Hayes Anthony J, Farrugia Brooke L, Biose Ifechukwude J, Bix Gregory J, Melrose James
Bioimaging Research Hub, Cardiff School of Biosciences, Cardiff University, Wales, United Kingdom.
Department of Biomedical Engineering, Melbourne School of Engineering, The University of Melbourne, Melbourne, VIC, Australia.
Front Cell Dev Biol. 2022 Apr 1;10:856261. doi: 10.3389/fcell.2022.856261. eCollection 2022.
This review highlights the multifunctional properties of perlecan (HSPG2) and its potential roles in repair biology. Perlecan is ubiquitous, occurring in vascular, cartilaginous, adipose, lymphoreticular, bone and bone marrow stroma and in neural tissues. Perlecan has roles in angiogenesis, tissue development and extracellular matrix stabilization in mature weight bearing and tensional tissues. Perlecan contributes to mechanosensory properties in cartilage through pericellular interactions with fibrillin-1, type IV, V, VI and XI collagen and elastin. Perlecan domain I - FGF, PDGF, VEGF and BMP interactions promote embryonic cellular proliferation, differentiation, and tissue development. Perlecan domain II, an LDLR-like domain interacts with lipids, Wnt and Hedgehog morphogens. Perlecan domain III binds FGF-7 and 18 and has roles in the secretion of perlecan. Perlecan domain IV, an immunoglobulin repeat domain, has cell attachment and matrix stabilizing properties. Perlecan domain V promotes tissue repair through interactions with VEGF, VEGF-R2 and α2β1 integrin. Perlecan domain-V LG1-LG2 and LG3 fragments antagonize these interactions. Perlecan domain V promotes reconstitution of the blood brain barrier damaged by ischemic stroke and is neurogenic and neuroprotective. Perlecan-VEGF-VEGFR2, perlecan-FGF-2 and perlecan-PDGF interactions promote angiogenesis and wound healing. Perlecan domain I, III and V interactions with platelet factor-4 and megakaryocyte and platelet inhibitory receptor promote adhesion of cells to implants and scaffolds in vascular repair. Perlecan localizes acetylcholinesterase in the neuromuscular junction and is of functional significance in neuromuscular control. Perlecan mutation leads to Schwartz-Jampel Syndrome, functional impairment of the biomechanical properties of the intervertebral disc, variable levels of chondroplasia and myotonia. A greater understanding of the functional working of the neuromuscular junction may be insightful in therapeutic approaches in the treatment of neuromuscular disorders. Tissue engineering of salivary glands has been undertaken using bioactive peptides (TWSKV) derived from perlecan domain IV. Perlecan TWSKV peptide induces differentiation of salivary gland cells into self-assembling acini-like structures that express salivary gland biomarkers and secrete α-amylase. Perlecan also promotes chondroprogenitor stem cell maturation and development of pluripotent migratory stem cell lineages, which participate in diarthrodial joint formation, and early cartilage development. Recent studies have also shown that perlecan is prominently expressed during repair of adult human articular cartilage. Perlecan also has roles in endochondral ossification and bone development. Perlecan domain I hydrogels been used in tissue engineering to establish heparin binding growth factor gradients that promote cell migration and cartilage repair. Perlecan domain I collagen I fibril scaffolds have also been used as an FGF-2 delivery system for tissue repair. With the availability of recombinant perlecan domains, the development of other tissue repair strategies should emerge in the near future. Perlecan co-localization with vascular elastin in the intima, acts as a blood shear-flow endothelial sensor that regulates blood volume and pressure and has a similar role to perlecan in canalicular fluid, regulating bone development and remodeling. This complements perlecan's roles in growth plate cartilage and in endochondral ossification to form the appendicular and axial skeleton. Perlecan is thus a ubiquitous, multifunctional, and pleomorphic molecule of considerable biological importance. A greater understanding of its diverse biological roles and functional repertoires during tissue development, growth and disease will yield valuable insights into how this impressive proteoglycan could be utilized successfully in repair biology.
