Liu Chia-Feng, Samsa William E, Zhou Guang, Lefebvre Véronique
Department of Cellular and Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland, OH, 44195, USA.
Department of Orthopaedics, Case Western Reserve University, Cleveland, OH, USA.
Semin Cell Dev Biol. 2017 Feb;62:34-49. doi: 10.1016/j.semcdb.2016.10.004. Epub 2016 Oct 19.
A milestone in the evolutionary emergence of vertebrates was the invention of cartilage, a tissue that has key roles in modeling, protecting and complementing the bony skeleton. Cartilage is elaborated and maintained by chondrocytes. These cells derive from multipotent skeletal progenitors and they perform highly specialized functions as they proceed through sequential lineage commitment and differentiation steps. They form cartilage primordia, the primary skeleton of the embryo. They then transform these primordia either into cartilage growth plates, temporary drivers of skeletal elongation and endochondral ossification, or into permanent tissues, namely articular cartilage. Chondrocyte fate decisions and differentiated activities are controlled by numerous extrinsic and intrinsic cues, and they are implemented at the gene expression level by transcription factors. The latter are the focus of this review. Meritorious efforts from many research groups have led over the last two decades to the identification of dozens of key chondrogenic transcription factors. These regulators belong to all types of transcription factor families. Some have master roles at one or several differentiation steps. They include SOX9 and RUNX2/3. Others decisively assist or antagonize the activities of these masters. They include TWIST1, SOX5/6, and MEF2C/D. Many more have tissue-patterning roles and regulate cell survival, proliferation and the pace of cell differentiation. They include, but are not limited to, homeodomain-containing proteins and growth factor signaling mediators. We here review current knowledge of all these factors, one superclass, class, and family at a time. We then compile all knowledge into transcriptional networks. We also identify remaining gaps in knowledge and directions for future research to fill these gaps and thereby provide novel insights into cartilage disease mechanisms and treatment options.
脊椎动物进化出现过程中的一个里程碑是软骨的形成,软骨是一种在骨骼塑形、保护和补充硬骨骨骼方面发挥关键作用的组织。软骨由软骨细胞构建和维持。这些细胞源自多能骨骼祖细胞,在经历一系列谱系定向和分化步骤时,它们执行高度专业化的功能。它们形成软骨原基,即胚胎的初级骨骼。然后,它们将这些原基转化为软骨生长板,这是骨骼伸长和软骨内骨化的临时驱动因素,或者转化为永久性组织,即关节软骨。软骨细胞的命运决定和分化活动受众多外在和内在信号的控制,并通过转录因子在基因表达水平上得以实现。转录因子是本综述的重点。在过去二十年中,许多研究团队付出了卓有成效的努力,已鉴定出数十种关键的软骨生成转录因子。这些调节因子属于所有类型的转录因子家族。有些在一个或几个分化步骤中起主导作用,包括SOX9和RUNX2/3等。其他一些则决定性地协助或拮抗这些主导因子的活性,包括TWIST1、SOX5/6和MEF2C/D等。还有更多转录因子具有组织模式形成作用,并调节细胞存活、增殖和细胞分化的速度,包括但不限于含同源结构域的蛋白质和生长因子信号传导介质。我们在此一次回顾一类、一个家族的所有这些因子的现有知识。然后将所有知识整合到转录网络中。我们还确定了知识上的剩余空白以及未来研究填补这些空白的方向,从而为软骨疾病机制和治疗方案提供新的见解。