ROS/TNF-α Crosstalk Triggers the Expression of IL-8 and MCP-1 in Human Monocytic THP-1 Cells via the NF-κB and ERK1/2 Mediated Signaling

Akhter, Nadeem; Wilson, Ajit; Thomas, Reeby; Al-Rashed, Fatema; Kochumon, Shihab; Al-Roub, Areej; Arefanian, Hossein; Madhoun, Ashraf Al; Al-Mulla, Fahd; Ahmad, Rasheed; Sindhu, Sardar

doi:10.3390/ijms221910519

Cited by 38 publications

(23 citation statements)

References 68 publications

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“…In consistent with previous reports ( 28 , 29 ), we identified that CCL2 was expressed in LECs, and that LEC-expressing CCL2 was regulated by S1pr1. Previous studies showed that ERK signaling pathway was involved in the regulation of the expression of multiple genes, including CCL2 ( 17 , 30 , 31 ). In consistence with these reports ( 17 , 30 , 31 ), our data showed that S1pr1 enhanced the expression of CCL2 in LECs via the ERK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

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Lymphatic endothelial sphingosine 1-phosphate receptor 1 enhances macrophage clearance via lymphatic system following myocardial infarction

Zhou

Zhao

et al. 2022

Front. Cardiovasc. Med.

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Lymphatic endothelial cell homeostasis plays important roles in normal physiological cardiac functions, and its dysfunction significantly influences pathological cardiac remodeling after myocardial infarction (MI). Our results revealed that sphingosine 1-phosphate receptor 1 (S1pr1) expression in cardiac lymphatic endothelial cells (LECs) was sharply changed after MI. It has been shown that S1pr1 tightly controlled LEC functions and homeostasis. We thus hypothesized that lymphatic endothelial S1pr1 might be involved in post-MI cardiac remodeling. We generated LEC-conditional S1pr1 transgenic mice, in which S1pr1 expression was reduced in cardiac LECs. We performed the left anterior descending coronary artery (LAD) ligation operation to induce MI in these mice. Cardiac functions and remodeling were examined by echocardiography analysis and serial histological analysis. Meanwhile, we performed adoptive cell transfer experiments to monitor macrophage trafficking in post-MI myocardium and their draining lymphatic system. Furthermore, in vitro cell culture experiments and mechanism studies were undertaken to uncover the molecular mechanism by which LEC-S1pr1 regulated cardiac inflammation and remodeling after MI. Our results showed that S1pr1 expression significantly decreased in cardiac LECs after MI. Our in vivo experiments showed that the reduced expression of LEC-S1pr1 deteriorated cardiac function and worsened pathological cardiac remodeling after MI. Our further results demonstrated that the reduced expression of LEC-S1pr1 did not influence macrophage infiltration in an early inflammatory phase of MI, but significantly affected macrophages clearance in the later phase of MI via afferent cardiac lymphatics, and thus influenced inflammatory responses and cardiac outcome after MI. Further study showed that S1P/S1pr1 activated ERK signaling pathway and enhanced CCL2 expression, which promoted macrophage trafficking in a paracrine manner. This study reveals that cardiac lymphatic endothelial cells tightly control macrophage trafficking via lymphatic vessels in injured hearts via S1P/S1pr1/ERK/CCL2 pathway and thus regulate post-MI immune modulation and heart repair. This study highlights the importance of cardiac lymphatic vessel system in orchestrating post-MI immune responses and cardiac remodeling by regulating macrophage transit in injured hearts. Our finding implies that a feasible modulation of S1pr1 signaling in LECs might provide a promising target to resolve excessive inflammation and to ameliorate adverse cardiac remodeling after MI.

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Section: Discussionmentioning

confidence: 99%

“…Previous studies showed that ERK signaling pathway was involved in the regulation of the expression of multiple genes, including CCL2 ( 17 , 30 , 31 ). In consistence with these reports ( 17 , 30 , 31 ), our data showed that S1pr1 enhanced the expression of CCL2 in LECs via the ERK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Lymphatic endothelial sphingosine 1-phosphate receptor 1 enhances macrophage clearance via lymphatic system following myocardial infarction

Zhou

Zhao

et al. 2022

Front. Cardiovasc. Med.

