MiR-182–5p/TLR4/NF-κB axis contributes to the protective effect of caffeic acid phenethyl ester against cadmium-induced spleen toxicity and associated damage in mice

Hao, Rili; Jiang, Yang; Li, Feng; Sun‐Waterhouse, Dongxiao

doi:10.1016/j.fct.2021.112654

Cited by 9 publications

(10 citation statements)

References 35 publications

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“…The spleen histomorphology of TDCPP-treated mice showed pathological changes. These pathomorphological alterations in the spleen are similar to previous findings, which showed that BDE-209 suppresses splenic cell immune and physiological functions by inducing inflammation and apoptosis, ultimately leading to splenic atrophy [ 35 ] and cadmium-induced spleen toxicity in mice [ 36 ], suggesting that these environmental pollutants cause splenic toxicity in a similar way. Body weight is one of the important indicators of the health of organisms and is influenced by several factors, such as excessive or insufficient energy intake and abnormal energy consumption, such as excessive exercise and disease.…”

Section: Discussionsupporting

confidence: 88%

Spleen Toxicity of Organophosphorus Flame Retardant TDCPP in Mice and the Related Mechanisms

Cao

Wei

et al. 2023

Toxics

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Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) is an organophosphorus flame retardant that has been utilized in recent years as a primary replacement for polybrominated diphenyl ethers (PBDEs) in a wide variety of fire-sensitive applications. However, the impact of TDCPP on the immune system has not been fully determined. As the largest secondary immune organ in the body, the spleen is considered to be an important study endpoint for determining immune defects in the body. The aim of this study is to investigate the effect of TDCPP toxicity on the spleen and its possible molecular mechanisms. In this study, for 28 consecutive days, TDCPP was administered intragastrically (i.g), and we assessed the general condition of mice by evaluating their 24 h water and food intake. Pathological changes in spleen tissues were also evaluated at the end of the 28-day exposure. To measure the TDCPP-induced inflammatory response in the spleen and its consequences, the expression of the critical players in the NF-κB pathway and mitochondrial apoptosis were detected. Lastly, RNA-seq was performed to identify the crucial signaling pathways of TDCPP-induced splenic injury. The results showed that TDCPP intragastric exposure triggered an inflammatory response in the spleen, likely through activating the NF-κB/IFN-γ/TNF-α/IL-1β pathway. TDCPP also led to mitochondrial-related apoptosis in the spleen. Further RNA-seq analysis suggested that the TDCPP-mediated immunosuppressive effect is associated with the inhibition of chemokines and the expression of their receptor genes in the cytokine–cytokine receptor interaction pathway, including four genes of the CC subfamily, four genes of the CXC subfamily, and one gene of the C subfamily. Taken together, the present study identifies the sub-chronic splenic toxicity of TDCPP and provides insights on the potential mechanisms of TDCPP-induced splenic injury and immune suppression.

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Section: Discussionsupporting

confidence: 88%

Spleen Toxicity of Organophosphorus Flame Retardant TDCPP in Mice and the Related Mechanisms

Cao

Wei

et al. 2023

Toxics

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“…Prior studies have identified miR-182-5p to regulating MAPK and NF-κB signaling pathways in colorectal cancer and spleen intoxication. (45,46) Assuming that inflammation plays a pivotal role in the pathogenesis of SONFH, (47)(48)(49) we analyzed a potential connection of these pro-inflammatory signaling pathways to the expression level of miR-182-5p. Our results showed that the phosphorylation levels of Erk1/2, p38 MAPK, and p65 pathway components were induced in SONFH-hBMSCs and inhibited in miR-182-5p mimic transfected SONFH-hBMSCs.…”

Section: Discussionmentioning

confidence: 99%

Low miR‐182‐5p Expressing Extracellular Vesicles Derived From Human Bone Marrow Stromal Cells of Subjects With Steroid‐Induced Osteonecrosis of the Femoral Head Aggravate Disease Progression

