中科院苏州纳米所的研究人员利用仿生学手段，成功揭示了古细菌的酸适应机制，相关成果近日发表于《科学报告》。
古细菌是一类不含细胞核和膜包围细胞器的单细胞生物，多生存于高温、高盐、高压或极端pH值等极端环境中。古细菌对极端环境的适应机制一直是微生物领域的研究热点之一。科学家曾经发现，在组成嗜酸古细菌细胞膜的脂质分子中，糖脂的比例远远高于其他种类生物的细胞膜，但由于缺乏合适的工具和手段，糖脂在质子防御中的作用并未得到足够充分的研究。
苏州纳米所马宏伟课题组创造性地引入仿生学手段，将内部富含羟基的表面高分子膜——聚甲基丙烯酸寡聚乙二醇酯作为仿生高分子层，模拟嗜酸古细菌表面糖脂所形成的富含羟基的糖被，从而定量研究羟基基团在嗜酸古细菌酸耐受机制中的作用。研究人员通过使用纳克级灵敏度的实时监测设备——石英晶体微天平，证实了该仿生高分子层具有显着的质子屏蔽作用，可在pH值为1.0的酸性液体环境中长期维持pH值≥5.0的局部微环境。通过共聚和嵌段聚合，研究人员成功对质子屏蔽能力进行了系统的研究和细致的调制，并初步验证了其在三维空间中的作用效果。
研究人员发现，当相同浓度的单体分子溶解于溶液中时，游离的羟基并不表现出质子屏蔽特性，说明该性能依赖于高分子主链对羟基的固定和富集。在自然界中，嗜酸古细菌则巧妙地利用了组成细胞膜的脂质分子骨架来“兼任”这一角色。脂质骨架致密排列，可行使固定和富集羟基的功能。
该仿生研究定量揭示了嗜酸古细菌的一项低pH适应机理，明确证实了羟基的质子屏蔽作用，其成果可应用于防酸材料的开发。而研究中所构建的仿生体系可继续应用于其他防酸分子和基团的评价与筛选，有望发展成为一套标准化的质子屏蔽研究系统。(生物谷Bioon.com)
doi:10.1038/srep00977
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Force and scleraxis synergistically promote the commitment of human ES cells derived MSCs to tenocytes
Xiao Chen, Zi Yin, Jia-lin Chen, Wei-liang Shen, Huan-huan Liu, Qiao-mei Tang, Zhi Fang,Lin-rong Lu, Junfeng Ji & Hong-wei Ouyang
As tendon stem/progenitor cells were reported to be rare in tendon tissues, tendons as vulnerable targets of sports injury possess poor self-repair capability. Human ESCs (hESCs) represent a promising approach to tendon regeneration. But their teno-lineage differentiation strategy has yet to be defined. Here, we report that force combined with the tendon-specific transcription factor scleraxis synergistically promoted commitment of hESCs to tenocyte for functional tissue regeneration. Force and scleraxis can independently induce tendon differentiation. However, force alone concomitantly activated osteogenesis, while scleraxis alone was not sufficient to commit, but augment tendon differentiation. Scleraxis synergistically augmented the efficacy of force on teno-lineage differentiation and inhibited the osteo-lineage differentiation by antagonized BMP signaling cascade. The findings not only demonstrated a novel strategy of directing hESC differentiation to tenocyte for functional tendon regeneration, but also offered insights into understanding the network of force, scleraxis and bmp2 controlling tendon-lineage differentiation.
