人造血干细胞可作为治疗受损肾脏修复的新手段吗？

lhj8100

随着医学技术的发展人类的很多急性疾病都能得到控制和治疗但目前我们对慢性病的控制和治疗好像很不如意，如慢性肾病，糖尿病。。。。。。
+ p& c4 }$ E0 U) z0 @3 O$ \+ g  y' U人造血干细胞可作为治疗受损肾脏修复的新手段吗？
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5 p4 |& x  ?3 a* U% x# l- ^2 t' `背景：鉴于目前尚无促进肾脏修复的有效手段，且肾脏难以完全修复，因此了解肾脏损伤后修复和再生机制具有重要的意义。在本研究中我们构建了小鼠缺血/再灌注模型，以微血管为重点，对CD34(+)造血干细胞促进肾脏修复再生的能力进行了研究* m& O2 [2 E, K& q
结果：小鼠肾脏受损后24小时，将人造血干细胞选择性注入免疫缺陷小鼠的肾脏的微血管周围和微血管内。补充人造血干细胞与肾脏微血管和小管上皮细胞的修复具有相关性，并可促进肾功能恢复，延长生存期。补充至肾脏部位的人造血干细胞可表达与循环内皮祖细胞一致的标记，并可合成高水平促血管生成因子，促进血管内皮和上皮细胞增殖。虽然纯化的人造血干细胞一注入肾脏就获得内皮祖细胞标记，但人内皮细胞在小鼠毛细血管壁的定植极为罕见，这表明人干细胞所介导的肾脏修复是通过旁分泌机制，而不是血管替换机制。! U' G: g9 }8 l3 m- v3 P
结论：此研究表明人造血干细胞可作为治疗受损肾脏修复的新手段- W. b+ Y* f: G4 A% _6 z
Mobilized Human Hematopoietic Stem/Progenitor Cells Promote Kidney Repair After Ischemia/Reperfusion Injury.
' t: `' D- |2 w) zLi B, Cohen A, Hudson TE, Motlagh D, Amrani DL, Duffield JS.' _; ~; [. m& m1 @3 p* t  w
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Laboratory of Inflammation Research, Renal Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass.
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BACKGROUND: -Understanding the mechanisms of repair and regeneration of the kidney after injury is of great interest because there are currently no therapies that promote repair, and kidneys frequently do not repair adequately. We studied the capacity of human CD34(+) hematopoietic stem/progenitor cells (HSPCs) to promote kidney repair and regeneration using an established ischemia/reperfusion injury model in mice, with particular focus on the microvasculature. Methods and Results-Human HSPCs administered systemically 24 hours after kidney injury were selectively recruited to injured kidneys of immunodeficient mice (Jackson Labs, Bar Harbor, Me) and localized prominently in and around vasculature. This recruitment was associated with enhanced repair of the kidney microvasculature, tubule epithelial cells, enhanced functional recovery, and increased survival. HSPCs recruited to kidney expressed markers consistent with circulating endothelial progenitors and synthesized high levels of proangiogenic cytokines, which promoted proliferation of both endothelial and epithelial cells. Although purified HSPCs acquired endothelial progenitor markers once recruited to the kidney, engraftment of human endothelial cells in the mouse capillary walls was an extremely rare event, indicating that human stem cell mediated renal repair is by paracrine mechanisms rather than replacement of vasculature. Conclusions-These studies advance human HSPCs as a promising therapeutic strategy for promoting renal repair after injury.

johnson

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