Nickel chloride-induced apoptosis via mitochondria- and Fas-mediated caspase-dependent pathways in broiler chickens

Guo, Hongrui; Cui, Hengmin; Fang, Jing; Zuo, Zhicai; Deng, Junliang; Wang, Xun; Zhao, Ling; Wu, Biao; Chen, Kejie

doi:10.18632/oncotarget.12946

Cited by 27 publications

(13 citation statements)

References 60 publications

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“…These findings are consistent with those of Zuo et al [36], in which nickel sulfate induces apoptosis in rat Leydig cells through activation of ROS-dependent mitochondria pathway. Likewise, the data of this study are compatible with our previous work that NiCl 2 induces apoptosis in the kidney of broiler chickens via mitochondria-dependent apoptotic pathway [37]. Interestingly, Z-YVAD-FMK (caspase-1 inhibitor) can decrease at least part of the apoptotic process.…”

Section: Discussionsupporting

confidence: 92%

Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Guo

Liu

Jian

et al. 2019

Aging

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Nickel (Ni), an environmental hazard, widely causes allergic contact hypersensitivity worldwide. Despite that Ni-stimulated pro-inflammatory response is vital in allergy, the underlying molecular mechanisms remain largely unclear. Here, we demonstrated that NiCl2 activated nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPKs) and interferon regulatory factor 3 (IRF3) signaling pathways in primary bone marrow-derived macrophages (BMDMs), leading to the altered transcription levels of interleukin-1β (IL-1β), -6, -8, -18, tumor necrosis factor-α (TNF-α) and interferon β (INF-β). We also found that nickel chloride (NiCl2) activated Nod-like receptor 3 (NLRP3) inflammasome pathway, resulting in the proteolytic cleavage and release of IL-1β. NiCl2 induced the accumulation of mitochondrial reactive oxygen species (mtROS) and the release of mitochondrial DNA (mtDNA), thus activating NLRP3 inflammasome pathway. Additionally, NiCl2-induced apoptosis was dependent on the generation of mtROS, and caspase-1 activation might also partly contribute to the apoptotic process. Altogether, abovementioned results indicate that NiCl2 induces inflammatory activation in BMDMs via NF-κB, MAPKs, IRF3 signaling pathways as well as NLRP3 inflammasome pathway, which provides a mechanism to improve the efficiency of treatment against Ni-induced allergic reactions.

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Section: Discussionsupporting

confidence: 92%

Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Guo

Liu

Jian

et al. 2019

Aging

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“…Our studies indicate that HTRA2 is important in CCL2/CCR2-mediated breast cancer cell growth and invasion, but not apoptosis. HTRA2 is best known for its role as an apoptotic inducer through binding and cleaving inhibitors of apoptosis proteins (Guo et al, 2016; Kilbride and Prehn, 2013). A few studies have indicated that HTRA2 may have other cellular functions.…”

Section: Discussionmentioning

confidence: 99%

Role of ALDH1A1 and HTRA2 expression to CCL2/CCR2 mediated breast cancer cell growth and invasion

Myers

Fang

et al. 2019

Biology Open

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Chemokines mediate immune cell trafficking during tissue development, wound healing and infection. The chemokine CCL2 is best known to regulate macrophage recruitment during wound healing, infection and inflammatory diseases. While the importance of CCL2/CCR2 signaling in macrophages during cancer progression is well documented, we recently showed that CCL2-mediated breast cancer progression depends on CCR2 expression in carcinoma cells. Using 3D Matrigel: Collagen cultures of SUM225 and DCIS.com breast cancer cells, this study characterized the mechanisms of CCL2/CCR2 signaling in cell growth and invasion. SUM225 cells, which expressed lower levels of CCR2 than DCIS.com cells, formed symmetrical spheroids in Matrigel: Collagen, and were not responsive to CCL2 treatment. DCIS.com cells formed asymmetric cell clusters in Matrigel: Collagen. CCL2 treatment increased growth, decreased expression of E-cadherin and increased TWIST1 expression. CCR2 overexpression in SUM225 cells increased responsiveness to CCL2 treatment, enhancing growth and invasion. These phenotypes corresponded to increased expression of Aldehyde Dehydrogenase 1A1 (ALDH1A1) and decreased expression of the mitochondrial serine protease HTRA2. CCR2 deficiency in DCIS.com cells inhibited CCL2-mediated growth and invasion, corresponding to decreased ALDH1A1 expression and increased HTRA2 expression. ALDH1A1 and HTRA2 expression were modulated in CCR2-deficient and CCR2-overexpressing cell lines. We found that ALDH1A1 and HTRA2 regulates CCR2-mediated breast cancer cell growth and cellular invasion in a CCL2/CCR2 context-dependent manner. These data provide novel insight on the mechanisms of chemokine signaling in breast cancer cell growth and invasion, with important implications on targeted therapeutics for anti-cancer treatment.

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“…In the cell caspase-8 and -10 cleave and activate the effectors of proteases, such as caspase-3, -6 and -7 that act on PARP, which lead to apoptosis (Figure 1). Moreover, some members of Bcl-2 family of proteins inhibit apoptosis [114]. In addition to its importance as a biological phenomenon, defective apoptotic processes have been involved in a wide variety of diseases.…”

Section: Nickel-induced Apoptosismentioning

confidence: 99%

Nickel: Human Health and Environmental Toxicology

Genchi

Carocci

Lauria

et al. 2020

IJERPH

892

383

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Nickel is a transition element extensively distributed in the environment, air, water, and soil. It may derive from natural sources and anthropogenic activity. Although nickel is ubiquitous in the environment, its functional role as a trace element for animals and human beings has not been yet recognized. Environmental pollution from nickel may be due to industry, the use of liquid and solid fuels, as well as municipal and industrial waste. Nickel contact can cause a variety of side effects on human health, such as allergy, cardiovascular and kidney diseases, lung fibrosis, lung and nasal cancer. Although the molecular mechanisms of nickel-induced toxicity are not yet clear, mitochondrial dysfunctions and oxidative stress are thought to have a primary and crucial role in the toxicity of this metal. Recently, researchers, trying to characterize the capability of nickel to induce cancer, have found out that epigenetic alterations induced by nickel exposure can perturb the genome. The purpose of this review is to describe the chemical features of nickel in human beings and the mechanisms of its toxicity. Furthermore, the attention is focused on strategies to remove nickel from the environment, such as phytoremediation and phytomining.

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Nickel chloride-induced apoptosis via mitochondria- and Fas-mediated caspase-dependent pathways in broiler chickens

Cited by 27 publications

References 60 publications

Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Nickel induces inflammatory activation via NF-κB, MAPKs, IRF3 and NLRP3 inflammasome signaling pathways in macrophages

Role of ALDH1A1 and HTRA2 expression to CCL2/CCR2 mediated breast cancer cell growth and invasion

Nickel: Human Health and Environmental Toxicology

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