TNFα-induced MMP-9 promotes macrophage recruitment into injured peripheral nerve

Shubayev, Veronica I.; Angert, Mila; Dolkas, Jennifer; Campana, W. Marie; Palenscar, Kai; Myers, Robert R.

doi:10.1016/j.mcn.2005.10.011

Cited by 148 publications

(165 citation statements)

References 59 publications

Supporting

Mentioning

156

Contrasting

Unclassified

Order By: Relevance

“…The macrophages begin clearing myelin from the distal stump within the first few days [36][37][38] and continue to clear myelin and axonal debris for two weeks. These macrophages are mainly of hematogenous origin [39,40] . Understanding the key factors that regulate rapid macrophage responses to nerve injury during WD, and comparing the gene-expression differences in the injured nerves, may provide insights into methods for slowing WD [41,42] .…”

Section: Discussionmentioning

confidence: 99%

“…Axons begin to grow into the distal endoneurial tubes 1 week after nerve injury [6,39,45] ; Schwann cell/axon contacts are re-established and remyelination occurs at about 2 weeks; and the proper target tissues are reinnervated at about 4 weeks after sciatic nerve injury. In this process, a large number of genes with marked up-or down-regulation were differentially expressed, indicating sustained regulation at consecutive time points, meaning regeneration/repair by means of a continuously progressive program [4,10,35] .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Expression changes and bioinformatic analysis of Wallerian degeneration after sciatic nerve injury in rat

Yao

Shen

et al. 2013

Neurosci. Bull.

View full text Add to dashboard Cite

Wallerian degeneration (WD) remains an important research topic. Many genes are differentially expressed during the process of WD, but the precise mechanisms responsible for these differentiations are not completely understood. In this study, we used microarrays to analyze the expression changes of the distal nerve stump at 0, 1, 4, 7, 14, 21 and 28 days after sciatic nerve injury in rats. The data revealed 6 076 differentially-expressed genes, with 23 types of expression, specifically enriched in genes associated with nerve development and axonogenesis, cytokine biosynthesis, cell differentiation, cytokine/chemokine production, neuron differentiation, cytokinesis, phosphorylation and axon regeneration. Kyoto Encyclopedia of Genes and Genomes pathway analysis gave findings related mainly to the MAPK signaling pathway, the Jak-STAT signaling pathway, the cell cycle, cytokine-cytokine receptor interaction, the p53 signaling pathway and the Wnt signaling pathway. Some key factors were NGF, MAG, CNTF, CTNNA2, p53, JAK2, PLCB1, STAT3, BDNF, PRKC, collagen II, FGF, THBS4, TNC and c-Src, which were further validated by real-time quantitative PCR, Western blot, and immunohistochemistry. Our findings contribute to a better understanding of the functional analysis of differentially-expressed genes in WD and may shed light on the molecular mechanisms of nerve degeneration and regeneration.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression changes and bioinformatic analysis of Wallerian degeneration after sciatic nerve injury in rat

Yao

Shen

et al. 2013

Neurosci. Bull.

View full text Add to dashboard Cite

show abstract

“…The addition of TNF to the cultures increased the levels of MMP production, reinforcing this hypothesis. TNF-␣ induces MMP-9 expression in many systems (24,38), while MMP-9 has the ability to activate TNF-␣ release from its membrane precursor (43). Endogenous TNF-␣ stimulates MMP-9 gene transcription in monocytes through NF-B activation (3), and p38 mitogen-activated protein kinase (MAPK) inhibitors were able to downregulate MMP-9 mRNA and protein expression (24).…”

Section: Discussionmentioning

confidence: 99%

High Matrix Metalloproteinase Production Correlates with Immune Activation and Leukocyte Migration in Leprosy Reactional Lesions

Teles

Amadeu

et al. 2010

Infect Immun

View full text Add to dashboard Cite

Matrix metalloproteinases (MMPs) compose a family of zinc-and calcium-dependent proteolytic enzymes responsible for extracellular matrix (ECM) remodeling and the regulation of the trans-ECM migration of leukocytes, an important step in inflammatory processes as well as infectious diseases. MMPs are functionally classified according to their relative substrate specificities but have been shown to overlap. Collagenases (MMP-1, -8, and -13) degrade type I collagen, whereas gelatinases A and B (MMP-2 and -9, respectively) degrade denatured type I (gelatin) and type IV collagens, a major component of the basement membrane. Collagenases are produced by many cell types including lymphocytes, granulocytes, astrocytes, and activated macrophages (10, 18).MMP secretion takes place under tight regulatory mechanisms including transcriptional controls in addition to their release as proenzymes, requiring activation by specific proteases and cytokines present in the milieu (2,3,16). Also, the postactivation of MMPs is controlled by metalloproteinase tissue inhibitors (tissue inhibitor of MMP [TIMP]), a family of specific inhibitors, that bind to MMPs in a stoichiometric ratio.

show abstract

“…One of the functions of TNF-α during Wallerian degeneration has been suggested to be the induction of macrophage recruitment for debris removal (Liefner et al, 2000). TNF-α-induced matrix metalloproteinase activity has also been shown to promote macrophage recruitment into injured nerves during delayed axonal degeneration (Shubayev et al, 2006). Indeed, TNF-α knockout mice exhibit slower macrophage migration into the injured nerve and delayed myelin clearance during Wallerian degeneration (Liefner et al, 2000).…”

Section: Interplay Of Tnf-α Signaling With Other Cellular Events Assomentioning

confidence: 99%

TNF-α signaling in glaucomatous neurodegeneration

Tezel

2008

Progress in Brain Research

236

190

View full text Add to dashboard Cite

Growing evidence supports the role of TNF-α as a mediator of neurodegeneration in glaucoma. Glial production of TNF-α is increased and its death receptor is up-regulated on retinal ganglion cells (RGCs) and optic nerve axons in glaucomatous eyes. This multifunctional cytokine can induce RGC death through receptor-mediated caspase activation, mitochondrial dysfunction, and oxidative stress. Opposing these cell-death promoting signals, binding of TNF receptors can also trigger the activation of survival signals. A critical balance between a variety of intracellular signaling pathways determines the predominant in vivo bioactivity of TNF-α as best exemplified by differential responses of RGCs and glia. In addition to the direct neurotoxicity of TNF-α to RGCs and their axons, potential interplay of TNF-α signaling with other cellular events associated with glaucomatous neurodegeneration may also contribute to secondary neurodegenerative injury. This review focuses on the present evidence supporting the involvement of TNF-α signaling in glaucomatous neurodegeneration and possible treatment targets to provide neuroprotection.

show abstract

TNFα-induced MMP-9 promotes macrophage recruitment into injured peripheral nerve

Cited by 148 publications

References 59 publications

Expression changes and bioinformatic analysis of Wallerian degeneration after sciatic nerve injury in rat

Expression changes and bioinformatic analysis of Wallerian degeneration after sciatic nerve injury in rat

High Matrix Metalloproteinase Production Correlates with Immune Activation and Leukocyte Migration in Leprosy Reactional Lesions

TNF-α signaling in glaucomatous neurodegeneration

Contact Info

Product

Resources

About