸形细胞组在培养10天时增殖有统计学显著增强(p<0.05),弹性蛋白以及II型和III型胶原蛋白的表达有统计学显著降低(p<0.05)。
FGF-2对正常和小耳畸形软骨细胞的作用支持其用于增加细胞数量,而OP-1维持软骨细胞表型,否则在培养中会以III型胶原蛋白表达增加和细胞去分化为成纤维细胞为特征。