p38/MKP-1–regulated AKT coordinates macrophage transitions and resolution of inflammation during tissue repair

Perdiguero, Eusebio; Sousa‐Victor, Pedro; Ruiz‐Bonilla, Vanessa; Jardı́, Mercè; Caelles, Carmé; Serrano, Antonio L.; Muñoz‐Cánoves, Pura

doi:10.1083/jcb.201104053

Cited by 205 publications

(229 citation statements)

References 46 publications

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“…It then depresses PTEN in anti-inflammatory macrophages, resulting in AKT activation to cause inflammation alleviation and wound healing (Perdiguero et al, 2011). Hence, we suggest that miR-21 is a highly interesting and significant player in downstream inflammatory pathways and post-host immune responses mediated by diverse immune cells; the expression of miR-21 in MSC-EXO may be involved in the modulation of the inflammatory response during tissue repair.…”

Section: Figure 1 Analysis Of Mirna Expression Profiling In Msc-exo mentioning

confidence: 98%

Mesenchymal stem cells-derived exosomal microRNAs contribute to wound inflammation

Hao

et al. 2016

Sci. China Life Sci.

116

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Clinical and experimental studies have highlighted the significance of inflammation in coordinating wound repair and regeneration. However, it remains challenging to control the inflammatory response and tolerance at systemic levels without causing toxicity to injured tissues. Mesenchymal stem cells (MSCs) possess potent immunomodulatory properties and facilitate tissue repair by releasing exosomes, which generate a suitable microenvironment for inflammatory resolution. Exosomes contain several effective bioactive molecules and act as a cell-cell communication vehicle to influence cellular activities in recipient cells. During this process, the horizontal transfer of exosomal microRNAs (miRNAs) to acceptor cells, where they regulate target gene expression, is of particular interest for understanding the basic biology of inflammation ablation, tissue homeostasis, and development of therapeutic approaches. In this review, we describe a signature of three specific miRNAs (miR-21, miR-146a, and miR-181) present in human umbilical cord MSC-derived exosomes (MSC-EXO) identified microarray chip analysis and focus on the inflammatory regulatory functions of these immune-related miRNAs. We also discuss the potential mechanisms contributing to the resolution of wound inflammation and tissue healing.

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Section: Figure 1 Analysis Of Mirna Expression Profiling In Msc-exo mentioning

confidence: 98%

Mesenchymal stem cells-derived exosomal microRNAs contribute to wound inflammation

Hao

et al. 2016

Sci. China Life Sci.

116

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“…77,78 MAP kinase phosphatase-1 (MKP-1) regulates cell remnant disposal, macrophage transition and muscle healing. 79,80 Gene expression analyses on sorted MKP-1 − / − muscle macrophages suggest that MKP-1 regulates the inflammatory response as well as the macrophage polarization via p38 MAPK downregulation. Another enzyme, the AMP-activated protein kinase (AMPK)-α1, which 'senses' the cellular energy levels, also regulates the inflammatory status of macrophages.…”

Section: The Predators: Macrophages Scavenge Muscle Debrismentioning

confidence: 99%

Cell death, clearance and immunity in the skeletal muscle

et al. 2016

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“…PKB has been demonstrated to be a crucial effector in macrophage survival [98,99]. Mechanistically, PKB mediates macrophage survival by cross-talking with NF-κB, p38 MAPK and antiapoptotic signals mediated by Mcl1 and Bcl-xL [98][99][100]. Notably, IKK deficiency in macrophages results in decreased viability accompanied with reduced activation of PKB [101], indicating a potential feedback between PKB-IKK/NF-κB in the regulation of macrophage survival.…”

Section: Pkb Regulated Macrophage Functionmentioning

confidence: 99%

PKB/Akt-dependent regulation of inflammation in cancer

Tang

Wang

Hemmings

et al. 2018

Seminars in Cancer Biology

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A B S T R A C TChronic inflammation is a major cause of human cancer. Clinical cancer therapies against inflammatory risk factors are strategically determined. To rationally guide a novel drug development, an improved mechanistic understanding on the pathological connection between inflammation and carcinogenesis is essential. PI3K-PKB signaling axis has been extensively studied and shown to be one of the key oncogenic drivers in most types of cancer. Pharmacological inhibition of the components along this signaling axis is of great interest for developing novel therapies. Interestingly, emerging studies have shown a close association between PKB activation and inflammatory activity in the vicinity of the tumor, and either blockade of PKB or attenuation of para-tumoral inflammation reveals a mutual-interactive pattern through pathway crosstalk. In this review, we intend to discuss recent advances of PKB-regulated chronic inflammation and its potential impacts on tumor development.

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p38/MKP-1–regulated AKT coordinates macrophage transitions and resolution of inflammation during tissue repair

Abstract: MKP-1 limits p38 MAPK signaling in macrophages to promote the resolution of the inflammatory response and tissue repair in muscle through an AKT-dependent mechanism.

Cited by 205 publications

References 46 publications

Mesenchymal stem cells-derived exosomal microRNAs contribute to wound inflammation

Mesenchymal stem cells-derived exosomal microRNAs contribute to wound inflammation

Cell death, clearance and immunity in the skeletal muscle

PKB/Akt-dependent regulation of inflammation in cancer

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