Multiple and early hyperbaric oxygen treatments enhance muscle healing after muscle contusion injury: a pilot study

2021 ◽  
pp. 227-239c
Author(s):  
Naoki Yamamoto ◽  
◽  
Takuya Oyaizu ◽  
Kazuyoshi Yagishita ◽  
Mitsuhiro Enomoto ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Pilot Study ◽  
Satellite Cell ◽  
Hyperbaric Oxygen ◽  
Muscle Regeneration ◽  
Muscle Injury ◽  
Treatment Protocol ◽  
Optimal Number ◽  
Optimal Timing ◽  
Contusion Injury

Background: The optimal timing of hyperbaric oxygen (HBO2) treatments for the best recovery following muscle injury has yet to be determined. Thus, the optimal number and timing of HBO2 treatments for maximal muscle regeneration were explored. Methods: The HBO2 treatment protocol consisted of 2.5 ATA 100% oxygen for 120 minutes. Muscle-injured rats were randomized to one of 10 groups: single HBO2 treatment immediately after injury (HBO 1T day 0), one day (HBO 1T day 1), three days (HBO 1T day 3) and five days (HBO 1T day 5) after injury; three HBO2 treatments from immediately after injury to two days after injury (HBO 3T day 0-2), from one to three days after injury (HBO 3T day 1-3), from three to five days after injury (HBO 3T day 3-5), from five to seven days after injury (HBO 3T day 5-7); five daily HBO2 treatments (HBO 5T); and no treatment (NT). Results: HBO 5T and HBO 3T day 0-2, days 1-3 and days 3-5 significantly promoted CD206-positive cell infiltration, satellite cell differentiation and muscle regeneration compared to the NT group. Conclusion: Five HBO2 treatments and three HBO2 treatments within three days of injury promote muscle regeneration.

Enhancement of satellite cell differentiation and functional recovery in injured skeletal muscle by hyperbaric oxygen treatment

2014 ◽  
Vol 116 (2) ◽  
pp. 149-155 ◽  
Author(s):  
Masaki Horie ◽  
Mitsuhiro Enomoto ◽  
Manabu Shimoda ◽  
Atsushi Okawa ◽  
Shumpei Miyakawa ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Hyperbaric Oxygen ◽  
Functional Recovery ◽  
Muscle Regeneration ◽  
Muscle Injury ◽  
Muscle Fibers ◽  
Maximum Force ◽  
Pcr Analysis ◽  
Regulatory Factor

Recently, the use of hyperbaric oxygen (HBO) treatments by elite athletes to accelerate recovery from muscle injuries has become increasingly popular. However, the mechanism of promoting muscle regeneration under HBO conditions has not yet been defined. In this study, we investigated whether HBO treatments promoted muscle regeneration and modulated muscle regulatory factor expression in a rat skeletal muscle injury model. Muscle injury was induced by injecting cardiotoxin (CTX) into the tibialis anterior (TA) muscles. As the HBO treatment, rats were placed in an animal chamber with 100% oxygen under 2.5 atmospheres absolute for 2 h/day, 5 days/wk for 2 wk. We then performed histological analyses, measured the maximum force-producing capacity of the regenerating muscle fibers, and performed quantitative RT-PCR analysis of muscle regulatory factor mRNAs. The cross-sectional areas and maximum force-producing capacity of the regenerating muscle fibers were increased by HBO treatment after injury. The mRNA expression of MyoD, myogenin, and IGF-1 increased significantly in the HBO group at 3 and 5 days after injury. The number of Pax7+/MyoD+, Pax7−/MyoD+, and Pax7+/BrdU+-positive nuclei was increased by HBO treatment. In this study, we demonstrated that HBO treatment accelerated satellite cell proliferation and myofiber maturation in rat muscle that was injured by a CTX injection. These results suggest that HBO treatment accelerates healing and functional recovery after muscle injury.

scholarly journals Effects of intramuscular administration of 1α,25(OH)2D3 during skeletal muscle regeneration on regenerative capacity, muscular fibrosis, and angiogenesis

2016 ◽  
Vol 120 (12) ◽  
pp. 1381-1393 ◽  
Author(s):  
Ratchakrit Srikuea ◽  
Muthita Hirunsai
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Protein Synthesis ◽  
Cell Differentiation ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Fiber Type ◽  
Fiber Formation ◽  
Skeletal Muscle Regeneration ◽  
Type Composition

