Effects of SW033291 on the myogenesis of muscle-derived stem cells and muscle regeneration

Dong, Yuanqiang; Li, Yuan; Zhang, Chuan; Chen, Haibin; Liu, Lijia; Chen, Simeng

doi:10.1186/s13287-020-1574-5

Cited by 8 publications

(5 citation statements)

References 67 publications

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“…In vitro , SW033291 enhanced myogenic differentiation and myotube formation via upregulating a series of myogenic markers with an activated PI3K/Akt pathway involved. Additionally, SW033291 incorporating the compound with MDSCs in fibrin gel significantly facilitates myofiber formation within the defect region with mild immune response, less fibrosis, and sufficient vascularization 143 . Together with these findings, PGE2 can facilitate the proliferation and differentiation of MDSCs.…”

Section: The Role Of Pge2 On Organ Repair and Regenerationmentioning

confidence: 99%

“…Researchers have successively clarified the repair capabilities of SW033291 in different injury models including liver resection 80 , I/R renal injury 22 , intestinal injury 80 , bone marrow transplantation 80 , 155 , 156 , bone marrow failure 166 , muscle defect 143 , or muscle aging 3 , which we have mentioned above. In fact, SW033291 was also explored in aspects of cervical ripening, drug-induced kidney injury, and pulmonary fibrosis.…”

Section: Pge2-based Therapeutic Strategies For Tissue Regenerationmentioning

confidence: 99%

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Role of prostaglandin E2 in tissue repair and regeneration

et al. 2021

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Tissue regeneration following injury from disease or medical treatment still represents a challenge in regeneration medicine. Prostaglandin E2 (PGE2), which involves diverse physiological processes via E-type prostanoid (EP) receptor family, favors the regeneration of various organ systems following injury for its capabilities such as activation of endogenous stem cells, immune regulation, and angiogenesis. Understanding how PGE2 modulates tissue regeneration and then exploring how to elevate the regenerative efficiency of PGE2 will provide key insights into the tissue repair and regeneration processes by PGE2. In this review, we summarized the application of PGE2 to guide the regeneration of different tissues, including skin, heart, liver, kidney, intestine, bone, skeletal muscle, and hematopoietic stem cell regeneration. Moreover, we introduced PGE2-based therapeutic strategies to accelerate the recovery of impaired tissue or organs, including 15-hydroxyprostaglandin dehydrogenase (15-PGDH) inhibitors boosting endogenous PGE2 levels and biomaterial scaffolds to control PGE2 release.

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Section: The Role Of Pge2 On Organ Repair and Regenerationmentioning

confidence: 99%

Section: Pge2-based Therapeutic Strategies For Tissue Regenerationmentioning

confidence: 99%

Role of prostaglandin E2 in tissue repair and regeneration

et al. 2021

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“…17 Subsequent studies demonstrated that SW033291 promotes splenic niche hematopoietic regeneration, bone regeneration, and skeletal muscle regeneration. [26][27][28][29] Other observed beneficial effects of SW033291 include suppression of pulmonary fibrosis and protection from renal injury. 18,19,[30][31][32] Our findings establish a previously unrecognized cardioprotective action of SW033291, and further highlight the potential of 15-PGDH inhibitors to block fibrosis across organ systems.…”

