Beneficial Effect of Mechanical Stimulation on the Regenerative Potential of Muscle-Derived Stem Cells Is Lost by Inhibiting Vascular Endothelial Growth Factor

Beckman, Sarah; Chen, Chien-Wen; Tang, Ying; Proto, Jonathan D.; Mlakar, Logan; Wang, Bing; Huard, Johnny

doi:10.1161/atvbaha.112.301166

Cited by 31 publications

(28 citation statements)

References 48 publications

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“…Interestingly, rats treated with CAR revealed a significantly higher VEGF immunoreactivity than the DOX-treated group. The mononuclear cells, especially activated T cells, enhance VEGF production in injured cardiac cells to promote healing [Beckman et al, 2013]. Thus, CAR could accelerate angiogenesis through induction of VEGF, which eventually could induce faster healing of the injured cardiac muscle.…”

Section: Discussionmentioning

confidence: 99%

Ameliorative Effect of Cardamom Aqueous Extract on Doxorubicin-Induced Cardiotoxicity in Rats

Gazia¹,

El-Magd²

2018

Cells Tissues Organs

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This study was conducted to evaluate the potential cardioprotective effect of cardamom (CAR) against myocardial injuries induced by doxorubicin (DOX) in rats through investigation of histological alterations and the associated oxidative stress, apoptosis, inflammation, and angiogenesis. This study included 30 adult male albino rats that were randomized to 3 groups (n = 10/group): group I (control), group II (DOX) rats injected with DOX (2.5 mg/kg body weight [BW] i.p.) every other day for 2 weeks, and group III (CAR+DOX) received CAR extract (200 mg/kg BW) orally for 3 weeks, and 1 week later (starting from the 2nd week) they were injected with DOX (2.5 mg/kg BW i.p.) every other day for 2 weeks. Rats treated with DOX alone exhibited notable myocardial damage (discontinuity and disorganization of cardiac muscle fibers, mononuclear cell infiltration, and apparent increases in collagen fiber deposition) accompanied by loss of function (revealed by elevated serum levels of lactate dehydrogenase, creatine kinase, and cardiac troponin), induction of oxidative stress (indicated by higher levels of nitric oxide and malondialdehyde, and lower levels of superoxide dismutase, catalase, and glutathione peroxidase), apoptosis (evidenced by high caspase 3 activity and immunostaining), and inflammation (marked by high cardiac NFκB level). However, administration of CAR not only ameliorated all deleterious effects of DOX but also induced angiogenesis, as indicated by a significant increase in VEGF immunoreactivity. These data indicate that CAR could relieve DOX-induced cardiotoxicity, at least in part, via reductions in oxidative stress, apoptosis, and inflammation and increased tissue regeneration via induction of angiogenesis. Therefore, CAR could be a promising cytoprotective agent against DOX cardiotoxicity.

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Section: Discussionmentioning

confidence: 99%

Ameliorative Effect of Cardamom Aqueous Extract on Doxorubicin-Induced Cardiotoxicity in Rats

Gazia¹,

El-Magd²

2018

Cells Tissues Organs

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“…Several strategies to enhance skeletal muscle regeneration through pericyte-mediated angiogenesis have also been proposed (Beckman et al, 2013). Human muscle pericytes form tight associations and interactions with endothelial cells in three-dimensional microvascular models in vitro, suggesting that they may be able to directly assist restoration of microvascular networks (C.W.…”

Section: Pericytes As Potential Cellular Therapeutic Agentsmentioning

confidence: 99%

Skeletal and cardiac muscle pericytes: Functions and therapeutic potential

Murray

Baily

Chen

et al. 2017

Pharmacology & Therapeutics

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Pericytes are periendothelial mesenchymal cells residing within the microvasculature. Skeletal muscle and cardiac pericytes are now recognized to fulfill an increasing number of functions in normal tissue homeostasis, including contributing to microvascular function by maintaining vessel stability and regulating capillary flow. In the setting of muscle injury, pericytes contribute to a regenerative microenvironment through release of trophic factors and by modulating local immune responses. In skeletal muscle, pericytes also directly enhance tissue healing by differentiating into myofibers. Conversely, pericytes have also been implicated in the development of disease states, including fibrosis, heterotopic ossication and calcification, atherosclerosis, and tumor angiogenesis. Despite increased recognition of pericyte heterogeneity, it is not yet clear whether specific subsets of pericytes are responsible for individual functions in skeletal and cardiac muscle homeostasis and disease.

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“…Previous work has provided evidence of compromised vasculature in the disease, including impaired angiogenesis [2] and decreased vascular density in the mdx mouse, the most widely used murine model of DMD [3], as well as in the golden-retriever model of muscular dystrophy [4]. As such, many groups have attempted to increase vascular density in dystrophic muscle by treating it with vascular endothelial growth factor (VEGF), a well-known and potent inducer of angiogenesis [5–7]. Histological markers of endothelial cells, cells that make up the luminal wall of vessels, demonstrate increased vascular density following VEGF treatment.…”

Section: Introductionmentioning

confidence: 99%

ANG1 treatment reduces muscle pathology and prevents a decline in perfusion in DMD mice

et al. 2017

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Vascular endothelial growth factor (VEGF) and other pro-angiogenic growth factors have been investigated to enhance muscle tissue perfusion and repair in Duchenne muscular dystrophy (DMD). Current understanding is limited by a lack of functional data following in vivo delivery of these growth factors. We previously used dynamic contrast-enhanced computed tomography to monitor disease progression in murine models of DMD, but no study to date has utilized this imaging technique to assess vascular therapy in a preclinical model of DMD. In the current study, we locally delivered VEGF and ANG1 alone or in combination to dystrophic hind limb skeletal muscle. Using functional imaging, we found the combination treatment as well as ANG1 alone prevented decline in muscle perfusion whereas VEGF alone had no effect compared to controls. These findings were validated histologically as demonstrated by increased alpha-smooth muscle actin-positive vessels in muscles that received either VEGF+ANG1 or ANG1 alone compared to the sham group. We further show that ANG1 alone slows progression of fibrosis compared to either sham or VEGF treatment. The findings from this study shed new light on the functional effects of vascular therapy and suggest that ANG1 alone may be a candidate therapy in the treatment of DMD.

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Beneficial Effect of Mechanical Stimulation on the Regenerative Potential of Muscle-Derived Stem Cells Is Lost by Inhibiting Vascular Endothelial Growth Factor

Cited by 31 publications

References 48 publications

Ameliorative Effect of Cardamom Aqueous Extract on Doxorubicin-Induced Cardiotoxicity in Rats

Ameliorative Effect of Cardamom Aqueous Extract on Doxorubicin-Induced Cardiotoxicity in Rats

Skeletal and cardiac muscle pericytes: Functions and therapeutic potential

ANG1 treatment reduces muscle pathology and prevents a decline in perfusion in DMD mice

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