The recent discovery of the vitamin D receptor (VDR) in regenerating muscle raises the question regarding the action of vitamin D3 on skeletal muscle regeneration. To investigate the action of vitamin D3 on this process, the tibialis anterior muscle of male C57BL/6 mice (10 wk of age) was injected with 1.2% BaCl2 to induce extensive muscle injury. The bioactive form of vitamin D3 [1α,25(OH)2D3] was administered daily via intramuscular injections during the regenerative phase (days 4-7 postinjury). Physiological and supraphysiological doses of 1α,25(OH)2D3 relative to 1 μg/kg muscle wet weight and mouse body weight were investigated. Muscle samples were collected on day 8 postinjury to examine proteins related to vitamin D3 metabolism (VDR, CYP24A1, and CYP27B1), satellite cell differentiation and regenerative muscle fiber formation [myogenin and embryonic myosin heavy chain (EbMHC)], protein synthesis signaling (Akt, p70 S6K1, 4E-BP1, and myostatin), fiber-type composition (fast and slow MHCs), fibrous formation (vimentin), and angiogenesis (CD31). Administration of 1α,25(OH)2D3 at physiological and supraphysiological doses enhanced VDR expression in regenerative muscle. Moreover, CYP24A1 and vimentin expression was increased, accompanying decreased myogenin and EbMHC expression at the supraphysiological dose. However, there was no change in CYP27B1, Akt, p70 S6K1, 4E-BP1, myostatin, fast and slow MHCs, or CD31 expression at any dose investigated. Taken together, administration of 1α,25(OH)2D3 at a supraphysiological dose decreased satellite cell differentiation, delayed regenerative muscle fiber formation, and increased muscular fibrosis. However, protein synthesis signaling, fiber-type composition, and angiogenesis were not affected by either 1α,25(OH)2D3 administration at a physiological or supraphysiological dose.

scholarly journals Reduced Dnmt3a increases Gdf5 expression with suppressed satellite cell differentiation and impaired skeletal muscle regeneration

2018 ◽  
Vol 32 (3) ◽  
pp. 1452-1467 ◽  
Author(s):  
Yukino Hatazawa ◽  
Yusuke Ono ◽  
Yuma Hirose ◽  
Sayaka Kanai ◽  
Nobuharu L. Fujii ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Differentiation ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration

scholarly journals MASTR directs MyoD-dependent satellite cell differentiation during skeletal muscle regeneration

2012 ◽  
Vol 26 (2) ◽  
pp. 190-202 ◽  
Author(s):  
M. H. Mokalled ◽  
A. N. Johnson ◽  
E. E. Creemers ◽  
E. N. Olson
Keyword(s):  
Skeletal Muscle ◽  
Cell Differentiation ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration

scholarly journals Sulfs are regulators of growth factor signaling for satellite cell differentiation and muscle regeneration

2007 ◽  
Vol 311 (2) ◽  
pp. 464-477 ◽  
Author(s):  
Aliete Langsdorf ◽  
Anh-Tri Do ◽  
Marion Kusche-Gullberg ◽  
Charles P. Emerson Jr. ◽  
Xingbin Ai
Keyword(s):  
Cell Differentiation ◽  
Growth Factor ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Growth Factor Signaling

scholarly journals Necdin mediates skeletal muscle regeneration by promoting myoblast survival and differentiation

2007 ◽  
Vol 179 (2) ◽  
pp. 305-319 ◽  
Author(s):  
Daniela Deponti ◽  
Stéphanie François ◽  
Silvia Baesso ◽  
Clara Sciorati ◽  
Anna Innocenzi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transgenic Mice ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Muscle Injury ◽  
Muscle Fibers ◽  
Skeletal Muscle Regeneration ◽  
Muscle Degeneration ◽  
Wild Type ◽  
Cell Type

Regeneration of muscle fibers that are lost during pathological muscle degeneration or after injuries is sustained by the production of new myofibers. An important cell type involved in muscle regeneration is the satellite cell. Necdin is a protein expressed in satellite cell–derived myogenic precursors during perinatal growth. However, its function in myogenesis is not known. We compare transgenic mice that overexpress necdin in skeletal muscle with both wild-type and necdin null mice. After muscle injury the necdin null mice show a considerable defect in muscle healing, whereas mice that overexpress necdin show a substantial increase in myofiber regeneration. We also find that in muscle, necdin increases myogenin expression, accelerates differentiation, and counteracts myoblast apoptosis. Collectively, these data clarify the function and mechanism of necdin in skeletal muscle and show the importance of necdin in muscle regeneration.

scholarly journals Noggin Combined With Dental Pulp Stem Cells Repair Muscle Injury Through Smad/Pax7 Signaling Pathway

2021 ◽  
Author(s):  
Meng-Han Zhang ◽  
Li-Ming Yu ◽  
Wei-Hua Zhang ◽  
Jia-Jia Deng ◽  
Bing-Jing Sun ◽  
...  
Keyword(s):  
Stem Cells ◽  
Signaling Pathway ◽  
Satellite Cell ◽  
Morphometric Analysis ◽  
Muscle Regeneration ◽  
Dental Pulp ◽  
Tibialis Anterior ◽  
Muscle Injury ◽  
Myogenic Differentiation ◽  
Tibialis Anterior Muscle

