Effects of Nogo-A Silencing on TNF-<i>α</i>and IL-6 Secretion and TH Downregulation in Lipopolysaccharide-Stimulated PC12 Cells

Zhong, Jianbin; Fan, Shengnuo; Yan, Zhenwen; Xiao, Shifu; Wan, Limei; Chen, Chibang; Zhong, Simin; Liu, Lu; Liu, Jun

doi:10.1155/2015/817914

Cited by 15 publications

(13 citation statements)

References 23 publications

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“…We found that LPS-treated Nogo-KO BMDM expressed signi cantly decreased levels of IL-6, TNF-α, IL-1β, NF-κB, CXCL1, and CXCL2 compared with WT BMDM, whereas iNOS was not signi cantly downregulated in LPS-treated Nogo-KO BMDM compared with WT BMDM (Fig. 4c-i), as previously described [40,45]. These results suggest that Nogo-A may be involved in the activation of pro-in ammatory factors in LPS-treated WT BMDM.…”

Section: Nogo De Ciency Suppresses Expression Of Pro-in Ammatory Factsupporting

confidence: 87%

“…Our current work demonstrated that Nogo-A knockdown (si-Nogo-A) in differentiated C2C12 cells caused a reduction in CHOP, IL-6 and, TNF-α expression at the mRNA level. A previous study also stated that Nogo-A silencing led to the downregulation of IL-6 and TNF-α in LPS-stimulated PC12 cells [45]. IF data showed substantially decreased Nogo-A and CHOP expression after Nogo-A was silenced.…”

Section: Discussionmentioning

confidence: 65%

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Nogo-A is critical for pro-inflammatory gene regulation in myocytes and macrophages

Ullah

Elfadl

Park

et al. 2020

Preprint

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Background: Nogo-A (Rtn 4A), a member of the reticulon 4 (Rtn4) protein family, is a neurite outgrowth inhibitor protein that is primarily expressed in the central nervous system (CNS). However, the role of Nogo-A in inflammatory mechanisms remains unclear. Therefore, in this study, we used Nogo-knockout (KO) mice to explore its potential role in the inflammatory process. Here, we investigated whether Nogo-A affects the inflammatory process through transcription factor C/EBP homologous protein (CHOP). Results: Our results demonstrated that Nogo-A, CHOP, and pro-inflammatory factors were activated in the following: notexin-induced muscle injury, in human Duchenne muscular dystrophy (DMD) patients, in dystrophin-deficient (mdx) mice, in differentiated C2C12 myoblast cells, and in lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDM). Moreover, we found that Nogo-KO BMDM exhibited lower migratory ability compared with wild type (WT) BMDM after LPS treatment. Conclusion: Our data demonstrated that the Nogo-A-CHOP signaling pathway regulated the inflammatory process in notexin-induced injured muscle, in mdx mice, in DMD patients, in differentiated C2C12 cells, and in LPS-stimulated BMDM. Taken together, these results suggest that Nogo-A plays a vital role in inflammatory processes, which resembles the pathological mechanisms observed in the CNS.

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Section: Nogo De Ciency Suppresses Expression Of Pro-in Ammatory Factsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 65%

Nogo-A is critical for pro-inflammatory gene regulation in myocytes and macrophages

Ullah

Elfadl

Park

et al. 2020

Preprint

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“…As the typical cytokines of M1 macrophage, IL-6 and TNF-α are crucial for regulating inflammatory response [25,26]. IL-6 is not only a hallmark of many human chronic inflammatory states, but it is also associated with the acute-phase reaction [27,28].…”

Section: Discussionmentioning

confidence: 99%

Geraniin Inhibits LPS-Induced THP-1 Macrophages Switching to M1 Phenotype via SOCS1/NF-κB Pathway