Kong

et al. 2023

J of Bone & Mineral Res

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Steroid‐induced osteonecrosis of the femoral head (SONFH) is a refractory, progressive disease. However, the underlying mechanisms that aggravate femoral head necrosis remain unclear. Extracellular vesicles (EVs) act as molecular carriers in intercellular communication. We hypothesize that EVs derived from human (h) bone marrow stromal cells (BMSC) resident in SONFH lesion areas promote the pathogenesis of SONFH. In the present study, we determined the modulatory effects of SONFH‐hBMSCs‐derived EVs on the pathogenesis of SONFH in vitro and in vivo. We found that the expression of hsa‐miR‐182‐5p was downregulated in SONFH‐hBMSCs and EVs isolated from those hBMSCs. After tail vein injection, EVs isolated from hBMSCs transfected with hsa‐miR‐182‐5p inhibitor aggravated femoral head necrosis in the SONFH mouse model. We conclude that miR‐182‐5p regulates bone turnover in the SONFH mouse model via targeting MYD88 and subsequent upregulation of RUNX2 expression. We further assume that EVs derived from hBMSCs resident in SONFH lesion areas aggravate femoral head necrosis by downregulating miR‐182‐5p secreted from hBMSC located outside these lesions. We suggest that miR‐182‐5p could provide a novel target for future therapeutic approaches to treat or prevent SONFH. © 2023 American Society for Bone and Mineral Research (ASBMR).

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“…Current research indicates that Cd exposure can induce autophagy inhibition and apoptosis via Nrf2‐regulated signal pathway related to antioxidation and oxidation in spleen (Qu et al, 2019). Cd‐induced apoptosis and inflammation in spleen can be triggered by miR182‐5p‐TLR4/NF‐κB axis (Hao et al, 2021). Co‐exposure (molybdenum and Cd) induced pyroptosis and autophagy may associate with PI3K/AKT axis in spleen (Xin et al, 2020; Yiming et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

“…apoptosis and inflammation in spleen can be triggered by miR182-5p-TLR4/NF-κB axis (Hao et al, 2021). Co-exposure (molybdenum and Cd) induced pyroptosis and autophagy may associate with PI3K/AKT axis in spleen (Xin et al, 2020;Yiming et al, 2021).…”

mentioning

confidence: 98%

Cadmium exposure induces necroptosis of porcine spleen via ROS‐mediated activation of STAT1/RIPK3 signaling pathway

Lei

Zhang

et al. 2023

Environ and Mol Mutagen

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Cadmium (Cd), a heavy metal, is used in a wide range of applications, such as plastics, electroplating process, electronics, and so forth. Due to its bioaccumulation ability, Cd can contaminate soil, water, air and food. To determine the effect of Cd exposure on the necroptosis in pig spleen and its mechanistic investigation, we constructed a model in pigs by feeding them food containing 20 mg/kg Cd. In this study, we analyzed the effects of Cd exposure on pig spleen through HE staining, Quantitative real‐time PCR (qRT‐PCR), Western blot (WB), and principal component analysis (PCA). Results show that Cd exposure can destroy the structure and function of pig spleen, which is closely related to necroptosis. Further results show that Cd exposure can induce necroptosis through ROS‐mediated activation of Signal transducer and activator of transcription 1/Receptor‐Interacting Serine/Threonine‐Protein Kinase 3 (STAT1/RIPK3) signaling pathway in pig spleen. Additionally, Cd exposure also can affect the stability of mitochondrial‐associated endoplasmic reticulum membrane (MAMs) structure, which also contributes to the process of necroptosis. Our study provides insights into the physiological toxicity caused by Cd exposure.

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MiR-182–5p/TLR4/NF-κB axis contributes to the protective effect of caffeic acid phenethyl ester against cadmium-induced spleen toxicity and associated damage in mice

Cited by 9 publications

References 35 publications

Spleen Toxicity of Organophosphorus Flame Retardant TDCPP in Mice and the Related Mechanisms

Spleen Toxicity of Organophosphorus Flame Retardant TDCPP in Mice and the Related Mechanisms

Low miR‐182‐5p Expressing Extracellular Vesicles Derived From Human Bone Marrow Stromal Cells of Subjects With Steroid‐Induced Osteonecrosis of the Femoral Head Aggravate Disease Progression

Cadmium exposure induces necroptosis of porcine spleen via ROS‐mediated activation of STAT1/RIPK3 signaling pathway

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