Analyses of caspase-1-regulated transcriptomes in various tissues lead to identification of novel IL-1β-, IL-18- and sirtuin-1-independent pathways

Li, Yafeng; Nanayakkara, Gayani; Sun, Yu; Li, Xinyuan; Wang, Luqiao; Cueto, Ramón; Shao, Ying; Fu, Hangfei; Johnson, Candice; Cheng, Jiali; Chen, Xiongwen; Hu, Wenhui; Yu, Jun; Choi, Eric T.; Wang, Hong; Yang, Xiaofeng

doi:10.1186/s13045-017-0406-2

Cited by 48 publications

(53 citation statements)

References 80 publications

(108 reference statements)

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“…It also plays a pivotal role in the cascade that leads to apoptosis in several organs and tissues, including the epithelial cells of intestine. Once activated, the inflammatory response increases expression of Caspase-1 by a positive feedback that worse the response 16 .…”

Section: ■ Discussionmentioning

confidence: 99%

The role of atenolol in the modulation of the expression of genes encoding pro- (caspase-1) and anti- (Bcl2L1) apoptotic proteins in endothelial cells exposed to intestinal ischemia and reperfusion in rats

et al. 2018

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Purpose: To investigate the role of atenolol in the gene expression of caspase 1 (Casp1) and Bcl2L1 on vascular endothelium of rat intestine after ischemia and reperfusion (IR). Methods: Eighteen adult male Wistar rats were randomly divided into 3 groups (n=6): SG (Sham group): no clamping of the superior mesenteric artery; IRG: IR plus saline group: IRG+At: IR plus Atenolol group. Rats from IRG and IRG+At were subjected to 60 min of intestinal ischemia and 120 min of reperfusion. Atenolol (2mg/kg) or saline were injected in the femoral vein 5 min before ischemia, 5 min and 55 min after reperfusion. Thereafter, intestinal segments were appropriately removed and processed for Endothelial Cell Biology Rat RT2 Profiler PCR Array. Results: the anti-apoptotic Bcl2L1 gene expression was significantly down-regulated (-1.10) in the IRG and significantly up-regulated in the IRG+At (+14.15). Meanwhile, despite Casp1 gene expression was upregulated in both groups, it was significantly higher in the IRG (+35.06) than the IRG+At (+6.68). Conclusions: Atenolol presents antiapoptotic effects on rat intestine subjected to IR partly by the up-regulation of the anti-apoptotic Bcl2L1 gene expression. Moreover, atenolol can mitigate the pro-apoptotic and pro-inflammatory effects of Casp1 gene on rat intestine after IR.

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Section: ■ Discussionmentioning

confidence: 99%

The role of atenolol in the modulation of the expression of genes encoding pro- (caspase-1) and anti- (Bcl2L1) apoptotic proteins in endothelial cells exposed to intestinal ischemia and reperfusion in rats

et al. 2018

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“…Interestingly, caspase-1 activation has been shown to not only result in pro-inflammatory cytokine production but also regulation of many other cellular pathways. A study by Li et al identified 40 genes regulated by caspase-1 in various tissues [126]. Previously, Grucel et al showed caspase-1 induced activation of sterol regulatory element binding proteins (SREBP) in response to bacterial pore forming toxins.…”

Section: Role Of Inflammasomes In Hcv-induced Inflammatory Responsementioning

confidence: 99%

Hepatitis C Virus and Inflammation

Kumar¹,

Ramachandran²,

Waris³

2018

Hepatitis C - From Infection to Cure

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Inflammation is often a rapid coordinated response generated in the host against evading microbial infections or tissue injury. Microorganisms like bacteria and viruses instigate inflammation mediated by pro-inflammatory cytokines and activate cascade of signaling events leading to the recruitment of inflammatory cells (neutrophils and macrophages). Although the main function of inflammation is the resolution of infection, several viruses, including the hepatitis C viruses (HCV) have evolved to utilize this host response and make the cellular environments conducive to infection. In majority of infected individuals, HCV causes persistent chronic liver inflammation leading to development of liver cirrhosis and hepatocellular carcinoma. HCV induces reactive oxygen species (ROS) and activates nuclear factor-κB (NF-κB) leading to the activation of cyclooxygenase-2 (Cox-2) that ultimately produces prostaglandin-E2 (PGE2), thus enhancing inflammatory process. Interestingly, HCV further activates NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome (a multiprotein complex) by recruiting adaptor protein apoptosis-associated speck-like protein containing a carboxy-terminal CARD (ASC) which are involved in activation of caspase-1 leading to production of interleukin-1beta (IL-1β) and interleukin-18 (IL-18). In this chapter we have highlighted the recent advancements in HCV-induced inflammatory responses and discussed potential future directions to understand the role of inflammation during HCV infection.

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“…Brie y, NlRP3 in ammasome composed of NLRP3, ASC and caspase-1, the activation of NLRP3 in ammasome ultimately process pro-IL-1β into IL-1β. Moreover, induce in ammatory response [12,13]. Originally NLRP3 was hypothesized to be a cytosolic receptor.…”

Section: Introductionmentioning

confidence: 99%

Selenium ameliorates S. aureus-induced inflammation through ROS-mediated NLRP3 inflammasome in bovine mammary epithelial cells

Bi¹,

Zhang²,

Tang³

2020

Preprint

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Background Some research has indicated that selenium (Se) plays a significant role during mastitis. However the intracellular anti-inflammatory effect of Se is not fully clear. Due to the ability of Staphylococcus aureus ( S. aureus ) to internalize into host cell, in this study we explored whether Se could regulate inflammation induced by S. aureus through reactive oxygen species (ROS)-mediated NLRP3 inflammasome in bMECs. Result bMECs were treated with 8 μmol/L Na 2 SeO 3 for 12 h before infected with S. aureus for 2 h. Through flow cytometry, Western blot and qPCR analysis, ROS and NLRP3 imflammasome were detected. Result shown that the production of ROS was increased by S. aureus , Se exerted strong inhibitory effects on the production of ROS; The protein expression of NLRP3 inflammasome including NLRP3, ASC and Caspase-1 increased significantly after S. aureus infection, Se played an important role in regulating the expression of NLRP3, ASC and Caspase-1; To further investigate the anti-inflammatory effect of Se, the expression level of IL-1β associated molecule pro-IL-1β and IL-1β were detected. Result shown that the mRNA expression of IL-1β was up-regulated by S. aureus and after Se treatment the expression level of IL-1β mRNA was markedly down-regulated, meanwhile Se play a regulation effect on the protein expression of Pro-IL-1β and IL-1β. Conclusions Here we show that ROS is involved in bMECs inflammation induced by S. aureus and Se ameliorates S. aureus -induced inflammation through ROS-mediated NLRP3 pathway in bMECs.

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Analyses of caspase-1-regulated transcriptomes in various tissues lead to identification of novel IL-1β-, IL-18- and sirtuin-1-independent pathways

Cited by 48 publications

References 80 publications

The role of atenolol in the modulation of the expression of genes encoding pro- (caspase-1) and anti- (Bcl2L1) apoptotic proteins in endothelial cells exposed to intestinal ischemia and reperfusion in rats

The role of atenolol in the modulation of the expression of genes encoding pro- (caspase-1) and anti- (Bcl2L1) apoptotic proteins in endothelial cells exposed to intestinal ischemia and reperfusion in rats

Hepatitis C Virus and Inflammation

Selenium ameliorates S. aureus-induced inflammation through ROS-mediated NLRP3 inflammasome in bovine mammary epithelial cells

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