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“…THP-1 cells were seeded in a 6-well plate at a density of 1 × 10 6 cells/well and then induced in RPMI 1640 medium with 100 ng/mL PMA for 48 h at 37 °C and 5% CO 2 . Cellular ROS was measured using a DCFH-DA probe (Sigma-Aldrich), as described previously [ 67 ]. The fluorescence intensity was measured using a flow cytometer (Beckman).…”

Section: Methodsmentioning

confidence: 99%

SHED-derived exosomes promote LPS-induced wound healing with less itching by stimulating macrophage autophagy

Xie

Cheng

et al. 2022

J Nanobiotechnol

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High-quality cutaneous wound healing is associated with rapid wound closure and a comfortable healing process. Currently, exosomes derived from mesenchymal stem cells displayed a prominent therapeutic effect on skin wound closure. But the therapeutic approaches for wound itching are very limited in clinical. Stem cells from human exfoliated deciduous teeth (SHED) may offer a unique exosome resource for cell-free therapeutics in potential clinical applications. Here, we investigated the common mechanisms underlying wound closure and unpleasant sensation of itching, focusing on the contribution of the SHED-derived exosome to immune response and wound itching during healing. The effects of SHED-derived exosomes on inflammatory wound healing were examined using lipopolysaccharide (LPS)-induced wounds in a mouse model. We found prolonged inflammation and distinct itch responses in skin wound tissue during LPS-induced wound healing. SHED-derived exosomes facilitated LPS-induced wound closure and relieved wound itching. Therefore, they are ideal for the treatment of wound healing. Macrophages in skin wound tissues are responsible for autophagy during wound healing. Macrophage autophagy also regulates cell proliferation, migration, and neuronal signal transduction in vitro. SHED-derived exosomes containing miR-1246 enhanced autophagy by regulating macrophage function through the AKT, ERK1/2, and STAT3 signaling pathways. Thus, SHED-derived exosomes promote wound healing with less itching in an LPS-induced wound model by stimulating macrophage autophagy, which has implications for the treatment of inflammatory wound healing. Graphical Abstract

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“…Relative gene expression to the lean AT control was also calculated using the comparative cycles to threshold (C T ) method, as has been described previously [ 43 ]. Results were normalized using glyceraldehyde 3-phosphate dehydrogenase ( GAPDH ), and means ± standard error of the mean (SEM) are expressed as fold changes in the expression relative to controls as indicated [ 44 ].…”

Section: Methodsmentioning

confidence: 99%

Dectin-1 as a Potential Inflammatory Biomarker for Metabolic Inflammation in Adipose Tissue of Individuals with Obesity

Madhoun

Kochumon

Al-Rashed

et al. 2022

Cells

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In obesity, macrophage activation and infiltration in adipose tissue (AT) underlie chronic low-grade inflammation-induced insulin resistance. Although dectin-1 is primarily a pathogen recognition receptor and innate immune response modulator, its role in metabolic syndromes remains to be clarified. This study aimed to investigate the dectin-1 gene expression in subcutaneous AT in the context of obesity and associated inflammatory markers. Subcutaneous AT biopsies were collected from 59 nondiabetic (lean/overweight/obese) individuals. AT gene expression levels of dectin-1 and inflammatory markers were determined via real-time reverse transcriptase-quantitative polymerase chain reaction. Dectin-1 protein expression was assessed using immunohistochemistry. Plasma lipid profiles were measured by ELISA. AT dectin-1 transcripts and proteins were significantly elevated in obese as compared to lean individuals. AT dectin-1 transcripts correlated positively with body mass index and fat percentage (r ≥ 0.340, p ≤ 0.017). AT dectin-1 RNA levels correlated positively with clinical parameters, including plasma C-reactive protein and CCL5/RANTES, but negatively with that of adiponectin. The expression of dectin-1 transcripts was associated with that of various proinflammatory cytokines, chemokines, and their cognate receptors (r ≥ 0.300, p ≤ 0.05), but not with anti-inflammatory markers. Dectin-1 and members of the TLR signaling cascade were found to be significantly associated, suggesting an interplay between the two pathways. Dectin-1 expression was correlated with monocyte/macrophage markers, including CD16 , CD68 , CD86 , and CD163 , suggesting its monocytes/macrophage association in an adipose inflammatory microenvironment. Dectin-1 expression was independently predicted by CCR5 , CCL20 , TLR2 , and MyD88 . In conclusion, dectin-1 may be regarded as an AT biomarker of metabolic inflammation in obesity.

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ROS/TNF-α Crosstalk Triggers the Expression of IL-8 and MCP-1 in Human Monocytic THP-1 Cells via the NF-κB and ERK1/2 Mediated Signaling

Cited by 38 publications

References 68 publications

Lymphatic endothelial sphingosine 1-phosphate receptor 1 enhances macrophage clearance via lymphatic system following myocardial infarction

Lymphatic endothelial sphingosine 1-phosphate receptor 1 enhances macrophage clearance via lymphatic system following myocardial infarction

SHED-derived exosomes promote LPS-induced wound healing with less itching by stimulating macrophage autophagy

Dectin-1 as a Potential Inflammatory Biomarker for Metabolic Inflammation in Adipose Tissue of Individuals with Obesity

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