歐洲分子生物學實驗室（EMBL）的科學家在原本令人失望的試驗結果得到了一項重要的發現。這項發現發表在本周Proceedings of the National Academy of Sciences的在線版本上。
該結果為某一理論，即當肌肉受傷時，巨噬細胞在其再生過程中承擔了決定性的角色，提供了確鑿的證據。
科學家還發現遺傳開關控制著該過程，這為新的療法開闢了道路，不僅僅可以是運動損傷同樣可以是疾病導致的，比如進行性假肥大性肌營養不良（Duchenne muscular dystrophy）。
正常情況下，巨噬細胞會吞食並消滅細菌和其他傳染源。它們就像清潔工人清除已經死亡的細胞，釋放促炎因子（pro-inflammatory factor），阻止感染。在清除殘骸以後，巨噬細胞會停止釋放這些促炎因子，並開始產生抗炎因子促進損傷區域的修復。巨噬細胞從清除殘骸到激發修復的變化就是巨噬細胞兩極化現象，Claus Nerlov和他的同事證實這對肌肉的再生來說是必不可少的。如果巨噬細胞不能發生這種改變那麼肌肉組織將不能修復，就會留下疤痕，而不是新的組織。
據介紹，有一種C/EBPβ的蛋白，發生炎症時該蛋白的產量增加。因此研究人員設計了C/EBPβ生成障礙的老鼠，以觀察不同細胞發展受到的影響，包括免疫系統。但令人失望的是，細胞幾乎沒有受到任何影響。除了巨噬細胞沒有出現兩極化，這種改進的老鼠能夠正常發育，有正常的血細胞，。
儘管這項試驗沒有出現科學家想要的關於血細胞發育的結果，但是對於肌肉再生研究來說這是一項新的發現。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS September 24, 2009, doi: 10.1073/pnas.0908641106
A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair
Daniela Ruffell1, Foteini Mourkioti1, Adriana Gambardella1, Peggy Kirstetter, Rodolphe G. Lopez, Nadia Rosenthal and Claus Nerlov2
Mouse Biology Unit, European Molecular Biology Laboratory, Via Ramarini 32, 00015 Monterotondo, Italy
Macrophages play an essential role in the resolution of tissue damage through removal of necrotic cells, thus paving the way for tissue regeneration. Macrophages also directly support the formation of new tissue to replace the injury, through their acquisition of an anti-inflammatory, or M2, phenotype, characterized by a gene expression program that includes IL-10, the IL-13 receptor, and arginase 1. We report that deletion of two CREB-binding sites from the Cebpb promoter abrogates Cebpb induction upon macrophage activation. This blocks the downstream induction of M2-specific Msr1, Il10, II13ra, and Arg-1 genes, whereas the inflammatory (M1) genes Il1, Il6, Tnfa, and Il12 are not affected. Mice carrying the mutated Cebpb promoter (βΔCre) remove necrotic tissue from injured muscle, but exhibit severe defects in muscle fiber regeneration. Conditional deletion of the Cebpb gene in muscle cells does not affect regeneration, showing that the C/EBPβ cascade leading to muscle repair is muscle-extrinsic. While βΔCre macrophages efficiently infiltrate injured muscle they fail to upregulate Cebpb, leading to decreased Arg-1 expression. CREB-mediated induction of Cebpb expression is therefore required in infiltrating macrophages for upregulation of M2-specific genes and muscle regeneration, providing a direct genetic link between these two processes.