The Relationship Between Src-Suppressed C Kinase Substrate and β-1,4 Galactosyltransferase-I in the Process of Lipopolysaccharide-Induced TNF-α Secretion in Rat Primary Astrocytes

Shao, Bai; Li, Chunmiao; Yang, Huiling; Shen, Aiguo; Wu, Xiaohong; Yuan, Qin; Wu, Xiujie; Kang, Lihua; Liu, Zhiqiang; Zhang, Guowei; Lü, Xiang; Cheng, Chun

doi:10.1007/s10571-011-9704-3

Cited by 10 publications

(6 citation statements)

References 46 publications

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“…Our results indicate that other CNS resident cells rather than neurons could be responsible for TNFα production rather than neurons. We were able to detect significant expression of TNFα in astroglial cultures treated with TLR3 and TLR4 agonists and these data came into agreement with previously reported results of the other studies [ 22 , 23 , 24 ]. According to our results, pre-incubation with RG leads to downregulation of TNFα secretion into media in LPS- or PIC-activated astroglial cultures.…”

Section: Discussionsupporting

confidence: 92%

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Rosiglitazone as a Modulator of TLR4 and TLR3 Signaling Pathways in Rat Primary Neurons and Astrocytes

Chistyakov

Azbukina

Лопачев

et al. 2018

IJMS

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An antidiabetic drug of the thiazolidinedione class, rosiglitazone (RG) demonstrates anti-inflammatory properties in various brain pathologies. The mechanism of RG action in brain cells is not fully known. To unravel mechanisms of RG modulation of toll-like receptor (TLR) signaling pathways, we compare primary rat neuron and astrocyte cultures stimulated with the TLR4 agonist lipopolysaccharide (LPS) and the TLR3 agonist poly I:C (PIC). Both TLR agonists induced tumor necrosis factor (TNFα) release in astrocytes, but not in neurons. Neurons and astrocytes released interleukin-10 (IL-10) and prostaglandin E2 (PGE2) in response to LPS and PIC. RG decreased TLR-stimulated TNFα release in astrocytes as well as potentiated IL-10 and PGE2 release in both astrocytes and neurons. RG induced phosphorylation of p38 and JNK MAPK (mitogen-activated protein kinase) in neurons. The results reveal new role of RG as a modulator of resolution of neuroinflammation.

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Section: Discussionsupporting

confidence: 92%

“…TLR4 and TLR3 mediated release of TNFα by astrocytes has already been clearly shown [ 22 , 23 , 24 ]. Some data obtained from nervous tissue pointed that neurons could also express TNFα (both on mRNA and protein levels) [ 25 , 26 ], however data at the cellular level are still missing.…”

Section: Resultsmentioning

confidence: 98%

Rosiglitazone as a Modulator of TLR4 and TLR3 Signaling Pathways in Rat Primary Neurons and Astrocytes

Chistyakov

Azbukina

Лопачев

et al. 2018

IJMS

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“…LPS‐induced responses include the release of TNFα in astrocytes (Shao et al . ). We detected no TNFα release in naïve cells, whereas addition of LPS increased the TNFα level to 250 ± 25 pg/mL (Fig.…”

Section: Resultsmentioning

confidence: 97%

Regulation of peroxisome proliferator‐activated receptor β/δ expression and activity levels by toll‐like receptor agonists and MAP kinase inhibitors in rat astrocytes

