美国伊利诺伊大学医学院的科学家对患急性肺损伤老鼠模型的研究表明，成体干细胞(adult stem cell)能够治疗急性肺损伤(acute lung injury,ALI)。这项研究报告发表在10月版的Stem Cells杂志上。
急性肺损伤的病理特点为肺泡毛细血管内皮细胞和肺泡上皮细胞损伤，表现为广泛肺水肿和微小肺不张。由于内皮细胞生命周期较长，新细胞的更新需要2～5年时间，因而在特定时间内，用于修复损伤的干细胞数目远远不够，并且内皮细胞修复非常复杂。该课题组提出，干细胞或许可以用于ALI治疗。
Wary及其同事在老鼠骨髓干细胞中找到了一些祖干细胞(progenitor stem cells)，因其细胞表面有Flk-1以及CD34蛋白，分别将其命名为Flk-1以及CD34。虽然骨髓干细胞中这类干细胞的含量极少，但研究人员还是成功地找到一种增加干细胞数量和“粘着度”的细胞培养方法。
这些干细胞可通过细胞表面的整合素(integrin)黏附到相应的靶点并进行修复。研究人员首先对小鼠注射一种物质引起小鼠出现急性肺损伤，然后在注射经过培养和纯化的Flk-1以及CD34干细胞。研究人员发现，这些祖细胞能够修复肺损伤，并防止肺部出现积水。
这项研究证实，干细胞疗法不仅是一种很有前景的治疗ALI的方法，还使研究人员进一步了解干细胞修复损伤的机制。（生物谷Bioon.com）
生物谷推荐原始出处：
STEM CELLS DOI:10.1002/stem.241
Requirement of α4β1 and α5β1 Integrin Expression in Bone-Marrow Derived Progenitor Cells in Preventing Endotoxin-Induced Lung Vascular Injury and Edema in Mice
Kishore K. Wary *, Stephen M Vogel, Sean Garrean, Yidan D. Zhao, Asrar B. Malik
Department of Pharmacology and Center for Lung and Vascular Biology, The University of Illinois, Chicago, IL 60612
The goal of this study was to determine the role of integrin-mediated adhesion of bone marrow derived progenitor cells (BMPCs) as a requirement for the endothelial barrier protection in a lung injury model. C57BL mice were used as the source for BMPCs, which were characterized as CD34+ and Flk1+ as well as expression of a repertoire of integrins. We used a mouse model of bacterial lipopolysaccharide (LPS)-induced lung vascular injury and edema formation to test the effects of BMPC integrin expression in preventing endothelial barrier injury. Adhesion of BMPCs to purified extracellular matrix proteins induced Fak phosphorylation and formation of branching point structures in a 4 and 5 integrin-dependent manner. BMPCs expressing red fluorescent protein (RFP) were administered via the retro-orbital venous route in mice treated intraperitonially (i.p.) with LPS [7.5 mg/kg body weight (BW). We observed increased retention of RFP-labeled Flk1+ and CD34+ BMPCs for up to 8 wk in mice injured with LPS. BMPC transplantation increased survival by 50% (at 72 to 96 hr after LPS) and reduced lung vascular injury and extravascular water content induced by LPS. However, blocking with anti-4 or anti-5 integrin antibody, or shRNA mediated silencing of 4 or 5 integrins in donor BMPCs failed to prevent the vascular injury or edema formation and mortality. Thus, 4 and 5 integrin-dependent adhesion of BMPCs in lung tissue plays a critical role in preventing lung vascular injury and increasing survival in a mouse model of LPS-induced acute lung injury.