Section: -Pgdh Inhibition As a Potential Therapy For Cardiac Diseasementioning

confidence: 99%

Inhibition of Eicosanoid Degradation Mitigates Fibrosis of the Heart

Rubino

Travers

Headrick

et al. 2023

Circulation Research

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BACKGROUND: Organ fibrosis due to excessive production of extracellular matrix by resident fibroblasts is estimated to contribute to >45% of deaths in the Western world, including those due to cardiovascular diseases such as heart failure. Here, we screened for small molecule inhibitors with a common ability to suppress activation of fibroblasts across organ systems. METHODS: High-content imaging of cultured cardiac, pulmonary, and renal fibroblasts was used to identify nontoxic compounds that blocked induction of markers of activation in response to the profibrotic stimulus, transforming growth factor-β1. SW033291, which inhibits the eicosanoid-degrading enzyme, 15-hydroxyprostaglandin dehydrogenase, was chosen for follow-up studies with cultured adult rat ventricular fibroblasts and human cardiac fibroblasts (CFs), and for evaluation in mouse models of cardiac fibrosis and diastolic dysfunction. Additional mechanistic studies were performed with CFs treated with exogenous eicosanoids. RESULTS: Nine compounds, including SW033291, shared a common ability to suppress transforming growth factor-β1–mediated activation of cardiac, pulmonary, and renal fibroblasts. SW033291 dose-dependently inhibited transforming growth factor-β1–induced expression of activation markers (eg, α-smooth muscle actin and periostin) in adult rat ventricular fibroblasts and normal human CFs, and reduced contractile capacity of the cells. Remarkably, the 15-hydroxyprostaglandin dehydrogenase inhibitor also reversed constitutive activation of fibroblasts obtained from explanted hearts from patients with heart failure. SW033291 blocked cardiac fibrosis induced by angiotensin II infusion and ameliorated diastolic dysfunction in an alternative model of systemic hypertension driven by combined uninephrectomy and deoxycorticosterone acetate administration. Mechanistically, SW033291-mediated stimulation of extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling was required for SW033291 to block CF activation. Of the 12 exogenous eicosanoids that were tested, only 12-hydroxyeicosatetraenoic acid, which signals through the G protein-coupled receptor, GPR31, recapitulated the suppressive effects of SW033291 on CF activation. CONCLUSIONS: Inhibition of degradation of eicosanoids, arachidonic acid-derived fatty acids that signal through G protein-coupled receptors, is a potential therapeutic strategy for suppression of pathological organ fibrosis. In the heart, we propose that 15-hydroxyprostaglandin dehydrogenase inhibition triggers CF-derived autocrine/paracrine signaling by eicosanoids, including 12-hydroxyeicosatetraenoic acid, to stimulate extracellular signal-regulated kinase 1/2 and block conversion of fibroblasts into activated cells that secrete excessive amounts of extracellular matrix and contribute of heart failure pathogenesis.

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“…In the field of TE to treat volumetric muscle loss defects, MDSCs, which adhere to scaffolds, can also play an important role, which has presented promising prospects for translating this method into the treatment of severe sarcopenia [ 77 , 78 ]. Dong et al [ 79 ] concluded that SW033291, a small-molecule inhibitor targeting 15-hydroxyprostaglandin dehydrogenase that subsequently elevates the production of prostaglandin E2 (PGE2), could promote the myogenic differentiation of MDSCs, which led to the repair of large skeletal muscle defects. Tamaki et al [ 80 , 81 ] successfully formed cardiomyocytes after myocardial infarction with the help of CD34( +)/CD45(−) MDSCs and suggested the possible future use of these cells for cardiac muscle repair in infarcted areas.…”

Section: Mdscs and Sarcopeniamentioning

confidence: 99%

The role and therapeutic potential of stem cells in skeletal muscle in sarcopenia

et al. 2022

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Sarcopenia is a common age-related skeletal muscle disorder featuring the loss of muscle mass and function. In regard to tissue repair in the human body, scientists always consider the use of stem cells. In skeletal muscle, satellite cells (SCs) are adult stem cells that maintain tissue homeostasis and repair damaged regions after injury to preserve skeletal muscle integrity. Muscle-derived stem cells (MDSCs) and SCs are the two most commonly studied stem cell populations from skeletal muscle. To date, considerable progress has been achieved in understanding the complex associations between stem cells in muscle and the occurrence and treatment of sarcopenia. In this review, we first give brief introductions to sarcopenia, SCs and MDSCs. Then, we attempt to untangle the differences and connections between these two types of stem cells and further elaborate on the interactions between sarcopenia and stem cells. Finally, our perspectives on the possible application of stem cells for the treatment of sarcopenia in future are presented. Several studies emerging in recent years have shown that changes in the number and function of stem cells can trigger sarcopenia, which in turn leads to adverse influences on stem cells because of the altered internal environment in muscle. A better understanding of the role of stem cells in muscle, especially SCs and MDSCs, in sarcopenia will facilitate the realization of novel therapy approaches based on stem cells to combat sarcopenia.

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Effects of SW033291 on the myogenesis of muscle-derived stem cells and muscle regeneration

Cited by 8 publications

References 67 publications

Role of prostaglandin E2 in tissue repair and regeneration

Role of prostaglandin E2 in tissue repair and regeneration

Inhibition of Eicosanoid Degradation Mitigates Fibrosis of the Heart

The role and therapeutic potential of stem cells in skeletal muscle in sarcopenia

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