Myogenic progenitors contribute to open but not closed fracture repair.
Myogenic progenitors contribute to open but not closed fracture repair.
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DOI：
10.1186/1471-2474-12-288
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发表时间：
2011-12-22
影响因子：
2.3
通讯作者：
Schindeler A
中科院分区：
文献类型：
--
作者：
Liu R;Birke O;Morse A;Peacock L;Mikulec K;Little DG;Schindeler A
骨修复依赖于能够分化和产生新骨的骨能力祖细胞的存在。肌肉被发现与骨科损伤密切相关，然而其能力使骨修复的细胞贡献仍然不明确。我们假设myod谱系的肌源性细胞能够促进骨修复。我们使用MyoD-Cre+:Z/AP+条件报告基因小鼠，其中myod谱系的所有细胞都被永久标记为人类碱性磷酸酶（hAP）报告基因。我们追踪了myod谱系细胞在小鼠胫骨愈合模型中的作用。在没有肌肉骨骼损伤的情况下，myod表达细胞仅限于骨骼肌，非肌肉组织中报告阳性细胞的存在可以忽略不计。在闭合性胫骨骨折模型中，hAP+细胞对愈合的骨痂没有显著贡献。相比之下，开放性胫骨骨折具有骨膜剥离和肌肉开窗，在开放性骨折骨痂中检测到高达50%的hAP+细胞。在修复的早期阶段，许多hAP+细胞表现出软骨细胞形态，在后期出现少量成骨细胞样hAP+细胞。hAP和II型和I型胶原染色的连续切片显示myod谱系细胞被软骨或骨基质包围，提示在修复过程中起功能作用。为了排除骨祖细胞在骨修复过程中自发表达MyoD的可能性，我们在胫骨上制造了一个干骺端钻孔缺损。在该模型中未观察到hAP+染色，这表明MyoD的表达不是内源性骨祖细胞的正常事件。这些数据首次证明肌肉细胞可以在骨修复中发挥重要的次要作用，这一知识可能导致骨科手术中重要的转化应用。请参阅相关文章：http://www.biomedcentral.com/1741-7015/9/136
Bone repair is dependent on the presence of osteocompetent progenitors that are able to differentiate and generate new bone. Muscle is found in close association with orthopaedic injury, however its capacity to make a cellular contribution to bone repair remains ambiguous. We hypothesized that myogenic cells of the MyoD-lineage are able to contribute to bone repair. We employed a MyoD-Cre+:Z/AP+ conditional reporter mouse in which all cells of the MyoD-lineage are permanently labeled with a human alkaline phosphatase (hAP) reporter. We tracked the contribution of MyoD-lineage cells in mouse models of tibial bone healing. In the absence of musculoskeletal trauma, MyoD-expressing cells are limited to skeletal muscle and the presence of reporter-positive cells in non-muscle tissues is negligible. In a closed tibial fracture model, there was no significant contribution of hAP+ cells to the healing callus. In contrast, open tibial fractures featuring periosteal stripping and muscle fenestration had up to 50% of hAP+ cells detected in the open fracture callus. At early stages of repair, many hAP+ cells exhibited a chondrocyte morphology, with lesser numbers of osteoblast-like hAP+ cells present at the later stages. Serial sections stained for hAP and type II and type I collagen showed that MyoD-lineage cells were surrounded by cartilaginous or bony matrix, suggestive of a functional role in the repair process. To exclude the prospect that osteoprogenitors spontaneously express MyoD during bone repair, we created a metaphyseal drill hole defect in the tibia. No hAP+ staining was observed in this model suggesting that the expression of MyoD is not a normal event for endogenous osteoprogenitors. These data document for the first time that muscle cells can play a significant secondary role in bone repair and this knowledge may lead to important translational applications in orthopaedic surgery. Please see related article: http://www.biomedcentral.com/1741-7015/9/136
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影响因子：
2.8
作者：
Harry, Lorraine E.;Sandison, Ann;Nanchahal, Jagdeep
通讯作者：
Nanchahal, Jagdeep
影响因子：
64.8
作者：
SASSOON, D;LYONS, G;BUCKINGHAM, M
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BUCKINGHAM, M
影响因子：
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作者：
SMITH, CK;JANNEY, MJ;ALLEN, RE
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ALLEN, RE
DOI：
10.1097/01.blo.0000031984.92980.5d
发表时间：
2002-10-01
影响因子：
4.2
作者：
Young, BH;Peng, HR;Huard, J
通讯作者：
Huard, J
影响因子：
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Bosch, P;Musgrave, DS;Huard, J
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Huard, J