本综述强调了基底膜聚糖(HSPG2)的多功能特性及其在修复生物学中的潜在作用。基底膜聚糖广泛存在于血管、软骨、脂肪、淋巴网状组织、骨骼、骨髓基质以及神经组织中。在成熟的负重和张力组织中,基底膜聚糖在血管生成、组织发育和细胞外基质稳定方面发挥作用。通过与原纤蛋白-1、IV型、V型、VI型和XI型胶原蛋白以及弹性蛋白的细胞周相互作用,基底膜聚糖有助于软骨的机械感觉特性。基底膜聚糖结构域I与成纤维细胞生长因子(FGF)、血小板衍生生长因子(PDGF)、血管内皮生长因子(VEGF)和骨形态发生蛋白(BMP)的相互作用促进胚胎细胞增殖、分化和组织发育。基底膜聚糖结构域II是一个低密度脂蛋白受体(LDLR)样结构域,可与脂质、Wnt和Hedgehog形态发生素相互作用。基底膜聚糖结构域III结合FGF-7和18,并在基底膜聚糖的分泌中起作用。基底膜聚糖结构域IV是一个免疫球蛋白重复结构域,具有细胞附着和基质稳定特性。基底膜聚糖结构域V通过与VEGF、VEGF受体2(VEGF-R2)和α2β1整合素相互作用促进组织修复。基底膜聚糖结构域V的LG1-LG2和LG3片段可拮抗这些相互作用。基底膜聚糖结构域V促进缺血性中风受损的血脑屏障的重建,具有神经发生和神经保护作用。基底膜聚糖-VEGF-VEGFR2、基底膜聚糖-FGF-2和基底膜聚糖-PDGF相互作用促进血管生成和伤口愈合。基底膜聚糖结构域I、III和V与血小板因子4以及巨核细胞和血小板抑制受体的相互作用促进细胞在血管修复中与植入物和支架的黏附。基底膜聚糖将乙酰胆碱酯酶定位于神经肌肉接头,在神经肌肉控制中具有重要功能。基底膜聚糖突变会导致施瓦茨-扬佩尔综合征、椎间盘生物力学特性的功能受损、不同程度的软骨发育异常和肌强直。深入了解神经肌肉接头的功能运作可能对神经肌肉疾病的治疗方法具有启发性。已经利用源自基底膜聚糖结构域IV的生物活性肽(TWSKV)进行唾液腺的组织工程。基底膜聚糖TWSKV肽诱导唾液腺细胞分化为自组装的腺泡样结构,这些结构表达唾液腺生物标志物并分泌α-淀粉酶。基底膜聚糖还促进软骨祖干细胞成熟以及多能迁移干细胞谱系的发育,这些干细胞谱系参与滑膜关节形成和早期软骨发育。最近的研究还表明,基底膜聚糖在成人人类关节软骨修复过程中显著表达。基底膜聚糖在软骨内成骨和骨骼发育中也发挥作用。基底膜聚糖结构域I水凝胶已用于组织工程,以建立促进细胞迁移和软骨修复的肝素结合生长因子梯度。基底膜聚糖结构域I胶原I原纤维支架也已用作组织修复的FGF-2递送系统。随着重组基底膜聚糖结构域的可得性,其他组织修复策略的开发在不久的将来应该会出现。基底膜聚糖与内膜中的血管弹性蛋白共定位,作为调节血容量和压力的血液剪切流内皮传感器,并且在小管液中与基底膜聚糖具有类似作用,调节骨骼发育和重塑。这补充了基底膜聚糖在生长板软骨和软骨内成骨中形成附属骨骼和中轴骨骼的作用。因此,基底膜聚糖是一种广泛存在、多功能且多形的分子,具有相当重要的生物学意义。深入了解其在组织发育、生长和疾病过程中的多种生物学作用和功能谱,将为如何在修复生物学中成功利用这种令人印象深刻的蛋白聚糖提供有价值的见解。