Effects of ASC Application on Endplate Regeneration Upon Glycerol-Induced Muscle Damage

Rigon, Matteo; Hörner, Sarah Janice; Straka, Tatjana; Gretz, Norbert; Hafner, Mathias; Rudolf, Rüdiger

doi:10.3389/fnmol.2020.00107

Cited by 4 publications

(3 citation statements)

References 63 publications

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“…Glycerolinduced muscle injury significantly promoted levels of melatonin and Pax7 protein expression in TA muscle, and decreased muscle-specific differentiation markers MyHC, desmin and Pax7, as indicated by IHC staining (Figure 6I). Previous research has demonstrated that glycerol causes muscle necrosis through the loss of dystrophin protein marker expression in fibers [34]. In this study, immunofluorescent data showed that melatonin significantly reversed dystrophin protein expression in muscle fibers (Figure 6K).…”

Section: Melatonin Improves In Vivo Skeletal Muscle Dystrophysupporting

confidence: 65%

Melatonin improves muscle injury and differentiation by increasing Pax7 expression

Su¹,

Tsai²,

Chen³

et al. 2023

Int. J. Biol. Sci.

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A balance between muscle injury and regeneration is critical for sustaining muscle function during myogenesis. Melatonin is well recognized for its involvement in neuroprotective activities, immune system regulation and suppression of inflammatory responses. This study set out to provide evidence that melatonin improves muscle regeneration during skeletal muscle differentiation. We began with cloning a stable cell line expressing Pax7 knockdown C2C12 cells. We then investigated markers of muscle degradation and regeneration after treating growth medium and differentiated medium with melatonin. Bioinformatics analysis of RNA sequencing results revealed that melatonin regulates muscle differentiation and that Wnt cascades are involved in the mechanism of muscle differentiation. Screening of miRNA online databases revealed that miR-3475-3p is a specific binding site on Pax7 and acts as a negative regulator of Pax7, which is involved in melatonin-induced muscle differentiation. We then investigated the effects of melatonin treatment in the early stage of glycerol-induced skeletal muscle injury in mice. Rotarod performance, micro-computed tomography and immunohistochemistry findings showed that melatonin-induced increases in Pax7 expression rapidly rescue skeletal muscle differentiation and improve muscle fiber morphology in glycerol-induced muscle injury. Our data support the hypothesis that melatonin rapidly rescues skeletal muscle differentiation and the melatonin/Pax7 axis could therefore serve as an important therapeutic target to optimize muscle healing after injury.

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Section: Melatonin Improves In Vivo Skeletal Muscle Dystrophysupporting

confidence: 65%

Melatonin improves muscle injury and differentiation by increasing Pax7 expression

Su¹,

Tsai²,

Chen³

et al. 2023

Int. J. Biol. Sci.

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“…Accompanying data strongly support previous findings that MSCs are entrapped within the lungs, retained within the lung microvasculature, and rapidly cleared within the first one to three days ( 49 , 50 ). So far, we were only able to track MSCs within a tissue when locally applied to the tissue, e,g, skin or muscle ( 51 , 52 ). Given that we did not observe differences between i.v.…”

Section: Discussionmentioning

confidence: 99%

Clinical-grade human skin-derived ABCB5+ mesenchymal stromal cells exert anti-apoptotic and anti-inflammatory effects in vitro and modulate mRNA expression in a cisplatin-induced kidney injury murine model

Rendra,

Crigna,

Daniele

et al. 2024

Front. Immunol.

