2010
DOI: 10.1523/jneurosci.2998-10.2010
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Mitogen-Activated Protein Kinase-Activated Protein Kinase 2 (MK2) Contributes to Secondary Damage after Spinal Cord Injury

Abstract: The inflammatory response contributes importantly to secondary tissue damage and functional deficits after spinal cord injury (SCI). In this work, we identified mitogen-activated protein kinase (MAPK)-activated protein kinase 2 (MAPKAPK2 or MK2), a downstream substrate of p38 MAPK, as a potential target using microarray analysis of contused spinal cord tissue taken at the peak of the inflammatory response. There was increased expression and phosphorylation of MK2 after SCI, with phospho-MK2 expressed in microg… Show more

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Cited by 55 publications
(54 citation statements)
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“…Microarray analysis of spinal cord tissues taken at the peak of the inflammatory response to spinal cord injury showed an increased expression of phosphorylated MK2 in microglia and also in neurons and astrocytes. Locomotor recovery was significantly improved in MK2-deficient animals and was associated with reduced neuronal and myelin loss, and decreased expression of proinflammatory cytokines and decreased protein nitrosylation (Ghasemlou et al, 2010).…”
Section: The Role Of Mk2 In Neuroinflammationmentioning
confidence: 95%
See 1 more Smart Citation
“…Microarray analysis of spinal cord tissues taken at the peak of the inflammatory response to spinal cord injury showed an increased expression of phosphorylated MK2 in microglia and also in neurons and astrocytes. Locomotor recovery was significantly improved in MK2-deficient animals and was associated with reduced neuronal and myelin loss, and decreased expression of proinflammatory cytokines and decreased protein nitrosylation (Ghasemlou et al, 2010).…”
Section: The Role Of Mk2 In Neuroinflammationmentioning
confidence: 95%
“…Thus, MK2 emerged as a potential anti-inflammatory target, as convincingly documented by the increasing number of publications and reviews related to MK2 inflammation. In addition, MK2 governs not only peripheral inflammation but also neuroinflammation, the inflammation of the brain (Culbert et al, 2006;Thomas et al, 2008b;Ghasemlou et al, 2010). As the prominent kinase phosphorylating heat shock protein 27 (Hsp27) (Stokoe et al, 1992), MK2 has become a promising target for cancer treatment.…”
Section: Introductionmentioning
confidence: 99%
“…Serial spinal cord cross-sections were stained with cresyl violet to measure motor neuron survival over a 2-mm segment of the spinal cord centered on spinal level L4-L5. Criteria used to identify motor neuron profiles were the appearance of Nissl substance, a euchromatic nucleus, and cells with a diameter of at least 12.5 μm, and the ventral horn was defined as the area below (i.e., ventral) a horizontal line drawn at the level of the central canal (72). Motor neurons in the ipsilateral and contralateral ventral horn were counted at 100-μm intervals in the spinal cords of hHsp27 Tg and LM control mice 55 days after SNT/resuture.…”
Section: Methodsmentioning
confidence: 99%
“…Its prototype is the extracellular signal-regulated kinase (ERK)/mitogen-and stress-activated kinase (MSK)/cyclic-adenosine monophosphate regulatory element binding protein (CREB) pathway, where ERK activates its downstream target, MSK, to phosphorylate CREB [76][77][78][79]. This phosphorylation and activation of CREB recruits CREB binding protein, a HAT that regulates local chromatin structure as part of CREB-dependent activation of nuclear gene transcription [80]. Second, the nuclear factor kappa B (NFκB) signaling pathway appears to control histone acetylation and chromatin structure in the CNS by mechanisms that are still being elucidated [81,82].…”
Section: Some Established Pathways Activated After Sci Alter Chromatimentioning
confidence: 99%