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Reduced nucleotomy-induced intervertebral disc disruption through spontaneous spheroid formation by the Low Adhesive Scaffold Collagen (LASCol).
Biomaterials ( IF 14.0 ) Pub Date : 2020-01-11 , DOI: 10.1016/j.biomaterials.2020.119781
Yoshiki Takeoka 1 , Takashi Yurube 1 , Koichi Morimoto 2 , Saori Kunii 2 , Yutaro Kanda 1 , Ryu Tsujimoto 1 , Yohei Kawakami 1 , Naomasa Fukase 1 , Toshiyuki Takemori 1 , Kaoru Omae 3 , Yuji Kakiuchi 1 , Shingo Miyazaki 1 , Kenichiro Kakutani 1 , Toru Takada 1 , Kotaro Nishida 1 , Masanori Fukushima 3 , Ryosuke Kuroda 1
Affiliation  

Back pain is a global health problem with a high morbidity and socioeconomic burden. Intervertebral disc herniation and degeneration are its primary cause, further associated with neurological radiculopathy, myelopathy, and paralysis. The current surgical treatment is principally discectomy, resulting in the loss of spinal movement and shock absorption. Therefore, the development of disc regenerative therapies is essential. Here we show reduced disc damage by a new collagen type I-based scaffold through actinidain hydrolysis-Low Adhesive Scaffold Collagen (LASCol)-with a high 3D spheroid-forming capability, water-solubility, and biodegradability and low antigenicity. In human disc nucleus pulposus and annulus fibrosus cells surgically obtained, time-dependent spheroid formation with increased expression of phenotypic markers and matrix components was observed on LASCol but not atelocollagen (AC). In a rat tail nucleotomy model, LASCol-injected and AC-injected discs presented relatively similar radiographic and MRI damage control; however, LASCol, distinct from AC, decelerated histological disc disruption, showing collagen type I-comprising LASCol degradation, aggrecan-positive and collagen type II-positive endogenous cell migration, and M1-polarized and also M2-polarized macrophage infiltration. Reduced nucleotomy-induced disc disruption through spontaneous spheroid formation by LASCol warrants further investigations of whether it may be an effective treatment without stem cells and/or growth factors for intervertebral disc disease.

中文翻译:

低粘附支架胶原蛋白(LASCol)通过自发球体形成减少了核仁切除​​术诱导的椎间盘破裂。

背痛是高发病率和社会经济负担的全球性健康问题。椎间盘突出和变性是其主要原因,进一步与神经系统神经根病,脊髓病和麻痹相关。当前的外科治疗主要是椎间盘切除术,导致脊柱运动的丧失和震动吸收。因此,椎间盘再生疗法的发展至关重要。在这里,我们显示了一种新的基于I型胶原的支架通过放线肌动蛋白水解低粘合支架胶原(LASCol)减少的椎间盘损伤,该支架具有高3D球体形成能力,水溶性,可生物降解性和低抗原性。通过手术获得的人椎间盘髓核和纤维环细胞,在LASCol上观察到随时间变化的球体形成,其中表型标记和基质成分的表达增加,但在Atelocollagen(AC)上未观察到。在大鼠尾部解剖模型中,LASCol注射和AC注射的椎间盘表现出相对相似的射线照相和MRI损伤控制。然而,不同于AC的LASCol减缓了组织学椎间盘的破坏,显示出包含I型胶原的LASCol降解,聚集蛋白聚糖阳性和II型胶原阳性的内源性细胞迁移,以及M1极化和M2极化的巨噬细胞浸润。LASCol通过自发的球体形成减少了核仁切除​​术诱导的椎间盘破裂,因此有必要进一步研究它是否可以有效治疗无椎间盘疾病的干细胞和/或生长因子。在大鼠尾部解剖模型中,LASCol注射和AC注射的椎间盘表现出相对相似的射线照相和MRI损伤控制。然而,不同于AC的LASCol减慢了组织学椎间盘的破坏,显示了包含I型胶原的LASCol降解,聚集蛋白聚糖阳性和II型胶原阳性的内源性细胞迁移,以及M1极化和M2极化的巨噬细胞浸润。LASCol通过自发的球体形成减少了核仁切除​​术诱导的椎间盘破裂,因此有必要进一步研究它是否可以有效治疗无椎间盘疾病的干细胞和/或生长因子。在大鼠尾部解剖模型中,LASCol注射和AC注射的椎间盘表现出相对相似的射线照相和MRI损伤控制。然而,不同于AC的LASCol减慢了组织学椎间盘的破坏,显示了包含I型胶原的LASCol降解,聚集蛋白聚糖阳性和II型胶原阳性的内源性细胞迁移,以及M1极化和M2极化的巨噬细胞浸润。LASCol通过自发的球体形成减少了核仁切除​​术诱导的椎间盘破裂,因此有必要进一步研究它是否可以有效治疗无椎间盘疾病的干细胞和/或生长因子。显示包含LASCol降解的I型胶原蛋白,聚集蛋白聚糖阳性和II型胶原蛋白阳性的内源性细胞迁移以及M1极化以及M2极化的巨噬细胞浸润。LASCol通过自发的球体形成减少了核仁切除​​术诱导的椎间盘破裂,因此有必要进一步研究它是否可以有效治疗无椎间盘疾病的干细胞和/或生长因子。显示包含LASCol降解的I型胶原蛋白,聚集蛋白聚糖阳性和II型胶原蛋白阳性的内源性细胞迁移以及M1极化以及M2极化的巨噬细胞浸润。LASCol通过自发的球体形成减少了核仁切除​​术诱导的椎间盘破裂,因此有必要进一步研究它是否可以有效治疗无椎间盘疾病的干细胞和/或生长因子。
更新日期:2020-01-13
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