Involvement of MAPKs and NF-κB in LPS-induced VCAM-1 expression in human tracheal smooth muscle cells

Lin, Wei‐Ning; Luo, Shue‐Fen; Lee, Chiang‐Wen; Wang, Chien-Chun; Wang, Jong‐Shyan; Yang, Che‐Hua

doi:10.1016/j.cellsig.2007.01.009

Cited by 42 publications

(33 citation statements)

References 54 publications

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“…TLR activation initiates a complex and integrated signaling cascade that activates EGFR in airway epithelial cells (19). LPS induces the expression of vascular cell adhesion molecule-1 (VCAM-1), a systemic inflammation marker, through EGFR-dependent activation of AKT (53,54).…”

Section: Discussionmentioning

confidence: 99%

Erlotinib protects against LPS-induced Endotoxicity because TLR4 needs EGFR to signal

Zhou

DeSantis

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Several components of the canonical pathway of response to lipopolysaccharide (LPS) are required for the EGF-dependent activation of NFκB. Conversely, the ability of Toll-like Receptor 4 (TLR4) to activate NFκB in response to LPS is impaired by down regulating EGF receptor (EGFR) expression or by using the EGFR inhibitor erlotinib. The LYN proto-oncogene (LYN) is required for signaling in both directions. LYN binds to the EGFR upon LPS stimulation, and erlotinib impairs this association. In mice, erlotinib blocks the LPS-induced expression of tumor necrosis factor α (TNFα) and interleukin-6 (IL-6) and ameliorates LPS-induced endotoxity, revealing that EGFR is essential for LPS-induced signaling in vivo.

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Section: Discussionmentioning

confidence: 99%

Erlotinib protects against LPS-induced Endotoxicity because TLR4 needs EGFR to signal

Zhou

DeSantis

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…Previous studies in human tubuloepithelial and vascular cells have shown that selective inhibitors of p38 (SB203580), JNK (SP600125), and ERK (PD98059) suppressed ICAM-1 expression by cytokines. 50,51 In endothelial cells, p38-mediated activation of NF-B and AP-1, resulted in increased expression of ICAM-1. 52 In response to CTGF stimulation in murine tubuloepithelial cells, ICAM-1 is up-regulated by both p38 and JNK activation.…”

Section: Discussionmentioning

confidence: 99%

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

Sánchez-López¹,

Rayego²,

Rodrigues‐Díez³

et al. 2009

Journal of the American Society of Nephrology

118

100

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Connective tissue growth factor (CTGF) is an important profibrotic factor in kidney diseases. Blockade of endogenous CTGF ameliorates experimental renal damage and inhibits synthesis of extracellular matrix in cultured renal cells. CTGF regulates several cellular responses, including adhesion, migration, proliferation, and synthesis of proinflammatory factors. Here, we investigated whether CTGF participates in the inflammatory process in the kidney by evaluating the nuclear factor-kappa B (NF-B) pathway, a key signaling system that controls inflammation and immune responses. Systemic administration of CTGF to mice for 24 h induced marked infiltration of inflammatory cells in the renal interstitium (T lymphocytes and monocytes/macrophages) and led to elevated renal NF-B activity. Administration of CTGF increased renal expression of chemokines (MCP-1 and RANTES) and cytokines (INF-␥, IL-6, and IL-4) that recruit immune cells and promote inflammation. Treatment with a NF-B inhibitor, parthenolide, inhibited CTGF-induced renal inflammatory responses, including the up-regulation of chemokines and cytokines. In cultured murine tubuloepithelial cells, CTGF rapidly activated the NF-B pathway and the cascade of mitogen-activated protein kinases, demonstrating crosstalk between these signaling pathways. CTGF, via mitogen-activated protein kinase and NF-B activation, increased proinflammatory gene expression. These data show that in addition to its profibrotic properties, CTGF contributes to the recruitment of inflammatory cells in the kidney by activating the NF-B pathway.

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“…It has been reported that tyrosine kinases are involved in LPS-induced specific gene expression in some cells [20,38]. In macrophages, tyrosine phosphorylation induced p38 mitogen-activated protein kinase activation to express NF-κB-dependent iNOS [39].…”

Section: Discussionmentioning

confidence: 99%

Action of Lipopolysaccharide on Interstitial Cells of Cajal from Mouse Small Intestine

et al. 2012

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Background and Purpose: Lipopolysaccharide (LPS) induces intestinal dysmotility by alteration of smooth muscle and enteric neuronal activities. However, there is no report on the modulatory effects of LPS on the interstitial cells of Cajal (ICCs). We investigated the effect of LPS and its signal transduction in ICCs. Methods: We performed whole-cell patch clamp and RT-PCR in cultured ICCs from mouse small intestine. Results: LPS suppressed the generation of pacemaker currents of ICCs. The mRNA transcripts for Toll-like receptor 4 (TLR4) were expressed in ICCs. However, the inhibitory action of LPS on pacemaker currents from TLR4^+/+ mice was not present in TLR4^–/– mice. The inhibitory effects of LPS on ICCs were blocked by glibenclamide (an inhibitor of ATP-sensitive K⁺ channels), NS-398 (a COX-2 inhibitor), AH6808 [a prostaglandin E₂ (PGE₂)-EP₂ receptor antagonist], ODQ (an inhibitor of guanylate cyclase) and L-NAME [an inhibitor of nitric oxide synthase (NOS)]. Furthermore, genistein and herbimycin A (tyrosine kinase inhibitors) blocked the LPS-induced inhibitory action on pacemaker activity in ICCs. Conclusions: LPS can activate ICCs to release NO and PGE₂ through TLR4 activation. The released NO and PGE₂ inhibit pacemaker currents by activating ATP-sensitive K⁺ channels. The LPS actions are mediated by tyrosine kinase signaling pathways.

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Involvement of MAPKs and NF-κB in LPS-induced VCAM-1 expression in human tracheal smooth muscle cells

Cited by 42 publications

References 54 publications

Erlotinib protects against LPS-induced Endotoxicity because TLR4 needs EGFR to signal

Erlotinib protects against LPS-induced Endotoxicity because TLR4 needs EGFR to signal

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

Action of Lipopolysaccharide on Interstitial Cells of Cajal from Mouse Small Intestine

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