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

Song, Juquan; Hornsby, Peter J.; Stanley, Morgan; AbdelFattah, Kareem R.; Wolf, Steven E.

doi:10.7243/2050-1218-3-3

Cited by 4 publications

(3 citation statements)

References 42 publications

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“…The same report showed that placement of extracellular matrix immediately after injury improved muscle function and brotic tissue remodeling, but there was no evidence of myo ber regeneration at day 28 [28]. We previously observed increased myogenesis in a cryoinjured mouse with UBM treatment [29]. In vitro, we found that UBM increases the protein expression of the proliferation marker PCNA in the mouse myoblast C2C12 cells, supporting a direct effect of UBM on muscle cells (Fig.…”

Section: Discussionsupporting

confidence: 70%

Improved Muscle Function After Injury with the Application of a Biological Decellularized Matrix

Ayadi¹,

Threlkeld²,

Wolf³

et al. 2020

Preprint

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Background: Skeletal muscle injury leads to loss of muscle function that lasts well into recovery and can be permanent. Application of the novel bio-scaffold termed porcine-derived urinary bladder matrix (UBM) has a potential benefit to mitigate injury through tissue regeneration. To date, findings of potential benefit in animal models were limited to short assessment times. The purpose of this study was to investigate whether UBM treatment 14 days after injury sustainably improves the recovery of muscle function in injured mice. Methods: C57BL/6 adult male mice received bilateral laceration injuries on the gastrocnemius (GN) muscle under anesthesia and were then treated with vehicle or 150 µg of UBM nanoparticles. Treatment was applied immediately after injury or 14 days later. Muscle isometric force was measured 60 days after injury. Previous time course analyses have shown that muscle function did not start to improve until after 42 days after injury. Therefore, we designed a second experiment to trace the time course of UBM effects on muscle function recovery by measuring the isometric muscle force at 49 and 90 days after injury. In vitro, we analyzed the effects of UBM on muscle cell proliferation and differentiation. Results: UBM promotes muscle cell proliferation and differentiation. Twitch (Pt), tetanic (Po) force and maximal fatigue were significantly decreased in the injured mice on day 60. Muscle fatigue maximum force significantly recovered when UBM treatment was applied 14 days after injury (p<0.05) but not when UBM was applied immediately after the injury. Time course analysis demonstrated that UBM improvement of Pt and Po was evident by day 49 after injury (p<0.05). However, no further muscle function improvement was observed on day 90. Conclusions: Delayed treatment with the UBM improves muscle function recovery following laceration injury starting 49 days after injury. These effects may be mediated by improvements in muscle cell proliferation and differentiation. This animal model is suitable to test other therapeutic strategies to improve muscle function after injury.

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Section: Discussionsupporting

confidence: 70%

Improved Muscle Function After Injury with the Application of a Biological Decellularized Matrix

Ayadi¹,

Threlkeld²,

Wolf³

et al. 2020

Preprint

Self Cite

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“…UBM has been shown to promote regeneration in soft tissue injury through a number of mechanisms. Remodeling UBM was shown to shift the local macrophage response in vivo towards a pro-healing, anti-inflammatory phenotype (13), and recruits progenitor cell proliferation and differentiation after traumatic muscle injury in mice (14). UBM similarly promoted muscle repair in patients with volumetric muscle loss in a clinical study (15).…”

Section: Introductionmentioning

confidence: 99%

Intra-articular Injection of Urinary Bladder Matrix Reduces Osteoarthritis Development

Jacobs

Rathod

Wolf

et al. 2016

AAPS J

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Micronized porcine urinary bladder matrix (UBM) is an extracellular matrix biomaterial that has immunomodulatory and pro-regenerative properties. The objective of this study was to assess the ability of UBM to alter disease progression in a mouse model of post-traumatic osteoarthritis (OA). Ten-week-old wild-type C57BL/6 male mice underwent anterior cruciate ligament transection (ACLT) to induce OA. Two weeks after ACLT, UBM (50 mg/mL) or saline was injected into the mouse joint. At 4 and 8 weeks post-ACLT, cartilage integrity was assessed using OARSI scoring of histology, pain was evaluated, and joints were harvested for quantitative RT-PCR analysis of cartilage-specific and inflammatory gene expression. UBM-treated animals showed improved cartilage integrity at 4 and 8 weeks and reduced pain at 4 weeks compared to saline-injected mice. Animals injected with UBM expressed higher levels of genes encoding structural cartilage proteins, such as collagen2α1 and aggrecan, as well as anti-inflammatory cytokines, including interleukins 10 and 4. UBM decreased cartilage degeneration in the murine ACLT model of OA, which may be due to reduced inflammation in the joint and maintenance of high expression levels of proteoglycans.

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“…This protein is required for the fusion of myogenic precursor cells to either new or previously existing fibers during the process of differentiation. In our previous study, we showed that MRFs, especially myogenin, increased in newly generated myotubes in mouse muscle following local cryoinjury (24). However, myogenin also contributes in the activation of muscle wasting.…”

Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Loss is Associated with TNF Mediated Insufficient Skeletal Myogenic Activation After Burn

Song

Saeman

Libero

et al. 2015

Shock

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Muscle loss accompanies severe burn; in this hyper-catabolic state, muscle undergoes atrophy through protein degradation and disuse. Muscle volume is related to the relative rates of cellular degradation and myogenesis. We hypothesize that muscle atrophy after injury is in part due to insufficient myogenesis associated with the hyper-inflammatory response. The aim of the study is to investigate the role of skeletal myogenesis and muscle cell homeostasis in response to severe burn. Twenty-eight male C57BL6 mice received 25% TBSA scald. Gluteus muscle from these animals was analysed at day 1, 3, 7 and 14 after injury. Six additional animals without burn served as controls. We showed muscle wet weight and protein content decreased at day 3 and 7 after burn, with elevated TNF mRNA expression (p< 0.05). Increased cell death was observed through TUNEL staining, and cleaved caspase-3 levels reached a peak in muscle lysate at day 3 (p < 0.05). The cell proliferation marker PCNA significantly increased after burn, associated with increased gene and protein expression of myogenesis markers Pax7 and myogenin. However, desmin mRNA expression and the ratio of desmin to PCNA protein expression significantly decreased at day 7 (p < 0.05). In vitro, the ratio of desmin to PCNA protein expression significantly decreased in C2C12 murine myoblasts after TNF-α stimulation for 24 hours. We showed that severe burn induces both increased cell death and proliferation. However, myogenesis does not counterbalance increased cell death after burn. Data suggest insufficient myogenesis might be associated with pro-inflammatory mediator TNF activity.

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

Cited by 4 publications

References 42 publications

Improved Muscle Function After Injury with the Application of a Biological Decellularized Matrix

Improved Muscle Function After Injury with the Application of a Biological Decellularized Matrix

Intra-articular Injection of Urinary Bladder Matrix Reduces Osteoarthritis Development

Skeletal Muscle Loss is Associated with TNF Mediated Insufficient Skeletal Myogenic Activation After Burn

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