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骨中的淋巴管支持受伤后的再生
作者:小柯机器人 发布时间:2023/1/27 22:39:31


英国牛津大学Anjali P. Kusumbe研究组发现,骨中的淋巴管支持受伤后的再生。相关论文于2023年1月19日发表于国际学术期刊《细胞》。

通过通过结合高分辨率光片成像和细胞特异性小鼠遗传学,研究人员证明了小鼠和人类骨骼中淋巴管的存在。研究人员发现骨骼中的淋巴管在遗传毒性压力下会扩张。血管内皮生长因子-C/VEGFR-3信号传导和基因毒性压力诱导的IL6驱动骨骼中的淋巴管生成。在淋巴管生成过程中,增殖的淋巴内皮细胞分泌的CXCL12对造血和骨再生至关重要。此外,淋巴管分泌的CXCL12触发了成熟的Myh11+CXCR4+周细胞的扩增,这些周细胞分化成骨细胞,有助于骨和造血的再生。在老年动物中,淋巴管和Myh11阳性细胞对基因毒性压力的这种扩张受到损害。这些数据表明,淋巴管生成是刺激造血和骨再生的一个治疗途径。

据了解,血液和淋巴管形成了一个多功能的运输网络,并提供诱导信号来调节组织的特定功能。骨骼中的血管调节成骨和造血,但目前的教条认为骨骼中缺乏淋巴管。

附:英文原文

Title: Lymphatic vessels in bone support regeneration after injury

Author: Lincoln Biswas, Junyu Chen, Jessica De Angelis, Amit Singh, Charlotte Owen-Woods, Zhangfan Ding, Joan Mane Pujol, Naveen Kumar, Fanxin Zeng, Saravana K. Ramasamy, Anjali P. Kusumbe

Issue&Volume: 2023/01/19

Abstract: Blood and lymphatic vessels form a versatile transport network and provide inductive signals to regulate tissue-specific functions. Blood vessels in bone regulate osteogenesis and hematopoiesis, but current dogma suggests that bone lacks lymphatic vessels. Here, by combining high-resolution light-sheet imaging and cell-specific mouse genetics, we demonstrate presence of lymphatic vessels in mouse and human bones. We find that lymphatic vessels in bone expand during genotoxic stress. VEGF-C/VEGFR-3 signaling and genotoxic stress-induced IL6 drive lymphangiogenesis in bones. During lymphangiogenesis, secretion of CXCL12 from proliferating lymphatic endothelial cells is critical for hematopoietic and bone regeneration. Moreover, lymphangiocrine CXCL12 triggers expansion of mature Myh11+ CXCR4+ pericytes, which differentiate into bone cells and contribute to bone and hematopoietic regeneration. In aged animals, such expansion of lymphatic vessels and Myh11-positive cells in response to genotoxic stress is impaired. These data suggest lymphangiogenesis as a therapeutic avenue to stimulate hematopoietic and bone regeneration.

DOI: 10.1016/j.cell.2022.12.031

Source: https://www.cell.com/cell/fulltext/S0092-8674(22)01574-4

期刊信息
Cell:《细胞》,创刊于1974年。隶属于细胞出版社,最新IF:66.85
官方网址:https://www.cell.com/
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