Midkine-deficient mice delayed degeneration and regeneration after skeletal muscle injury
Midkine-deficient mice delayed degeneration and regeneration after skeletal muscle injury
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DOI:
10.1016/j.acthis.2013.08.009
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发表时间:
2014-01-01
影响因子:
2.5
通讯作者:
Yoshida, Yoshihiro
中科院分区:
文献类型:
--
作者:
Ikutomo, Masako;Sakakima, Harutoshi;Yoshida, Yoshihiro
Midkine (MK), a heparin-binding growth factor, was previously found to be expressed in the rat myotubeforming stage. We investigated MK gene-deficient (Mdk(-/-)) mice in terms of skeletal muscle degeneration and regeneration after injury by bupivacaine injection into the tibialis anterior muscle. Injured muscles showed intense inflammatory cell infiltration. Myotubes, myofibers with centrally located nuclei in their cytoplasm, were significantly smaller in Mdk(-/-) mice than in wild type (Mdk(+/+)) mice 7 days after injury (p = 0.02). The distribution of myotube sizes showed quantitative differences between the two groups at 5 and 7 days, but not at 14 days. Many small myotubes were found in the regenerative area of Mdk(-/1-) mice compared with that of Mdk(+/+)mice 5 and 7 days after injury. The expression of Iba1, a macrophage marker, was significantly lower in Mdk(-/-) mice 3 days after injury (p = 0.01). The number of desminpositive cells like myoblasts in Mdk(-/-) mice was significantly fewer than that in Mdleif mice 3 days after injury. Our results suggested that deletion of MK results in a delay in regeneration, preceded by decelerated migration of macrophages to the damaged area, and that MK has a role in cell differentiation and maturation after skeletal muscle injury. (c) 2013 Elsevier GmbH. All rights reserved.