The HMGB1 signaling pathway activates the inflammatory response in Schwann cells

Man, Lili; Liu, Fan; Wang, Yongjun; Song, Honghua; Xu, Hongbo; Zhu, Ziwen; Zhang, Qing

doi:10.4103/1673-5374.167773

Cited by 21 publications

(10 citation statements)

References 34 publications

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“…Schwann cells express RAGE and several TLRs (with upregulation of TLR-1 in injured nerves) and inflammatory cytokine expression of Schwann cells (IL-1β, IL-6 and TNF) is upregulated following peripheral nerve injury [ 261 ]. Endothelial cells express RAGE, TLRs, NLRP-1, and NLRP-3.…”

Section: Mechanisms Linking Amyloid and Peripheral Neuropathymentioning

confidence: 99%

Amyloid Proteins and Peripheral Neuropathy

Asiri

Engelsman

Eijkelkamp

et al. 2020

Cells

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Painful peripheral neuropathy affects millions of people worldwide. Peripheral neuropathy develops in patients with various diseases, including rare familial or acquired amyloid polyneuropathies, as well as some common diseases, including type 2 diabetes mellitus and several chronic inflammatory diseases. Intriguingly, these diseases share a histopathological feature—deposits of amyloid-forming proteins in tissues. Amyloid-forming proteins may cause tissue dysregulation and damage, including damage to nerves, and may be a common cause of neuropathy in these, and potentially other, diseases. Here, we will discuss how amyloid proteins contribute to peripheral neuropathy by reviewing the current understanding of pathogenic mechanisms in known inherited and acquired (usually rare) amyloid neuropathies. In addition, we will discuss the potential role of amyloid proteins in peripheral neuropathy in some common diseases, which are not (yet) considered as amyloid neuropathies. We conclude that there are many similarities in the molecular and cell biological defects caused by aggregation of the various amyloid proteins in these different diseases and propose a common pathogenic pathway for “peripheral amyloid neuropathies”.

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Section: Mechanisms Linking Amyloid and Peripheral Neuropathymentioning

confidence: 99%

Amyloid Proteins and Peripheral Neuropathy

Asiri

Engelsman

Eijkelkamp

et al. 2020

Cells

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“…It remains to be solved why RAGE inactivation has such contrasting effects on axonal regeneration between the hyperglycemic and normoglycemic conditions. The RAGE ligands other than AGEs, in particular, S100B, and high-mobility group box 1 have been suggested to activate the RAGE signaling pathway in Schwann cells and macrophages to promote their migration to injured sites, thereby contributing to axonal regeneration with functional repair ( 51 , 57 – 59 ). Under diabetic conditions, however, the AGE–RAGE signaling axis that is detrimental to axonal regeneration may surpass the non-AGE-mediated RAGE signaling axes described above.…”

Section: Impaired Axonal Regeneration In Animal Models Of Diabetesmentioning

confidence: 99%

Impaired Axonal Regeneration in Diabetes. Perspective on the Underlying Mechanism from In Vivo and In Vitro Experimental Studies

Sango

Mizukami

Horie³

et al. 2017

Front. Endocrinol.

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Axonal regeneration after peripheral nerve injury is impaired in diabetes, but its precise mechanisms have not been elucidated. In this paper, we summarize the progress of research on altered axonal regeneration in animal models of diabetes and cultured nerve tissues exposed to hyperglycemia. Impaired nerve regeneration in animal diabetes can be attributed to dysfunction of neurons and Schwann cells, unfavorable stromal environment supportive of regenerating axons, and alterations of target tissues receptive to reinnervation. In particular, there are a number of factors such as enhanced activity of the negative regulators of axonal regeneration (e.g., phosphatase and tensin homolog deleted on chromosome 10 and Rho/Rho kinase), delayed Wallerian degeneration, alterations of the extracellular matrix components, enhanced binding of advanced glycation endproducts (AGEs) with the receptor for AGE, and delayed muscle reinnervation that can be obstacles to functional recovery after an axonal injury. It is also noteworthy that we and others have observed excessive neurite outgrowth from peripheral sensory ganglion explants from streptozotocin (STZ)-diabetic mice in culture and enhanced regeneration of small nerve fibers after sciatic nerve injury in STZ-induced diabetic rats. The excess of abortive neurite outgrowth may lead to misconnections of axons and target organs, which may interfere with appropriate target reinnervation and functional repair. Amelioration of perturbed nerve regeneration may be crucial for the future management of diabetic neuropathy.

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“…Interestingly, these factors belong to HMGB1 signaling pathways identified in a web-based pathway analysis. HMGB1 has been shown to activate pro-inflammatory signals in the literature 54 – 56 and promote autophagy of tumor-associated myeloid cells such as MDSCs 57 . This could explain the decreased MDSCs and pro-tumor TAMs in p65KO group compared to p65 controls.…”

Section: Discussionmentioning

confidence: 99%

Canonical NFκB signaling in myeloid cells is required for the glioblastoma growth

Achyut

Angara

Jain

et al. 2017

Sci Rep

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Tumor development and therapeutic resistance are linked with tumor-associated macrophage (TAM) and myeloid-derived suppressor cell (MDSC) infiltration in tumors via chemokine axis. Chemokine expression, which determines the pro or anti-inflammatory status of myeloid cells, are partly regulated by the nuclear factor-kappa B (NF-κB) pathway. Here, we identified that conditional deletion of canonical NF-κB signaling (p65) in myeloid cells inhibited syngeneic glioblastoma (GBM) through decreased CD45 infiltration in tumors, as characterized by decreased TAMs (CD206+) and MDSCs (Gr1+ CD11b+), increased dendritic cells (CD86+) and cytotoxic T cells (CD8+) in the p65 knockout (KO) mice. Proinflammatory cytokines (IFNγ, MCP1, MIP1α, and TNFα) and myeloid differentiation factor (Endoglin) were increased in myeloid cells from p65 KO tumor, which demonstrated an influence on CD8+T cell proliferation. In contrast, p65KO athymic chimeric mice with human GBM, failed to inhibit tumor growth, confirming the contribution of T cells in an immune competent model. The analysis of human datasets and GBM tumors revealed higher expression of p65 in GBM-associated CD68+ macrophages compared to neighboring stroma. Thus, canonical NF-κB signaling has an anti-inflammatory role and is required for macrophage polarization, immune suppression, and GBM growth. Combining an NF-κB inhibitor with standard therapy could improve antitumor immunity in GBM.

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The HMGB1 signaling pathway activates the inflammatory response in Schwann cells

Cited by 21 publications

References 34 publications

Amyloid Proteins and Peripheral Neuropathy

Amyloid Proteins and Peripheral Neuropathy

Impaired Axonal Regeneration in Diabetes. Perspective on the Underlying Mechanism from In Vivo and In Vitro Experimental Studies

Canonical NFκB signaling in myeloid cells is required for the glioblastoma growth

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