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Acute kidney injury (AKI) is characterized by a rapid reduction in renal function and glomerular filtration rate (GFR). The broadly used anti-cancer chemotherapeutic agent cisplatin often induces AKI as an adverse drug side effect. Therapies targeted at the reversal of AKI and its potential progression to chronic kidney disease or end-stage renal disease are currently insufficiently effective. Mesenchymal stromal cells (MSCs) possess diverse immunomodulatory properties that confer upon them significant therapeutic potential for the treatment of diverse inflammatory disorders. Human dermal MSCs expressing ATP-Binding Cassette member B5 (ABCB5) have shown therapeutic efficacy in clinical trials in chronic skin wounds or recessive dystrophic epidermolysis bullosa. In preclinical studies, ABCB5+ MSCs have also shown to reverse metabolic reprogramming in polycystic kidney cells, suggesting a capacity for this cell subset to improve also organ function in kidney diseases. Here, we aimed to explore the therapeutic capacity of ABCB5+ MSCs to improve renal function in a preclinical rat model of cisplatin-induced AKI. First, the anti-apoptotic and immunomodulatory capacity was compared against research-grade adipose stromal cells (ASCs). Then, cross-species immunomodulatory capacity was checked, testing first inhibition of mitogen-driven peripheral blood mononuclear cells and then modulation of macrophage function. Finally, therapeutic efficacy was evaluated in a cisplatin AKI model. First, ABCB5+ MSCs suppressed cisplatin-induced apoptosis of human conditionally-immortalized proximal tubular epithelial cells in vitro, most likely by reducing oxidative stress. Second, ABCB5+ MSCs inhibited the proliferation of either human or rat peripheral blood mononuclear cells, in the human system via the Indoleamine/kynurenine axis and in the murine context via nitric oxide/nitrite. Third, ABCB5+ MSCs decreased TNF-α secretion after lipopolysaccharide stimulation and modulated phagocytosis and in both human and rat macrophages, involving prostaglandin E2 and TGF-β1, respectively. Fourth, clinical-grade ABCB5+ MSCs grafted intravenously and intraperitoneally to a cisplatin-induced AKI murine model exerted modulatory effects on mRNA expression patterns toward an anti-inflammatory and pro-regenerative state despite an apparent lack of amelioration of renal damage at physiologic, metabolic, and histologic levels. Our results demonstrate anti-inflammatory and pro-regenerative effects of clinical grade ABCB5+ MSCs in vitro and in vivo and suggest potential therapeutic utility of this cell population for treatment or prevention of cisplatin chemotherapy-induced tissue toxicity.

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“…Impaired muscle regeneration is associated with muscle injuries or myopathy [ 66 , 67 ]. Previous research has shown that glycerol injury induces early fibrosis in rat skeletal muscle [ 68 ] and disrupts neuromuscular junctions in skeletal muscle [ 69 ]. Our in vivo results revealed the rapid appearance of early-stage muscle injury after glycerol treatment.…”

Section: Discussionmentioning

confidence: 99%

HMGB1 Promotes In Vitro and In Vivo Skeletal Muscle Atrophy through an IL-18-Dependent Mechanism

Tang

Chang

et al. 2022

Cells

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Skeletal muscle atrophy occurs due to muscle wasting or reductions in protein associated with aging, injury, and inflammatory processes. High-mobility group box-1 (HMGB1) protein is passively released from necrotic cells and actively secreted by inflammatory cells, and is implicated in the pathogenesis of various inflammatory and immune diseases. HMGB1 is upregulated in muscle inflammation, and circulating levels of the proinflammatory cytokine interleukin-18 (IL-18) are upregulated in patients with sarcopenia, a muscle-wasting disease. We examined whether an association exists between HMGB1 and IL-18 signaling in skeletal muscle atrophy. HMGB1-induced increases of IL-18 levels enhanced the expression of muscle atrophy markers and inhibited myogenic marker expression in C2C12 and G7 myoblast cell lines. HMGB1-induced increases of IL-18 production in C2C12 cells involved the RAGE/p85/Akt/mTOR/c-Jun signaling pathway. HMGB1 short hairpin RNA (shRNA) treatment rescued the expression of muscle-specific differentiation markers in murine C2C12 myotubes and in mice with glycerol-induced muscle atrophy. HMGB1 and IL-18 signaling was suppressed in the mice after HMGB1 shRNA treatment. These findings suggest that the HMGB1/IL-18 axis is worth targeting for the treatment of skeletal muscle atrophy.

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Effects of ASC Application on Endplate Regeneration Upon Glycerol-Induced Muscle Damage

Cited by 4 publications

References 63 publications

Melatonin improves muscle injury and differentiation by increasing Pax7 expression

Melatonin improves muscle injury and differentiation by increasing Pax7 expression

Clinical-grade human skin-derived ABCB5+ mesenchymal stromal cells exert anti-apoptotic and anti-inflammatory effects in vitro and modulate mRNA expression in a cisplatin-induced kidney injury murine model

HMGB1 Promotes In Vitro and In Vivo Skeletal Muscle Atrophy through an IL-18-Dependent Mechanism

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