Haydont Valérie, Vozenin-Brotons Marie-Catherine
Laboratoire UPRES EA 27-10, Radiosensibilite des tumeurs et tissus sains, Institut de Radioprotection et de Sûreté Nucléaire/Institut Gustave Roussy, Villejuif, France.
World J Gastroenterol. 2007 May 21;13(19):2675-83. doi: 10.3748/wjg.v13.i19.2675.
Recent advances in cell and molecular radiobiology clearly showed that tissue response to radiation injury cannot be restricted to a simple cell-killing process, but depends upon continuous and integrated pathogenic processes, involving cell differentiation and crosstalk between the various cellular components of the tissue within the extracellular matrix. Thus, the prior concept of primary cell target in which a single-cell type (whatever it's epithelial or endothelial cells) dictates the whole tissue response to radiation injury has to be replaced by the occurrence of coordinated multicellular response that may either lead to tissue recovery or to sequel development. In this context, the present review will focus on the maintenance of the radiation-induced wound healing and fibrogenic signals triggered by and through the microenvironment toward the mesenchymal cell compartment, and will highlight how sequential and sustained modifications in cell phenotypes will in cascade modify cell-to-cell interactions and tissue composition.
细胞与分子放射生物学的最新进展清楚地表明，组织对辐射损伤的反应不能局限于简单的细胞杀伤过程，而是取决于连续且整合的致病过程，这涉及细胞分化以及细胞外基质中组织的各种细胞成分之间的相互作用。因此，先前认为单一细胞类型（无论是上皮细胞还是内皮细胞）决定整个组织对辐射损伤反应的原代细胞靶点概念，必须被协调的多细胞反应所取代，这种反应可能导致组织恢复或后遗症发展。在此背景下，本综述将聚焦于由微环境触发并通过微环境向间充质细胞区室传递的辐射诱导伤口愈合和纤维化信号的维持，并将强调细胞表型的连续和持续改变如何级联改变细胞间相互作用和组织组成。
