Regulation of Muscle Stem Cell Functions: A Focus on the p38 MAPK Signaling Pathway

Segalés, Jessica; Perdiguero, Eusebio; Muñoz‐Cánoves, Pura

doi:10.3389/fcell.2016.00091

Cited by 162 publications

(127 citation statements)

References 156 publications

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“…Compared to wild type controls, the fraction of cells in SC in Pax7 −/− mice was markedly diminished at the neonatal stage (Fig.2f, g) and progressively declined by 3 weeks of age (Fig.2f, g). At birth, the decrease in Pax7 −/− cells within the SC population was paralleled by an increase in the fraction of cells in P1 (Fig.2g), and was accompanied by alteration of a key signaling pathway involved in the regulation of myogenic commitment 23–26 , as shown by increased phosphorylation of MAPKAPK2 (Supplementary Fig.2a), a direct target of p38α/β MAPK 27 . In one rare Pax7 −/− mouse that survived to three weeks of age, a majority of α7integrin + /CD9 + muscle cells were in P2 and P3.…”

Section: Resultsmentioning

confidence: 96%

High-resolution myogenic lineage mapping by single-cell mass cytometry

et al. 2017

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Muscle regeneration is a dynamic process during which cell state and identity change over time. A major roadblock has been a lack of tools to resolve a myogenic progression in vivo. Here we capitalize on a transformative technology, single-cell mass cytometry (CyTOF), to identify in vivo skeletal muscle stem cell and previously unrecognized progenitor populations that precede differentiation. We discovered two cell surface markers, CD9 and CD104, whose combined expression enabled in vivo identification and prospective isolation of stem and progenitor cells. Data analysis using the X-shift algorithm paired with single-cell force directed layout visualization, defined a molecular signature of the activated stem cell state (CD44+/CD98+/MyoD+) and delineated a myogenic trajectory during recovery from acute muscle injury. Our studies uncover the dynamics of skeletal muscle regeneration in vivo and pave the way for the elucidation of the regulatory networks that underlie cell-state transitions in muscle diseases and aging.

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Section: Resultsmentioning

confidence: 96%

High-resolution myogenic lineage mapping by single-cell mass cytometry

et al. 2017

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“…Losmapimod was initially developed as a p38 MAPK inhibitor intended for treatment of cardiovascular disease and COPD. P38 MAPKs are a class of mitogen-activated protein kinases that are responsive to stress stimuli, such as cytokines, ultraviolet irradiation, and heat shock, and are involved in cell differentiation, apoptosis and autophagy (Segales et al, 2016). Four p38 MAPKs have been identified, including p38-α (MAPK14), -β (MAPK11), -γ (MAPK12/ERK6), and -δ (MAPK13/ SAPK4).…”

Section: Down-regulation Of P38 Mapks Does Not Affect the Anti-lasv Amentioning

confidence: 99%

Identification of a clinical compound losmapimod that blocks Lassa virus entry

et al. 2019

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A B S T R A C TLassa virus (LASV) causes Lassa hemorrhagic fever in humans and poses a significant threat to public health in West Africa. Current therapeutic treatments for Lassa fever are limited, making the development of novel countermeasures an urgent priority. In this study, we identified losmapimod, a p38 mitogen-activated protein kinase (MAPK) inhibitor, from 102 screened compounds as an inhibitor of LASV infection. Losmapimod exerted its inhibitory effect against LASV after p38 MAPK down-regulation, and, interestingly, had no effect on other arenaviruses capable of causing viral hemorrhagic fever. Mechanistic studies showed that losmapimod inhibited LASV entry by affecting the stable signal peptide (SSP)-GP2 subunit interface of the LASV glycoprotein, thereby blocking pH-dependent viral fusion. As an aryl heteroaryl bis-carboxyamide derivative, losmapimod represents a novel chemical scaffold with anti-LASV activity, and it provides a new lead structure for the future development of LASV fusion inhibitors.

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“…p38-MAPK is one of the activations of mitogen-activated protein kinase (MAPK) families and acts as intracellular signal transduction pathway [13,26]. p38-MAPK is implicated in the oxidative stress stimulus-induced Reactive oxygen species (ROS) production [27,28].…”

Section: Discussionmentioning

confidence: 99%

Apocynin Attenuates Cobalt Chloride-Induced Pheochromocytoma Cell Apoptosis by Inhibiting P38-MAPK/Caspase-3 Pathway

Liu

Zhu

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Apocynin, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, has been identified as a potential neuroprotectant. In this study, we aimed to investigate the protective effect of apocynin against cobalt chloride (CoCl₂)-induced pheochromocytoma (PC12) cell apoptosis. Methods: The PC12 cell culture was pretreated with apocynin and/or SB203580 (p38 mitogen-activated protein kinase [p38-MAPK] inhibitor) at different time points prior to CoCl₂ incubation. The cell viability, apoptosis rate, DAN damage, and antioxidant activity were detected using cell counting kit-8 (CCK-8), flow cytometry, enzyme-linked immunosorbent assay (ELISA), and comet assay respectively. The protein and mRNA expressions of p38-MAPK and caspase-3 in the cells were measured by qRT-PCR and Western blotting. Results: Apocynin inhibited CoCl₂-mediated apoptosis, reduced oxidative stress, and down-regulated the expression of p38-MAPK and caspase-3. Conclusions: Our findings show that apocynin attenuated CoCl₂-induced apoptosis by potently restraining p38-MAPK-caspase-3 signaling pathway in PC12 cells, suggesting that apocynin may be a potent prophylactic reagent against CoCl₂-mediated PC12 cell apoptosis.

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Regulation of Muscle Stem Cell Functions: A Focus on the p38 MAPK Signaling Pathway

Cited by 162 publications

References 156 publications

High-resolution myogenic lineage mapping by single-cell mass cytometry

High-resolution myogenic lineage mapping by single-cell mass cytometry

Identification of a clinical compound losmapimod that blocks Lassa virus entry

Apocynin Attenuates Cobalt Chloride-Induced Pheochromocytoma Cell Apoptosis by Inhibiting P38-MAPK/Caspase-3 Pathway

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