Abstract Background: A proper stem cell source is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an available source for the treatment of muscle injury due to their high reproductive and differential activities. However, the application of DPSCs in muscle regeneration is incompletely understood. Noggin, a secreted BMP antagonist promoted by Wnt-1, is required for embryonic myogenesis. Our research is to study whether Noggin can promote myogenic differentiation of DPSCs, and then to investigate the repair effect of Noggin combined with DPSCs in muscle injury.Methods: DPSCs were treated with Noggin to induce myogenic differentiation in vitro. The levels of myogenic markers (MyoD, Desmin, MRF4 and MyHC), and satellite cell markers (Pax3, Pax7, Six1 and Eya2) were detected during this process. Next, we blocked the effect of Noggin by adding BMP, and Samd phosphorylation level was tested. Then, we implanted Noggin-pretreated DPSC combined Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML). After 30-day recovery, morphometric analysis of the tibialis anterior muscle was performed.Results: Noggin effectively increased myotube formation in DPSCs. We also found Noggin accelerated the skeletal myogenic differentiation of DPSCs and promote Pax7+ satellite-like cell generation. These satellite-like cells had the capacity to generate myofibers and could self-renew. Pax7 and Pax3 levels were repressed when blocked the effect of Noggin by adding BMP, and Noggin eliminated the level of BMP/Smad phosphorylation. This suggested that Noggin facilitated the skeletal myogenic differentiation of DPSCs via Smad/Pax7 pathway. Morphometric analysis of muscle cross-sections revealed that DPSCs therapy could increase repair size and decrease scar tissue in tibialis anterior muscle of VML. Moreover, Noggin-treated DPSCs can benefit to Pax7+ satellite cell pool and promote muscle regeneration. Conclusions: This work reveals that Noggin can promote the generation of satellite-like cells for the myogenic process in DPSCs through Smad/Pax7 signaling pathway, and these satellite-like cells bioconstructs might possess a relatively fast capacity to regenerate for muscle injury.

P.19.9 Gαi2 signaling is required for skeletal muscle regeneration and for satellite cell differentiation

2013 ◽  
Vol 23 (9-10) ◽  
pp. 838
Author(s):  
G.C. Minetti ◽  
J.N. Feige ◽  
F. Bombard ◽  
L. Birnbaumer ◽  
D.J. Glass ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Differentiation ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration

scholarly journals Vitamin D Promotes Skeletal Muscle Regeneration and Mitochondrial Health

2021 ◽  
Vol 12 ◽  
Author(s):  
Christine M. Latham ◽  
Camille R. Brightwell ◽  
Alexander R. Keeble ◽  
Brooke D. Munson ◽  
Nicholas T. Thomas ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Muscle Damage ◽  
Muscle Regeneration ◽  
Muscle Injury ◽  
Time Course ◽  
Active Form ◽  
Skeletal Muscle Regeneration ◽  
Optimal Timing

Vitamin D is an essential nutrient for the maintenance of skeletal muscle and bone health. The vitamin D receptor (VDR) is present in muscle, as is CYP27B1, the enzyme that hydroxylates 25(OH)D to its active form, 1,25(OH)D. Furthermore, mounting evidence suggests that vitamin D may play an important role during muscle damage and regeneration. Muscle damage is characterized by compromised muscle fiber architecture, disruption of contractile protein integrity, and mitochondrial dysfunction. Muscle regeneration is a complex process that involves restoration of mitochondrial function and activation of satellite cells (SC), the resident skeletal muscle stem cells. VDR expression is strongly upregulated following injury, particularly in central nuclei and SCs in animal models of muscle injury. Mechanistic studies provide some insight into the possible role of vitamin D activity in injured muscle. In vitro and in vivo rodent studies show that vitamin D mitigates reactive oxygen species (ROS) production, augments antioxidant capacity, and prevents oxidative stress, a common antagonist in muscle damage. Additionally, VDR knockdown results in decreased mitochondrial oxidative capacity and ATP production, suggesting that vitamin D is crucial for mitochondrial oxidative phosphorylation capacity; an important driver of muscle regeneration. Vitamin D regulation of mitochondrial health may also have implications for SC activity and self-renewal capacity, which could further affect muscle regeneration. However, the optimal timing, form and dose of vitamin D, as well as the mechanism by which vitamin D contributes to maintenance and restoration of muscle strength following injury, have not been determined. More research is needed to determine mechanistic action of 1,25(OH)D on mitochondria and SCs, as well as how this action manifests following muscle injury in vivo. Moreover, standardization in vitamin D sufficiency cut-points, time-course study of the efficacy of vitamin D administration, and comparison of multiple analogs of vitamin D are necessary to elucidate the potential of vitamin D as a significant contributor to muscle regeneration following injury. Here we will review the contribution of vitamin D to skeletal muscle regeneration following injury.

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