A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair
By D. Ruffell, F. Mourkioti, A. Gambardella, Peggy Kirstetter, R. G. Lopez, Nadia A. Rosenthal, C. Nerlov. Proceedings of the National Academy of Sciences of the United States of America, 2009
631 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/92f71ad2580adf4332f86a4785b9a3772bb553e3
How researchers see this paper
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In Immunology
- Xiangming Zou
- G. Chinetti-Gbaguidi
- Nicolas A. Dumont
- Michael A. Rudnicki
- G. Harry
- Bart Staels
- Yan-Cun Liu
- Yong-ming Yao
In Molecular Biology
- C. Bentzinger
- Nicolas A. Dumont
- Marie-Claude Sincennes
- Xiangming Zou
- P. Muñoz-Cánoves
- Michael A. Rudnicki
- G. Harry
- A. Serrano
Citations in the corpus
- Microglial M1/M2 polarization and metabolic states (2016, background): “While the initial response of macrophages to injury has been known for some time, positive influences on tissue remodelling have been recognized more recently (Longbrake et al., 2007; Ruffell et al., 2009; Deng et al., 2012; Novak and Koh, 2013; Shechter and Schwartz, 2013; Shechter et al., 2013).”
- Microglia/Macrophage Polarization Dynamics Reveal Novel Mechanism of Injury Expansion After Focal Cerebral Ischemia (2012, background): “A CREB-C/EBPβ cascade also was shown to induce M2 macrophage- specific gene expression and promote muscle injury repair.(26) The identification of these critical molecules brings hope to therapies that promote healthy microglia/macrophage responses even under pathological conditions.”
- Satellite Cells and Skeletal Muscle Regeneration (2015, positive): “Consistently, the suppression of M2 macrophages in vivo leads to reduced myogenin expression and impaired fiber growth (86, 253).”
- 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action. (2013, background): “This indicates a possible feed-forward loop-inflammation stimulating the HPA axis to secrete glucocorticoids, both of which induce C/EBP in turn increasing 11 -HSD1, further amplifying local glucocorticoid signaling and shaping the trajectory of an inflammatory response via pro-resolution macrophage”
- Macrophages are required for adult salamander limb regeneration (2013, background): “In mice, macrophage depletion or disruption of macrophage transcriptional regulation after skeletal muscle injury results in incomplete muscle repair and induction of fibrotic scarring (18, 19).”
- Macrophage Polarization in Inflammatory Diseases (2014, background): “The alternatively activated macrophages secrete anti-inflammatory mediators, promote tissue repair, and regulate immune response in the initiation, development, and cessation of many inflammatory diseases through signal pathways including STATs, interferon regulatory factors (IRFs), NF-κB, AP1, PPAR”
- Aberrant repair and fibrosis development in skeletal muscle (2011, background): “Mutant mice were able to remove necrotic tissue from injured muscle, but they exhibited severe defects in myofiber regeneration [43].”
- Macrophage phenotypes in atherosclerosis (2014, background): “The CCAAT/enhancer-binding protein (C/EBP) transcription factor family, which comprises six members (a-f), and the cAMP-responsive element-binding protein (CREB) have been shown to play roles in macrophage activation (94).”