Comparative evaluation of IGF-I gene transfer and IGF-I protein administration for enhancing skeletal muscle regeneration after injury

Schertzer, Jonathan D.; Lynch, Gordon S.

doi:10.1038/sj.gt.3302817

Cited by 67 publications

(60 citation statements)

References 40 publications

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“…10 A comparative study of IGF-1 gene and protein delivery clearly shows superior functional effects of gene delivery approach. 11 Significant progress has been made for enhanced and localized overexpression of IGF-1 in the heart using both viral and nonviral vectors. 12,13 IGF-1 gene delivery has also been combined with other growth factors and with heart cell therapy to promote donor cell survival, engraftment, and differentiation as a part of the multimodal therapy approach.…”

mentioning

confidence: 99%

IGF-1–Overexpressing Mesenchymal Stem Cells Accelerate Bone Marrow Stem Cell Mobilization via Paracrine Activation of SDF-1α/CXCR4 Signaling to Promote Myocardial Repair

Haider

Jiang

Idris

et al. 2008

Circulation Research

394

211

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mentioning

confidence: 99%

IGF-1–Overexpressing Mesenchymal Stem Cells Accelerate Bone Marrow Stem Cell Mobilization via Paracrine Activation of SDF-1α/CXCR4 Signaling to Promote Myocardial Repair

Haider

Jiang

Idris

et al. 2008

Circulation Research

394

211

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“…13 In brief, mice were anesthetized deeply with sodium pentobarbitone (60 mg/kg i.p., Nembutal; Rhone Merieux, Pinkenba, QLD, Australia), and an adequate depth of anesthesia was maintained, such that the mice were unresponsive to tactile stimulation. The right hindlimb was shaved, and a small portion of the anterior aspect of the TA muscle was surgically exposed.…”

Section: Myotoxic Injury Of Tibialis Anterior Musclesmentioning

confidence: 99%

“…8,9 The importance of IGF-I in skeletal muscle regeneration has been demonstrated in transgenic mice, where overexpression of IGF-I localized to skeletal muscle maintained regenerative capacity in aged mice 10 and reduced the dystrophic pathology in mdx mice, an animal model of Duchenne muscular dystrophy. 11,12 In addition, we have shown previously that exogenous administration of recombinant human IGF-I (rhIGF-I) increased the rate of functional recovery after myotoxic injury 13 and improved the dystrophic pathology in mdx mice. 14 -16 Although rhIGF-I administration and transgenic IGF-I overexpression have beneficial effects on skeletal muscle, their mechanism of action seems to be vastly different.…”

mentioning

confidence: 99%

Modulation of Insulin-like Growth Factor (IGF)-I and IGF-Binding Protein Interactions Enhances Skeletal Muscle Regeneration and Ameliorates the Dystrophic Pathology in mdx Mice

Schertzer

Gehrig

Ryall

et al. 2007

The American Journal of Pathology

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Administration of recombinant human insulin-like growth factor-I (rhIGF-I) has beneficial effects in animal models of muscle injury and muscular dystrophy. However, the results of these studies may have been confounded by interactions of rhIGF-I with endogenous IGF-binding proteins (IGFBPs). To date, no study has examined whether inhibiting IGFBP interactions with endogenous IGF-I can improve muscle fiber regeneration or muscular pathologies. We tested the hypothesis that reducing IGFBP interactions with endogenous IGF-I would enhance muscle regeneration after myotoxic injury and improve the dystrophic pathology in mdx mice. We administered an IGF-I aptamer (NBI-31772; 6 mg/kg per day, continuous infusion) to C57BL/10 mice undergoing regeneration after myotoxic injury or to mdx dystrophic mice. NBI-31772 binds all six IGFBPs with high affinity and releases "free" endogenous IGF-I. NBI-31772 treatment increased the rate of functional repair in fast-twitch tibialis anterior muscles after notexin-induced injury as evidenced by an increase in maximum force producing capacity (P o ) at 10 days after injury. In contrast, NBI-31772 administration for 28 days did not alter P o of extensor digitorum longus (EDL) and soleus muscles or normalized force of diaphragm muscle strips from mdx mice. Although IG-FBP inhibition reduced the susceptibility of the fasttwitch EDL and the diaphragm muscle to contractionmediated damage, it increased muscle fatigability during repeated maximal contractions. Skeletal muscle injury and degeneration can result from trauma caused by mechanical (laceration, crush, strain), chemical (myotoxin), or metabolic (temperature) factors and is a major contributor to the etiology of myopathies, such as the muscular dystrophies. Although muscle fibers have an inherent capacity to regenerate when damaged, the regeneration process is often slow, inefficient, and incomplete with respect to functional restoration.

