RETRACTED ARTICLE: TN-2 modulates LPS-induced inflammatory response in human renal tubular epithelial cells by blocking TLR4-mediated NF-κB activation via MyD88- and TRIF-dependent mechanism

Liu, Yun; Ma, Dawei; Zhang, Lu; Cui, Yan; Guο, Minghao

doi:10.1007/s00011-015-0853-6

Cited by 3 publications

(1 citation statement)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[49][50][51][52] TLR4 plays a crucial role in the recognition of Gram-negative bacteria following LPS stimulation. 53 The MYD88-dependent and -independent signaling intermediates are downstream transduction pathways of TLR4, 54 which lead to the activation of the transcription factor NFKB and upregulation of inflammatory mediators. The regulative relationship between TLR4 and the MTOR pathway has been investigated in a few studies.…”

Section: Discussionmentioning

confidence: 99%

Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury

et al. 2016

View full text Add to dashboard Cite

MTOR (mechanistic target of rapamycin [serine/threonine kinase]) plays a crucial role in many major cellular processes including metabolism, proliferation and macroautophagy/autophagy induction, and is also implicated in a growing number of proliferative and metabolic diseases. Both MTOR and autophagy have been suggested to be involved in lung disorders, however, little is known about the role of MTOR and autophagy in pulmonary epithelium in the context of acute lung injury (ALI). In the present study, we observed that lipopolysaccharide (LPS) stimulation induced MTOR phosphorylation and decreased the expression of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3 β)-II, a hallmark of autophagy, in mouse lung epithelium and in human bronchial epithelial (HBE) cells. The activation of MTOR in HBE cells was mediated by TLR4 (toll-like receptor 4) signaling. Genetic knockdown of MTOR or overexpression of autophagy-related proteins significantly attenuated, whereas inhibition of autophagy further augmented, LPS-induced expression of IL6 (interleukin 6) and IL8, through NFKB signaling in HBE cells. Mice with specific knockdown of Mtor in bronchial or alveolar epithelial cells exhibited significantly attenuated airway inflammation, barrier disruption, and lung edema, and displayed prolonged survival in response to LPS exposure. Taken together, our results demonstrate that activation of MTOR in the epithelium promotes LPS-induced ALI, likely through downregulation of autophagy and the subsequent activation of NFKB. Thus, inhibition of MTOR in pulmonary epithelial cells may represent a novel therapeutic strategy for preventing ALI induced by certain bacteria.

show abstract

Section: Discussionmentioning

confidence: 99%

Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury

et al. 2016

View full text Add to dashboard Cite

show abstract

RETRACTED: Long non-coding RNA TUG1 protects renal tubular epithelial cells against injury induced by lipopolysaccharide via regulating microRNA-223

Deng

Zhang

2018

Biomedicine & Pharmacotherapy

View full text Add to dashboard Cite

Clinopodium chinense Attenuates Palmitic Acid-Induced Vascular Endothelial Inflammation and Insulin Resistance through TLR4-Mediated NF-κB and MAPK Pathways

et al. 2019

View full text Add to dashboard Cite

Elevated palmitic acid (PA) levels are associated with the development of inflammation, insulin resistance (IR) and endothelial dysfunction. Clinopodium chinense (Benth.) O. Kuntze has been shown to lower blood glucose and attenuate high glucose-induced vascular endothelial cells injury. In the present study we investigated the effects of ethyl acetate extract of C. chinense (CCE) on PA-induced inflammation and IR in the vascular endothelium and its molecular mechanism. We found that CCE significantly inhibited PA-induced toll-like receptor 4 (TLR4) expression in human umbilical vein endothelial cells (HUVECs). Consequently, this led to the inhibition of the following downstream adapted proteins myeloid differentiation primary response gene 88, Toll/interleukin-1 receptor domain-containing adaptor-inducing interferon-[Formula: see text] and TNF receptor-associated factor 6. Moreover, CCE inhibited the phosphorylation of Ikappa B kinase [Formula: see text], nuclear factor kappa-B (NF-[Formula: see text]B), c-Jun N-terminal kinase, extracellular regulated protein kinases, p38-mitogen-activated protein kinase (MAPK) and subsequently suppressed the release of tumor necrosis factor-[Formula: see text], interleukin-1[Formula: see text] (IL-1[Formula: see text]) and IL-6. CCE also inhibited IRS-1 serine phosphorylation and ameliorated insulin-mediated tyrosine phosphorylation of IRS-1. Moreover, CCE restored serine/threonine kinase and endothelial nitric oxide synthase (eNOS) activation and thus increased insulin-mediated nitric oxide (NO) production in PA-treated HUVECs. This led to reverse insulin mediated endothelium-dependent relaxation, eNOS phosphorylation and NO production in PA-treated rat thoracic aortas. These results suggest that CCE can significantly inhibit the inflammatory response and alleviate impaired insulin signaling in the vascular endothelium by suppressing TLR4-mediated NF-[Formula: see text]B and MAPK pathways. Therefore, CCE can be considered as a potential therapeutic candidate for endothelial dysfunction associated with IR and diabetes.

show abstract

RETRACTED ARTICLE: TN-2 modulates LPS-induced inflammatory response in human renal tubular epithelial cells by blocking TLR4-mediated NF-κB activation via MyD88- and TRIF-dependent mechanism

Cited by 3 publications

References 33 publications

Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury

Activation of MTOR in pulmonary epithelium promotes LPS-induced acute lung injury

RETRACTED: Long non-coding RNA TUG1 protects renal tubular epithelial cells against injury induced by lipopolysaccharide via regulating microRNA-223

Clinopodium chinense Attenuates Palmitic Acid-Induced Vascular Endothelial Inflammation and Insulin Resistance through TLR4-Mediated NF-κB and MAPK Pathways

Contact Info

Product

Resources

About