Liu

Peng

et al. 2016

Inflammation

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M1 macrophage polarization is proved to promote inflammation in atherosclerosis process. In this study, we evaluated the inhibitory effect of geraniin, a bioactive polyphenolic compound, on the LPS-induced switch of THP-1 macrophages to M1 phenotype, and we propose a molecular basis for its action. Flow cytometry analysis indicated that geraniin significantly inhibited LPS-induced M1 macrophage polarization. Geraniin downregulated the protein and the mRNA level of typical cytokines of M1 macrophage, including tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), indicating that geraniin can suppress typical mediators of M1 macrophage at the transcriptional level. Moreover, geraniin inhibited LPS-induced reactive oxygen species (ROS) and nitric oxide (NO) production, as well as inducible nitric oxide synthase (iNOS) activity, in THP-1 macrophages. Furthermore, western blot analysis indicated that geraniin decreased both LPS-induced phosphorylation of NF-κB-p65 and NF-κB-p65 expression without affecting the level of IκB-α. This suggested that geraniin inhibited NF-κB, a transcription factor pivotal in the LPS-induced expression of pro-inflammatory genes and an important player in M1 macrophage polarization. Moreover, an electrophoretic mobility shift assay (EMSA) demonstrated that geraniin blocked the LPS-induced translocation of NF-κB to the nucleus. Moreover, we found that geraniin up-regulated the expression of SOCS1, an upstream regulator of NF-κB activation that can directly bind to NF-κB-p65 and downregulate it, thus inhibiting NF-κB activation. In conclusion, geraniin inhibits LPS-induced THP-1 macrophages switching to M1 phenotype through SOCS1/NF-κB pathway.

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“…Tyrosine hydroxylase is the rate-limiting enzyme that converts tyrosine to L-DOPA (L-3, 4 dihydroxyphenylalanine). Therefore, the decrease in TH could be explained by a transient dysregulation in its expression that may have been induced by the localized and moderate inflammation resulting from ET injection (Zhong et al, 2015). Moreover, the transient change in the number of TH-ir neurons may be attributed to the mild dosage of ET that was administered.…”

Section: Discussionmentioning

confidence: 99%

Intranigral Injection of Endotoxin Suppresses Proliferation of Hippocampal Progenitor Cells

et al. 2019

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Brain inflammation can result in functional disorders observed in several neurodegenerative diseases and that can be also associated with reduced neurogenesis. In this study, we investigate the effect of mild inflammation, induced by unilateral injection of Endotoxin (ET) in the substantia nigra (SN)/Ventral Tegmental Area, on the proliferation and survival of stem/progenitor cells in the dentate gyrus (DG) of the hippocampus. Adult female rats received unilateral injection of ET (2 μg/2 μl saline) or sterile saline (2 μl) in the right SN followed by 5′-Bromo-2′-deoxyuridine (BrdU) injections (66 mg/kg/injection). Intranigral ET injection induced bilateral decrease in the number of newly born BrdU positive cells in the DG. This effect was paralleled by a significant decrease in the exploratory behavior of rats, as assessed by the Y-maze novel arm exploration task. ET also induced a transient decrease in the number of tyrosine hydroxylase-positive cells in the injected SN, impaired motor behavior, and caused microglial activation in the SN. This study provides an experimental simulation of the remote effects of moderate and reversible neuroinflammation resulting in impaired communication between midbrain dopaminergic neurons and the hippocampus.

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Effects of Nogo-A Silencing on TNF-αand IL-6 Secretion and TH Downregulation in Lipopolysaccharide-Stimulated PC12 Cells

Cited by 15 publications

References 23 publications

Nogo-A is critical for pro-inflammatory gene regulation in myocytes and macrophages

Nogo-A is critical for pro-inflammatory gene regulation in myocytes and macrophages

Geraniin Inhibits LPS-Induced THP-1 Macrophages Switching to M1 Phenotype via SOCS1/NF-κB Pathway

Intranigral Injection of Endotoxin Suppresses Proliferation of Hippocampal Progenitor Cells

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