Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury (Q28574797)

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English	Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury	scientific journal article

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scholarly article

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PubMed publication ID

31 January 2017

Inhibition of EGFR/MAPK signaling reduces microglial inflammatory response and the associated secondary damage in rats after spinal cord injury (English)

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PubMed publication ID

31 January 2017

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5

object named as

Qiang Zhang

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31 January 2017

10

object named as

Wei Wang

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31 January 2017

author name string

Wen-Sheng Qu

1

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31 January 2017

Dai-Shi Tian

2

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PubMed publication ID

31 January 2017

Zhi-Bao Guo

3

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PubMed publication ID

31 January 2017

Jun Fang

4

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PubMed publication ID

31 January 2017

Zhi-Yuan Yu

6

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PubMed publication ID

31 January 2017

Min-Jie Xie

7

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PubMed publication ID

31 January 2017

Hua-Qiu Zhang

8

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PubMed publication ID

31 January 2017

Jia-Gao Lü

9

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PubMed publication ID

31 January 2017

publication date

23 July 2012

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31 January 2017

Journal of Neuroinflammation

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PubMed publication ID

31 January 2017

9

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31 January 2017

178

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31 January 2017

Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment

1 reference

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Epidermal growth factor receptor inhibition modulates the microenvironment by vascular normalization to improve chemotherapy and radiotherapy efficacy

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Inhibiting epidermal growth factor receptor improves structural, locomotor, sensory, and bladder recovery from experimental spinal cord injury.

1 reference

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Interleukin-1 beta induction of neuron apoptosis depends on p38 mitogen-activated protein kinase activity after spinal cord injury

1 reference

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Signal transduction by the c-Jun N-terminal kinase (JNK) — from inflammation to development

1 reference

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Pro-inflammatory cytokines and lipopolysaccharide induce changes in cell morphology, and upregulation of ERK1/2, iNOS and sPLA₂-IIA expression in astrocytes and microglia.

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Microglial p38α MAPK is a key regulator of proinflammatory cytokine up-regulation induced by toll-like receptor (TLR) ligands or beta-amyloid (Aβ)

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The alternative and terminal pathways of complement mediate post-traumatic spinal cord inflammation and injury

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Role of microglia in neurotrauma

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The effect of epidermal growth factor in the injured brain after trauma in rats

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FoxO transcription factors promote autophagy in cardiomyocytes

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A straight alley version of the BBB locomotor scale

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Resection of glial scar following spinal cord injury

1 reference

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29 September 2017

Inflammation: beneficial or detrimental after spinal cord injury?

1 reference

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Methanol extract of Ficus leaf inhibits the production of nitric oxide and proinflammatory cytokines in LPS-stimulated microglia via the MAPK pathway

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EGFR inhibitor-mediated apoptosis in solid tumors.

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Inflammation and brain edema: new insights into the role of chemokines and their receptors

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EGFR activation mediates inhibition of axon regeneration by myelin and chondroitin sulfate proteoglycans

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Inflammation and apoptosis: linked therapeutic targets in spinal cord injury

1 reference

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Importance of MAPK pathways for microglial pro-inflammatory cytokine IL-1 beta production

1 reference

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Minocycline treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome after spinal cord injury.

1 reference

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Cytokines: powerful regulators of glial cell activation

1 reference

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Role of p38 and p44/42 mitogen-activated protein kinases in microglia

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Transforming growth factor-alpha (TGF-alpha) and epidermal growth factor-receptor (EGF-R) immunoreactivity in normal and pathologic brain.

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Mechanisms of secondary injury to spinal cord axons in vitro: role of Na , Na( )-K( )-ATPase, the Na( )-H exchanger, and the Na( )-Ca2 exchanger.

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Functional plasticity of microglia: a review

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Activation of p-38alpha MAPK contributes to neuronal hyperexcitability in caudal regions remote from spinal cord injury

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3 June 2018

The Rheb-mTOR pathway is upregulated in reactive astrocytes of the injured spinal cord.

