Microvesicles packaging IL-1β and TNF-α enhance lung inflammatory response to mechanical ventilation in part by induction of cofilin signaling

Zhang, Suisui; Dai, Huijun; Zhu, Lingyu; Lin, Fei; Hu, Zhaokun; Ren, Jing; Zhang, Weikang; Zhao, Chen; Hong, Xueqi; Zhong, Jian‐Hong; Pan, Linghui

doi:10.1016/j.intimp.2018.07.034

Cited by 20 publications

(12 citation statements)

References 50 publications

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“…In addition, MVs not only mediate inflammation through the NF‐κB signalling pathway, but also activate similar pro‐inflammatory responses in target cells through a variety of pathways. For example, MVs enhance lung inflammation by carrying IL‐1β and TNF‐α, or increase the expression level of mRNA in receptor cells. Circulating MVs bind to the cell membrane and transfer monomer C‐reactive proteins to the cell surface.…”

Section: Mechanism Of Mvs and Its Active Molecules In Exerting Biologmentioning

confidence: 99%

The role of microvesicles and its active molecules in regulating cellular biology

Tan

Miao

et al. 2019

J Cellular Molecular Medi

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Cell‐derived microvesicles are membrane vesicles produced by the outward budding of the plasma membrane and released by almost all types of cells. These have been considered as another mechanism of intercellular communication, because they carry active molecules, such as proteins, lipids and nucleic acids. Furthermore, these are present in circulating fluids, such as blood and urine, and are closely correlated to the progression of pathophysiological conditions in many diseases. Recent studies have revealed that microvesicles have a dual effect of damage and protection of receptor cells. However, the nature of the active molecules involved in this effect remains unclear. The present study mainly emphasized the mechanism of microvesicles and the active molecules mediating the different biological effects of receptor cells by affecting autophagy, apoptosis and inflammation pathways. The effective ways of blocking microvesicles and its active molecules in mediating cell damage when microvesicles exert harmful effects were also discussed.

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Section: Mechanism Of Mvs and Its Active Molecules In Exerting Biologmentioning

confidence: 99%

The role of microvesicles and its active molecules in regulating cellular biology

Tan

Miao

et al. 2019

J Cellular Molecular Medi

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“…At 6 weeks after HCC Huh-7 cells had been injected into mice, lung tissue samples were harvested, fixed with 4% paraformaldehyde, and stained with hematoxylin and eosin as described [16]. The sample slices were assessed by a pathologist who was blinded to experimental conditions.…”

Section: Hematoxylin and Eosin Stainingmentioning

confidence: 99%

“…RNA samples were reverse-transcribed into cDNA using a reverse transcription kit (Toyobo, Osaka, Japan). Quantitative real-time PCR was performed [15][16][17] on an ABI PRISM 7500 sequence detection system (Applied Biosystems, CA, USA) using the following primers for PNO1: 5'-TGTTAAACCCCTAAAGGGAGACC-3'(forward), 5'-CCTTGTCCGTGTCACATTCTCT-3'(reverse), and the following primers for GAPDH as endogenous control: 5'-GGCACAGTCAAGGCTGAGAATG-3' (forward) and 5'-ATGGTGGTGAAGACGCCAGTA-3' (reverse). The PCR conditions consisted of a 10 minutes step at 95°C, 40 cycles at 95°C for 15 seconds each and 1 minute at 65°C.…”

Section: Quantitative Rt-pcrmentioning

confidence: 99%

Celecoxib Inhibits Hepatocellular Carcinoma Cell Growth and Migration by Targeting PNO1

Dai

Zhang

et al. 2019

Med Sci Monit

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Background: Celecoxib has shown anti-tumor activities against several types of cancer. Although the majority of research focuses on its mechanism via cyclooxygenase-2 (COX-2) enzyme inhibition, we identified a distinct mechanism behind celecoxib anti-cancer abilities. Material/Methods: We treated hepatocellular carcinoma (HCC) Huh-7 cells and tumor xenograft mice models with celecoxib to test its effects on the tumor. Using gene chip method to identify the differential expressed genes after celecoxib treatment and using pathway enrichment analysis to predict the potential pathways for further study. We transfected cells with lentiviral shRNA to detect the effect of RNA binding gene partner of NOB1 (PNO1) on tumor growth in vitro and in vivo. Further we performed western blot to detect the effect of PNO1 on the protein kinase B (AKT) pathway. Results: Celecoxib inhibited HCC cell growth in vitro and in vivo, and gene chip and pathway enrichment analysis revealed that PNO1 may be the potential target of celecoxib in HCC cells. Celecoxib significantly reduced levels of PNO1 in tumor tissue. Knockdown of PNO1 remarkably suppressed tumor growth and metastasis in vitro and in vivo. Disruption of PNO1 expression significantly reduced protein kinase B (AKT)/rapamycin (mTOR) signaling, indicating that this pathway may be involved in PNO1-mediated tumorigenic activity. Conclusions: Celecoxib may exert its anti-tumor activity by inhibiting PNO1, and that AKT/mTOR signaling helps mediate the oncogenic effects of PNO1. This work offers the first evidence for a role of PNO1 as an HCC oncogene, which may open new avenues for prevention and treatment of HCC.

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“…Plasma membrane receptors for cytokines or growth factors can be shed due to protease-mediated cleavage, or released in association with plasma membrane-derived microvesicles/microparticles (MVs/MPs) (1, 2), thus deeply affecting signaling by the cognate cytokine (3). Although not routinely used in the diagnosis of inflammation, measurement of soluble cytokine receptor is gaining interest for the differential diagnosis of selected immune-related disorders.…”

Section: Introductionmentioning

confidence: 99%

The P2X7 Receptor Is Shed Into Circulation: Correlation With C-Reactive Protein Levels

et al. 2019

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The P2X7 receptor (P2X7R) is a key pro-inflammatory plasma membrane receptor responsible for NLRP3 inflammasome activation and IL-1β release. Various inflammatory plasma membrane receptors (e.g., IL-1 type I receptor, TNF type I and II receptors, IL-2 receptor) are shed under different pathophysiological conditions. In the present study, we show that the full length P2X7R is released into circulation in patients as well as in healthy subjects. Blood levels of shed P2X7R (sP2X7R) correlate to those of the inflammatory marker C reactive protein (CRP). Blood sP2X7R ranged from 16.74 to 82.17 ng/L, mean ± SE 40.97 ± 3.82 ( n = 26) in healthy subjects, from 33.1 to 484.0 ng/L, mean ± SE 114.78 ± 12.22 ( n = 45) in patients with CRP <3 mg/L, and from 63.65 to 1092.3 ng/L, mean ± SE 204.2 ± 30.94 ( n = 42) in patients with CRP >3 mg/L. sP2X7R in plasma was largely associated to microvesicles/microparticles. Peripheral blood monocytes from healthy subjects released sP2X7R upon stimulation with the semi-selective P2X7R agonist benzoyl ATP. These data show that the P2X7R can be released into circulation, and that its blood levels increase in various disease conditions.

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Microvesicles packaging IL-1β and TNF-α enhance lung inflammatory response to mechanical ventilation in part by induction of cofilin signaling

Cited by 20 publications

References 50 publications

The role of microvesicles and its active molecules in regulating cellular biology

The role of microvesicles and its active molecules in regulating cellular biology

Celecoxib Inhibits Hepatocellular Carcinoma Cell Growth and Migration by Targeting PNO1

The P2X7 Receptor Is Shed Into Circulation: Correlation With C-Reactive Protein Levels

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