Identification of ASK1, MKK4, JNK, c-Jun, and caspase-3 as a signaling cascade involved in cadmium-induced neuronal cell apoptosis

Kim, Sun Don; Moon, Chang Kyu; Eun, Su-Yong; Ryu, Pan Dong; Jo, Sangmee Ahn

doi:10.1016/j.bbrc.2004.11.173

Cited by 139 publications

(102 citation statements)

References 39 publications

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“…Our results are supported by a recent study, which showed that H 2 O 2 induction of ROS contributes to p38MAPK activation (18). Collectively, the findings from our group and others (18)(19)(20) support the notion that ROS activation of the p38MAPK pathway may be a common mechanism by which oxidative stress or hypoxia/ ischemia induces neuronal cell death or neurodegenerative disorders.…”

supporting

confidence: 81%

“…Under oxidative stress, ROS, including free radicals such as superoxide (O 2 -), hydroxyl radical (HO -) and H 2 O 2 , are generated at high levels (12,30). Excessive amounts of ROS induced by oxidative stress may modify protein, lipids and DNA and alter their functions, resulting in apoptosis of neuronal cells (19,31). Our previous study and other studies (6) have demonstrated that CoCl 2 elicits oxidative stress, which contributes to neuronal apoptosis.…”

Section: Discussionmentioning

confidence: 93%

“…In neuronal cells, the p38 signaling pathway is preferentially activated by inflammatory cytokines and environmental stress, such as osmotic stress, ultraviolet light, heat shock and hypoxia. It can also be activated by ROS (12,(18)(19)(20)(21). Previous studies have demonstrated that p38MAPK activation is implicated in neuronal damage associated with ischemia and neurodegenerative disease (32), and it is one of the apoptotic markers during PC12 cell death induced by a variety of stimuli (15)(16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

“…p38MAPK has been demonstrated to be one of the apoptotic markers during PC12 cell death induced by various stimuli (15)(16)(17)(18). Notably, excessive ROS have been shown to activate members of MAPKs, including extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun-N-terminal kinase (JNK) and p38MAPK in various types of cells (19)(20)(21). Recently, studies have found that H 2 O 2 induction of ROS inhibits serine/threonine protein phosphatase 2A (PP2A), a major negative regulator of phosphorylated (p)-ERK1/2, JNK and p38MAPK (22,23) and protein phosphatase 5 (PP5), a negative regulator of the JNK cascade involved in stress responses (24,25), leading to activation of the ERK1/2, JNK and p38MAPK pathways, thereby resulting in neuronal apoptosis (18).…”

Section: Introductionmentioning

confidence: 99%

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Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

et al. 2011

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Abstract. The present study investigated whether there is an interaction between reactive oxygen species (ROS) and p38 mitogen-activated protein kinase (MAPK) during chemical hypoxia-induced injury in PC12 cells. The results of the present study showed that cobalt chloride (CoCl 2 ), a chemical hypoxia agent, markedly induced ROS generation and phosphorylation of p38MAPK, as well as neuronal injuries. N-acetylcysteine (NAC), a ROS scavenger, blocked CoCl 2 -induced phosphorylation of p38MAPK. In addition, SB203580, an inhibitor of p38MAPK attenuated not only CoCl 2 -induced activation of p38MAPK, but also ROS production. These results suggest that ROS and p38MAPK are capable of interacting positively during chemical hypoxia. Furthermore, NAC and SB203580 markedly prevented CoCl 2 -induced cytotoxicity, apoptosis and a loss of mitochondrial membrane potential. Taken together, our findings suggest that the positive interaction between CoCl 2 induction of ROS and p38MAPK activation may play a significant role in CoCl 2 -induced neuronal injuries. We provide new insights into the mechanisms responsible for CoCl 2 -induced injuries in PC12 cells.

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supporting

confidence: 81%

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

et al. 2011

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“…While, the exact mechanism on how oxidative stress induced by MC-RR leading to plant cell apoptosis remains to be poorly understood. The data from other groups (Kim et al, 2005) suggested that ROS activation of the mitogen activated protein kinase (MAPK) cascades might be a common mechanism by which oxidative stress induces cell death. Chen et al (2009) identified that oxidative stress activates the MAPK pathway by induction of ROS and inhibition of PP 2A leading to apoptosis of neuronal cells.…”

Section: Resultsmentioning

confidence: 99%

Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis

Huang

Liu

2014

Journal of Environmental Sciences

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Cadmium Compounds

Saghir,

Ewert,

Shekh

et al. 2023

Patty's Toxicology

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Cadmium (Cd) is a soft, malleable, silvery bluish‐gray, relatively rare metal, occurs mainly with Zn, Pb, and Cu. Cadmium is used in nickel–cadmium batteries; pigments, protective plating on steel, ceramics, and glass; stabilizers for PVC; and as a component in various alloys. Production of Cd was ∼20 tons in 1920 and is well over 25,000 tons now. Cadmium is released into the atmosphere from both natural and anthropogenic sources. In workplace, Cd dust and fume arise from smelting nonferrous metals and in the production of Cd‐containing materials. Cadmium in air range 0.1–5 ng/m 3 in rural, 1–20 ng/m 3 in urban, and 15–150 ng/m 3 in industrialized areas. Little or no differences are noted in Cd levels between indoor and outdoor air; however, smoking substantially increases indoor air Cd concentrations as it is present in tobacco. Cadmium can cause severe acute or chronic toxicity; although, acute toxicity is less common. Most cases are from chronic exposure; even low‐level chronic exposure can affect many organs with the kidneys and bones being the principal targets. OSHA has three occupational exposure limits for Cd: AL of 2.5 μg/m 3 (8‐h TWA), PEL of 5 μg/m 3 , and SECAL of 15 or 50 μg/m 3 , depending on the processes involved. SECAL requires that the levels are achieved by combination of engineering and work practice control methods and respirators to the extent feasible to protect workers from exposures above PEL. This chapter covers toxicity of a number of Cd compounds along with regulations based on the available data.

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Identification of ASK1, MKK4, JNK, c-Jun, and caspase-3 as a signaling cascade involved in cadmium-induced neuronal cell apoptosis

Cited by 139 publications

References 39 publications

Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

Interaction between ROS and p38MAPK contributes to chemical hypoxia-induced injuries in PC12 cells

Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis

Cadmium Compounds

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