Monocyte depletion increases local proliferation of macrophage subsets after skeletal muscle injury.
Monocyte depletion increases local proliferation of macrophage subsets after skeletal muscle injury.
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DOI：
10.1186/1471-2474-14-359
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发表时间：
2013-12-19
影响因子：
2.3
通讯作者：
Duchesne E
中科院分区：
文献类型：
--
作者：
Côté CH;Bouchard P;van Rooijen N;Marsolais D;Duchesne E
M1和M2巨噬细胞的连续积累对于急性损伤后骨骼肌的恢复至关重要。虽然M1蓄积被认为依赖于单核细胞浸润，但M2蓄积的机制仍存在争议，但可能涉及浸润前体。然而，单核细胞的强烈耗竭仅部分损害骨骼肌愈合，支持存在减轻浸润巨噬细胞祖细胞损失的替代机制。因此，本研究的目的是调查是否发生在受损骨骼肌内的巨噬细胞亚群的增殖，并确定是否单核细胞耗竭导致损伤后巨噬细胞增殖增加。在大鼠胫骨前肌内注射布比卡因造成损伤。从损伤前24小时开始，通过每日静脉注射脂质体包封的氯膦酸盐耗尽血液单核细胞。在单独的实验中，还进行后肢照射以防止驻留细胞增殖。安乐死后，收集血液和肌肉用于巨噬细胞/单核细胞亚群的流式细胞术分析。氯膦酸盐诱导单核细胞消耗80%-90%，但仅导致M1和M2巨噬细胞积聚分别减少57%和41%，在损伤后2天。相反，损伤后4天，单核细胞耗竭大鼠中M1巨噬细胞的数量是非耗竭大鼠的2.4倍。这与增殖性M1巨噬细胞数量增加16倍有关，而在辐照动物中则减少了46%。M2巨噬细胞的增殖在损伤后4天通过氯膦酸盐处理增加了10倍。M2巨噬细胞的积累部分受损的照射，无论单核细胞耗竭。M1和M2亚群在骨骼肌损伤后增殖，并且在单核细胞耗竭的情况下其增殖增强。我们的研究支持这样的结论，即浸润和驻留前体都可能有助于M1或M2巨噬细胞在肌肉损伤中的积聚。
Sequential accumulation of M1 and M2 macrophages is critical for skeletal muscle recovery after an acute injury. While M1 accumulation is believed to rely on monocyte infiltration, the mechanisms of M2 accumulation remain controversial, but could involve an infiltrating precursor. Yet, strong depletion of monocytes only partially impairs skeletal muscle healing, supporting the existence of alternative mechanisms to palliate the loss of infiltrating macrophage progenitors. The aims of this study are thus to investigate if proliferation occurs in macrophage subsets within injured skeletal muscles; and to determine if monocyte depletion leads to increased proliferation of macrophages after injury. Injury was induced by bupivacaine injection in the tibialis anterior muscle of rats. Blood monocytes were depleted by daily intravenous injections of liposome-encapsulated clodronate, starting 24 h prior to injury. In separate experiments, irradiation of hind limb was also performed to prevent resident cell proliferation. Upon euthanasia, blood and muscles were collected for flow cytometric analyses of macrophage/monocyte subsets. Clodronate induced a 80%-90% depletion of monocyte but only led to 57% and 41% decrease of M1 and M2 macrophage accumulation, respectively, 2 d following injury. Conversely, the number of M1 macrophages in monocyte-depleted rats was 2.4-fold higher than in non-depleted rats 4 d after injury. This was associated with a 16-fold increase in the number of proliferative M1 macrophages, which was reduced by 46% in irradiated animals. Proliferation of M2 macrophages was increased tenfold by clodronate treatment 4 d post injury. The accumulation of M2 macrophages was partially impaired by irradiation, regardless of monocyte depletion. M1 and M2 subsets proliferate after skeletal muscle injury and their proliferation is enhanced under condition of monocyte depletion. Our study supports the conclusion that both infiltrating and resident precursors could contribute to M1 or M2 macrophage accumulation in muscle injury.
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影响因子：
15.3
作者：
Celada, A;Borras, FE;Maki, RA
通讯作者：
Maki, RA
影响因子：
3.7
作者：
Khallou-Laschet J;Varthaman A;Fornasa G;Compain C;Gaston AT;Clement M;Dussiot M;Levillain O;Graff-Dubois S;Nicoletti A;Caligiuri G
通讯作者：
Caligiuri G
影响因子：
3.6
作者：
Gross, JG;Bou-Gharios, G;Morgan, JE
通讯作者：
Morgan, JE
影响因子：
4
作者：
Hodgetts, SI;Grounds, MD
通讯作者：
Grounds, MD
DOI：
10.1084/jem.20070075
发表时间：
2007-05-14
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Arnold L;Henry A;Poron F;Baba-Amer Y;van Rooijen N;Plonquet A;Gherardi RK;Chazaud B
通讯作者：
Chazaud B