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ERK1/2 and p38 mitogen-activated protein kinase mediate iNOS-induced spinal neuron degeneration after acute traumatic spinal cord injury

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Angiotensin II triggers EGFR tyrosine kinase-dependent Ca2 influx in afferent arterioles

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Depletion of hematogenous macrophages promotes partial hindlimb recovery and neuroanatomical repair after experimental spinal cord injury

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Epidermal growth factor receptor immunoreactivity in rat brain astrocytes. Response to injury

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Cell cycle inhibition attenuates microglia induced inflammatory response and alleviates neuronal cell death after spinal cord injury in rats

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Activation of epidermal growth factor receptor causes astrocytes to form cribriform structures

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Epidermal Growth Factor is a Motility Factor for Microglial Cells In Vitro: Evidence for EGF Receptor Expression

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The influence of p38 mitogen-activated protein kinase inhibitor on synthesis of inflammatory cytokine tumor necrosis factor alpha in spinal cord of rats with chronic constriction injury.

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Activated microglia initiate motor neuron injury by a nitric oxide and glutamate-mediated mechanism

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Regulation of interleukin-1beta by the interleukin-1 receptor antagonist in the glutamate-injured spinal cord: endogenous neuroprotection

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Effects of Etanercept and Minocycline in a rat model of spinal cord injury

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Immunomodulatory effects of etanercept in an experimental model of spinal cord injury

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Tumor Necrosis Factor-α Antagonist Reduces Apoptosis of Neurons and Oligodendroglia in Rat Spinal Cord Injury

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Evidence for the role of mitogen-activated protein kinase signaling pathways in the development of spinal cord injury

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Continuous intrathecal infusion of SB203580, a selective inhibitor of p38 mitogen-activated protein kinase, reduces the damage of hind-limb function after thoracic spinal cord injury in rat

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JNK inhibition and inflammation after cerebral ischemia

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alpha(2)-Adrenergic receptors activate MAPK and Akt through a pathway involving arachidonic acid metabolism by cytochrome P450-dependent epoxygenase, matrix metalloproteinase activation and subtype-specific transactivation of EGFR.

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Effects of microglia-derived cytokines on astrocyte proliferation

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Cellular and molecular mechanisms of glial scarring and progressive cavitation: in vivo and in vitro analysis of inflammation-induced secondary injury after CNS trauma.

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Hypothalamic lesions that induce female precocious puberty activate glial expression of the epidermal growth factor receptor gene: differential regulation of alternatively spliced transcripts

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Behavioral assessment of functional deficit in rats with contusive spinal cord injury

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Inhibiting epidermal growth factor receptor attenuates reactive astrogliosis and improves functional outcome after spinal cord injury in rats

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Severity-dependent expression of pro-inflammatory cytokines in traumatic spinal cord injury in the rat

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Delayed neuronal damage related to microglia proliferation after mild spinal cord compression injury

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Beneficial Effect of Interleukin-1 Receptor Antagonist Protein on Spinal Cord Injury Recovery in the Rat

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Growth hormone-induced tyrosine phosphorylation of EGF receptor as an essential element leading to MAP kinase activation and gene expression

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

[Pathophysiology of acute spinal cord injury]

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Optimized protocols for isolation of primary motor neurons, astrocytes and microglia from embryonic mouse spinal cord.

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Vascular permeability in experimental spinal cord injury

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Effect of bacterial wall lipopolysaccharide (LPS) on morphology, motility, and cytoskeletal organization of microglia in cultures

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

The dual role of tumor necrosis factor-alpha in the pathophysiology of spinal cord injury

1 reference

https://pubmed.ncbi.nlm.nih.gov/22824323

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.1186/1742-2094-9-178

1 reference

Consolidated OpenCitations Corpus – April 2017

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Dimensions Publication ID

1 reference

9 September 2019

https://scigraph.springernature.com/pub.10.1186/1742-2094-9-178

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

PMC publication ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

PubMed publication ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

ResearchGate publication ID

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