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“…doi: 10.7243/2050-1218-3-3 such as growth factors with the aim of recovering body function, and have been applied in clinical studies of skeletal muscle regeneration in trauma patients [7][8][9]. A side from the viability of the cell itself, the extracellular environment is considered one of the most important factors for cell growth into functional tissue.…”

Section: Introductionmentioning

confidence: 99%

Porcine urinary bladder extracellular matrix activates skeletal myogenesis in mouse muscle cryoinjury

Song¹,

Hornsby²,

Stanley³

et al. 2014

J Regen Med Tissue Eng

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Background: Accelerated muscle regeneration is highly desirable after direct injury in trauma patients. Though the advantage of extracellular matrix extracted from porcine urine bladder (UBM) on tissue regeneration is feasible, the mechanisms by which skeletal myogenesis is improved are not clear. The current study aim was to determine whether UBM affects skeletal satellite cells during muscle repair after cryoinjury. Methods: RAG2-/-, γc -/-mice underwent bilateral gluteus muscle cryoinjury under general anesthesia. 200µg UBM suspended in 20 µl of Matrigel solution was implanted on one side of the wound intramuscularly, and 20µl of vehicle was applied on the contralateral side as a sham treatment. Five animals without any operation served as baseline. Mice were sacrificed from days 1 to 28 after injury for muscle tissue collection. Tissue morphology was estimated via H&E staining. Satellite cell proliferation was examined by immunofluorescence staining and western blot. Myogenesis markers were assessed by qPCR. Results: H&E staining results showed that muscle regeneration area increased in both sham and UBM treated muscles following injury. The number of regenerating myotubes was significantly higher in UBM treated tissue at 28 days (p<0.05, vs. sham group). Both Pax7 + and Ki-67 + satellite cell number significantly increased in muscle with UBM treatment compared to sham treated muscles (p<0.05). Protein levels of proliferating cell nuclear antigen (PCNA) were greater in muscle with UBM treatment at day 14 and 28 (p<0.05). MyoD1 and myogenin mRNA levels were also significantly higher in UBM treated animal muscle at day 28 (p<0.05). Conclusion: UBM treatment increased skeletal satellite cell proliferation and myogenic differentiation at 28 days after local muscle injury.

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Comparative evaluation of IGF-I gene transfer and IGF-I protein administration for enhancing skeletal muscle regeneration after injury

Cited by 67 publications

References 40 publications

IGF-1–Overexpressing Mesenchymal Stem Cells Accelerate Bone Marrow Stem Cell Mobilization via Paracrine Activation of SDF-1α/CXCR4 Signaling to Promote Myocardial Repair

IGF-1–Overexpressing Mesenchymal Stem Cells Accelerate Bone Marrow Stem Cell Mobilization via Paracrine Activation of SDF-1α/CXCR4 Signaling to Promote Myocardial Repair

Modulation of Insulin-like Growth Factor (IGF)-I and IGF-Binding Protein Interactions Enhances Skeletal Muscle Regeneration and Ameliorates the Dystrophic Pathology in mdx Mice

Porcine urinary bladder extracellular matrix activates skeletal myogenesis in mouse muscle cryoinjury

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