LPS-induced Apoptosis is Partially Mediated by Hydrogen Sulphide in RAW 264.7 Murine Macrophages

Leema, George; Tamizhselvi, Ramasamy; Sirajudeen, Kns; Manickam, Venkatraman

doi:10.1080/08820139.2019.1566355

Cited by 36 publications

(21 citation statements)

References 40 publications

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“…A decrease of H 2 S level in murine macrophages following 24 hr of LPS or IFN‐γ stimulation was observed (early phase), but the H 2 S content was restored to normal level after 48 hr of stimulation (late phase), which was associated with the feedback regulation between CBS and CSE 54 . It is worthy of note that H 2 S production was correlated with LPS‐induced macrophage late‐stage apoptosis, which could be blocked by the addition of H 2 S inhibitor 55 . Therefore, it is possible that sustained LPS stimulation renders macrophages that undergo apoptosis through the production of H 2 S (Fig.…”

Section: H2s Signalling In Macrophage Activation and Inflammasome Formentioning

confidence: 98%

“…54 It is worthy of note that H 2 S production was correlated with LPS-induced macrophage late-stage apoptosis, which could be blocked by the addition of H 2 S inhibitor. 55 Therefore, it is possible that sustained LPS stimulation renders macrophages that undergo apoptosis through the production of H 2 S (Fig. 2).…”

Section: H 2 S Signalling In Macrophage Activation and Inflammasome Fmentioning

confidence: 99%

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The role of hydrogen sulphide signalling in macrophage activation

et al. 2020

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Section: H2s Signalling In Macrophage Activation and Inflammasome Formentioning

confidence: 98%

Section: H 2 S Signalling In Macrophage Activation and Inflammasome Fmentioning

confidence: 99%

The role of hydrogen sulphide signalling in macrophage activation

et al. 2020

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“…Pro-inflammatory agents, such as liposaccharide (LPS), tend to upregulate CSE, and anti-inflammatory and cytoprotective agents, such as steroids and statins, inhibit its expression [104][105][106][107]. Bacterial LPS increases CSE expression and concomitant H 2 S production in macrophages via activation of the p38 MAP kinase pathway, and glucocorticoids prevent this upregulation [104,105,108]. CSE upregulation in macrophages is also dependent on activation of the NF-κB and ERK pathways [109].…”

Section: H 2 S In Immune Cellsmentioning

confidence: 99%

Hyperhomocysteinemia and Cardiovascular Disease: Is the Adenosinergic System the Missing Link?

Paganelli

Mottola

Fromonot

et al. 2021

IJMS

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The influence of hyperhomocysteinemia (HHCy) on cardiovascular disease (CVD) remains unclear. HHCy is associated with inflammation and atherosclerosis, and it is an independent risk factor for CVD, stroke and myocardial infarction. However, homocysteine (HCy)-lowering therapy does not affect the inflammatory state of CVD patients, and it has little influence on cardiovascular risk. The HCy degradation product hydrogen sulfide (H2S) is a cardioprotector. Previous research proposed a positive role of H2S in the cardiovascular system, and we discuss some recent data suggesting that HHCy worsens CVD by increasing the production of H2S, which decreases the expression of adenosine A2A receptors on the surface of immune and cardiovascular cells to cause inflammation and ischemia, respectively.

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“…RAW 264.7 cells were cultured in DMEM (Himedia) and 10% FBS (Invitrogen, USA) media containing 1% antibiotic-antimycotic solution (100X, Gibco) as described previously (George, Ramasamy, & Sirajudeen, 2019). The 3T3-L1 pre-adipocytes were grown as previously described (Shihabudeen, Roy, James, & Thirumurugan, 2015).…”

Section: Cell Culturementioning

confidence: 99%

New insights into TNFα/PTP1B and PPARγ pathway through RNF213- a link between inflammation, obesity, insulin resistance and Moyamoya disease

Sarkar

Thirumurugan

2020

Preprint

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AbstractDiabetic patients are always at a higher risk of ischemic diseases like coronary artery diseases. One such ischemic carotid artery disease is Moyamoya. Moyamoya disease (MMD) has been associated with diabetes Type-I and II and the causality was unclear. RNF213 is the major susceptible gene for MMD. To understand the association between diabetes mellitus and MMD we chose the major players from both the anomalies, insulin and RNF213. But before establishing a role of RNF213 in insulin regulating pathway we had to understand the involvement of RNF213 within different biological systems. For this we have adopted a preliminary computational approach to understand the prominent interactions of RNF213. Our first objective was to construct an interactome for RNF213. We have analyzed several curated databases and adapted a list of RNF213 interacting partners to develop its interactome. Then to understand the involvement of this interactome in biological functions we have analyzed major biological pathways, biological processes and prominent clusters related to this interactome through computational approach. Then to develop a pathway that might give clue for RNF213 involvement in insulin regulatory pathway we have validated the intercluster and intracluster predictions and identified a regulatory pathway for RNF213. RNF213 interactome was observed to be involved in adaptive immunity with 4 major clusters; one of the cluster involved TNFα. Immune system involves several pathways, and therefore at this point we have chosen an event-based strategy to obtain an explicit target. Immunity is mediated by many pro-inflammatory cytokines like TNFα. TNFα-mediated inflammation, obesity and insulin resistance are associated. Therefore we chose to explore the role of RNF213 in TNFα-mediated inflammation in macrophages and inflammation-mediated insulin-resistance in adipocytes. We have observed an enhancement of RNF213 gene expression by LPS mediated pro-inflammatory stimuli and suppression by PPARγ-mediated anti-inflammatory, insulin sensitizing stimuli in macrophages. A more significant response was observed in adipocytes as well. Administration of the pro-inflammatory cytokine TNFα was able to impede the reduction in RNF213 expression during adipogenesis and this effect was observed to be mediated by PTP1B. Inactivation of PTP1B abolished RNF213 expression which in turn enhanced the adipogenesis process through enhanced PPARγ. Constitutive expression of RNF213 suppressed the adipocyte differentiation by the inhibition of PPARγ. We could show the expression of RNF213 has been regulated by TNFα/PTP1B pathway and PPARγ. The constitutive expression of RNF213 during adipogenesis appears to be an adipostatic measure that obese patients acquire to inhibit further adipogenesis. This is verified in silico by analyzing the gene expression data obtained from Gene Expression Omnibus database, which showed a higher expression of RNF213 in adipose tissue samples of obese people. Overall this study gives new insights in the TNFα-mediated pathway in adipogenesis and suggests a role of RNF213 in adipogenesis via this pathway.

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LPS-induced Apoptosis is Partially Mediated by Hydrogen Sulphide in RAW 264.7 Murine Macrophages

Cited by 36 publications

References 40 publications

The role of hydrogen sulphide signalling in macrophage activation

The role of hydrogen sulphide signalling in macrophage activation

Hyperhomocysteinemia and Cardiovascular Disease: Is the Adenosinergic System the Missing Link?

New insights into TNFα/PTP1B and PPARγ pathway through RNF213- a link between inflammation, obesity, insulin resistance and Moyamoya disease

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