Midkine-deficient mice delayed degeneration and regeneration after skeletal muscle injury

Ikutomo, Masako; Sakakima, Harutoshi; Matsuda, Fumiyo; Yoshida, Yasuhiko

doi:10.1016/j.acthis.2013.08.009

Cited by 25 publications

(19 citation statements)

References 40 publications

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“…Muscle regeneration after the injection of bupivacaine hydrochloride into tibialis anterior muscles was delayed in Mdk−/− mice, and the diameter of myotubes was significantly smaller in Mdk−/− mice than in Mdk+/+ mice 5 and 7 days after injury. No significant difference was observed between these mice at 14 days (Ikutomo et al ., ). However, the number of macrophages in the injured muscle, as assessed by the expression of a macrophage marker, was significantly lower in Mdk−/− mice than in Mdk+/+ mice 3 days after injury.…”

Section: Mk In Related Diseasesmentioning

confidence: 97%

“…However, the number of macrophages in the injured muscle, as assessed by the expression of a macrophage marker, was significantly lower in Mdk−/− mice than in Mdk+/+ mice 3 days after injury. These results indicate that the deletion of MK results in a delay in regeneration of injured muscle preceded by the decreased migration of macrophages to the damaged area (Ikutomo et al ., ).…”

Section: Mk In Related Diseasesmentioning

confidence: 97%

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Midkine in repair of the injured nervous system

Yoshida

Sakakima

Matsuda

et al. 2014

British J Pharmacology

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Midkine (MK) is a growth factor with neurotrophic and neurite outgrowth activities. It was expressed in the peri-ischaemic area in the acute phase of cerebral infarction in rat brains. Astrocytes were the origin of MK in this occasion. MK has been assessed in terms of its effects on neural injury. The administration of MK into the lateral ventricle immediately prior to ischaemia prevented cell death in the hippocampal CA1 neurons degenerated by transient forebrain ischaemia in gerbils. MK administration was also beneficial in rats with neural injury, especially after kainic acid-induced seizures. Gene therapy with mouse MK cDNA using an adenovirus was effective in reducing the cerebral infarction volume and in increasing the number of neuronal precursor cells in the subventricular zone of the rat brain. MK mRNA and MK protein were found in spinal cord motor neurons of the anterior horn in both the acute phase of sciatic nerve injury and 3 weeks later. MK immunoreactivity was also found in the proximal side of a sciatic nerve-injured site in sciatic nerve axons. MK receptors were expressed in Schwann cells after injury, suggesting crosstalk between axons and Schwann cells. MK was also present in nerve terminals and influenced ACh receptor clustering during neuromuscular development in Xenopus. Thus, MK may also be involved in reinforcing and maintaining the synapse. All these findings indicate the therapeutic potential of MK for promoting repair of the nervous system after injury.LINKED ARTICLESThis article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-4

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Section: Mk In Related Diseasesmentioning

confidence: 97%

Section: Mk In Related Diseasesmentioning

confidence: 97%

Midkine in repair of the injured nervous system

Yoshida

Sakakima

Matsuda

et al. 2014

British J Pharmacology

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“…Anecdotally speaking, it seems that “centrally located nuclei” is favored by non-English speaker groups, mostly scattered through Europe or East Asia, even though “central nuclei” remains prevalent (Musarò et al, 2007; Coletti et al, 2013; Ikutomo et al, 2014). …”

Section: Temporal and Geographical Distributionmentioning

confidence: 99%

The Need for a Consensus on the Locution “Central Nuclei” in Striated Muscle Myopathies

Mazzotti¹,

Coletti

2016

Front. Physiol.

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“…MDK is a heparin-binding growth factor that is reported to promote the proliferation, differentiation, survival, adhesion and migration of cells [31,32,33,34]. Deletion of MDK results in a delay in regeneration, preceded by decelerated migration of macrophages to the damaged area after skeletal muscle injury [35]. In this study, recombinant MDK promoted the proliferation and migration of LGE cells.…”

Section: Resultsmentioning

confidence: 81%

Improvement of Radiotherapy-Induced Lacrimal Gland Injury by Induced Pluripotent Stem Cell-Derived Conditioned Medium via MDK and Inhibition of the p38/JNK Pathway

Zhang

Deng

Jiao

et al. 2014

IJMS

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Radiation therapy is the most widely used and effective treatment for orbital tumors, but it causes dry eye due to lacrimal gland damage. Induced pluripotent stem cell-derived conditioned medium (iPSC-CM) has been shown to rescue different types of tissue damage. The present study investigated the mechanism of the potential radioprotective effect of IPS cell-derived conditioned medium (iPSC-CM) on gamma-irradiation-induced lacrimal gland injury (RILI) in experimental mice. In this study, we found that iPSC-CM ameliorated RILI. iPSC-CM markedly decreased radiotherapy induced inflammatory processes, predominantly through suppressing p38/JNK signaling. Further signaling pathway analyses indicated that iPSC-CM could suppress Akt (Protein Kinase B, PKB) phosphorylation. High levels of midkine (MDK) were also found in iPSC-CM and could be involved in lacrimal gland regeneration by promoting cell migration and proliferation. Thus, our study indicates that inhibiting the p38/JNK pathway or increasing the MDK level might be a therapeutic target for radiation-induced lacrimal gland injury.

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Midkine-deficient mice delayed degeneration and regeneration after skeletal muscle injury

Cited by 25 publications

References 40 publications

Midkine in repair of the injured nervous system

Midkine in repair of the injured nervous system

The Need for a Consensus on the Locution “Central Nuclei” in Striated Muscle Myopathies

Improvement of Radiotherapy-Induced Lacrimal Gland Injury by Induced Pluripotent Stem Cell-Derived Conditioned Medium via MDK and Inhibition of the p38/JNK Pathway

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