Chistyakov

Aleshin

Sergeeva

et al. 2014

Journal of Neurochemistry

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Peroxisome proliferator-activated receptor b/d (PPARb/d) is a potential regulator of neuroinflammation. Toll-like receptors (TLR) are innate immunity-related receptors of inflammatory stimuli. In the present report, we evaluate the molecular mechanisms of regulation of mRNA, protein, and transcriptional activity levels of PPARb/d by agonists of TLR4, TLR1/2, and TLR5, using lipopolysaccharide (LPS), peptidoglycan, and flagellin, respectively. We found that these stimuli increase the PPARb/d levels in astrocytes. Expression and activity of PPARb/d are separately regulated by inhibitors of p38, MEK1/ 2, extracellular signal-regulated kinases 1/2, and c-Jun Nterminal Kinase mitogen-activated protein kinases. The LPSinduced kinetics of PPARb/d expression is similar to that of the proinflammatory gene cyclooxygenase 2. Moreover, for both genes the expression depends on nuclear factor kappa-lightchain-enhancer of activated B cells and p38, and is induced after inhibition of protein synthesis. The up-regulation of the expression after inhibition of protein synthesis signifies the participation of a labile protein in regulation of PPARb/d expression. In contrast to cyclooxygenase 2, the cycloheximide-sensitive PPARb/d expression was not responsive to nuclear factor kappa-light-chain-enhancer of activated B cells inhibition. Measurements of PPARb/d mRNA stability showed that the PPARb/d mRNA levels are regulated post-transcriptionally. We found that in LPS-stimulated astrocytes, the halflife of PPARb/d mRNA was 50 min. Thus, we demonstrate that PPARb/d expression and activity are regulated in TLR agoniststimulated astrocytes by mechanisms that are widely used for regulation of proinflammatory genes.

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“…The PKC pathway regulates cytoskeletal protein activity and endothelial cell barrier function by modulating its downstream substrate SSeCKS. PKC-mediated upregulation of SSeCKS activates F-actin, which leads to NF- κ B activation in HPMEC, resulting in ALI [ 40 ]. Because rescue of aquaporin 5 (AQP-5) and matrix metalloproteinase 9 (MMP-9) and inhibition of apoptosis may lead to NF- κ B attenuation [ 41 ], we speculate that NF- κ B may be a key mediator of apoptosis, AQP-5/MMP-9, and PKC/SSeCKS/F-actin signaling pathways during AP-induced ALI.…”

Section: Pkc Pathwaymentioning

confidence: 99%

Signal Pathways and Markers Involved in Acute Lung Injury Induced by Acute Pancreatitis

Zhou

Wang

2021

Disease Markers

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Acute pancreatitis (AP) is a common acute abdominal disease with a mortality rate of about 30%. Acute lung injury (ALI) is a common systemic complication of acute pancreatitis, with progressive hypoxemia and respiratory distress as the main manifestations, which can develop into acute respiratory distress syndrome or even multiple organ dysfunction syndrome (MODS) in severe cases, endangering human health. In the model of AP, pathophysiological process of the lung can be summarized as oxidative stress injury, inflammatory factor infiltration, and alveolar cell apoptosis. However, the intrinsic mechanisms underlying AP and how it leads to ALI are not fully understood. In this paper, we summarize recent articles related to AP leading to ALI, including the signal transduction pathways and biomarkers of AP-ALI. There are factors or pathway aggravating ALI, the JAK2-STAT3 signaling pathway, NLRP3/NF-κB pathway, mitogen-activated protein kinase, PKC pathway, neutrophil protease (NP)-LAMC2-neutrophil pathway, and the P2X7 pathway, and there are important transcription factors in the NRF2 signal transduction pathway which could give researchers better understanding of the underlying mechanisms controlling AP and ALI and lay the foundation for finally curing ALI induced by AP.

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The Relationship Between Src-Suppressed C Kinase Substrate and β-1,4 Galactosyltransferase-I in the Process of Lipopolysaccharide-Induced TNF-α Secretion in Rat Primary Astrocytes

Cited by 10 publications

References 46 publications

Rosiglitazone as a Modulator of TLR4 and TLR3 Signaling Pathways in Rat Primary Neurons and Astrocytes

Rosiglitazone as a Modulator of TLR4 and TLR3 Signaling Pathways in Rat Primary Neurons and Astrocytes

Regulation of peroxisome proliferator‐activated receptor β/δ expression and activity levels by toll‐like receptor agonists and MAP kinase inhibitors in rat astrocytes

Signal Pathways and Markers Involved in Acute Lung Injury Induced by Acute Pancreatitis

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