Research Advances on Pathways of Nickel-Induced Apoptosis

Guo, Hongrui; Lian, Chen; Cui, Hengmin; Peng, Xi; Fang, Jing; Zuo, Zhuang; Deng, Junliang; Wang, Xun; Wu, Biao

doi:10.3390/ijms17010010

Cited by 66 publications

(36 citation statements)

References 190 publications

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“…Under ER stress, PERK phosphorylates eIF‐2α causing a translational arrest. However, prolonged ER stress can promote apoptosis . The immediate cellular response to ER stress is to reduce the protein load within the ER by attenuating general translation via activating PERK/eIF‐2α pathway .…”

Section: Discussionmentioning

confidence: 99%

“…ER stress can facilitate the translocation of the activated caspase‐12 to cytoplasm, which specially interacted with caspase‐9 . All these apoptosis responses eventually led to activation of caspase‐3, as the most important effector of caspases . The activities of caspase‐9 and −3, as well as the transcriptional status, were increased significantly after exposing to high doses of Cd, Cr or their mixture in rat liver .…”

Section: Discussionmentioning

confidence: 99%

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Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

Chang

Liu

Tian

et al. 2017

Environmental Toxicology

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Nickel oxide nanoparticles (nano NiO) could induce hepatocyte apoptosis, while its potential mechanisms are unclear. This study aimed to explore the role of endoplasmic reticulum (ER) stress pathways in hepatocyte apoptosis induced by nano NiO. Male Wistar rats were administrated with nano NiO (0.015, 0.06, and 0.24 mg/kg b.w.) and micro NiO (0.24 mg/kg b.w.) by intratracheal instillation twice a week for 6 weeks. We measured the hepatocyte apoptosis levels by TdT-mediated dUTP nick-end labeling (TUNEL) staining, ER stress related gene and protein expression levels in rat liver. The results showed that the TUNEL positive cells increased after exposure nano NiO, hinting hepatocyte apoptosis. The up-regulated gene and protein levels of 78 kD glucose regulated protein and CCAAT/enhancer binding protein homologous protein suggested that nano NiO triggered ER stress. Nano NiO exposure contributed to the increased protein contents of inositol-requiring enzyme 1 (IRE-1)α, p-IRE-1α, X box protein-1S, pancreatic ER kinase (PERK), p-PERK, eukaryotic initiation factor-2 alpha (eIF-2α), p-eIF-2α, caspase-12, -9, and -3, implicating that nano NiO can activate the pathways of ER stress-mediated apoptosis. These findings indicate that the ER stress pathways may play an important role in hepatocyte apoptosis induced by nano NiO.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

Chang

Liu

Tian

et al. 2017

Environmental Toxicology

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“…ciałek apoptotycznych). Ostatnim etapem apoptozy jest ich fagocytoza przez otaczają-ce keratynocyty, komórki dendrytyczne i makrofagi bez wywołania stanu zapalnego [2][3][4].…”

Section: Wstępunclassified

“…Keratynocyty łuszczycowe są oporne na sygnały przekazywane przez TNF-α, co prowadzi do paradoksalnego wzrostu stężenia TNF-α w zmianach skórnych oraz surowicy pacjentów z łuszczycą [4]. Stało się to powodem szerokiego stosowania w łusz-czycy terapii biologicznej skierowanej przeciw TNF-α.…”

Section: Apoptoza W łUszczycyunclassified

Selected aspects of apoptosis in psoriasis

Myśliwiec¹,

Baran²,

Flisiak³

2017

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StreSzczenIeApoptoza jest procesem fizjologicznej, programowanej śmierci komó-rek, która w odróżnieniu od nekrozy nie powoduje stanu zapalnego. Ma podstawowe znaczenie dla funkcjonowania różnych tkanek i narządów. Równowaga pomiędzy proliferacją a apoptozą keratynocytów jest istotna dla prawidłowej homeostazy naskórka. W schorzeniach skóry może dochodzić do pobudzenia apoptozy, co prowadzi zazwyczaj do chorób o ostrym przebiegu, lub jej zahamowania, co skutkuje częściej rozwojem chorób przewlekłych. Łuszczyca jest przewlekłą chorobą zapalną charakteryzującą się nadmierną proliferacją oraz zaburzeniem różnicowania keratynocytów. Keratynocyty łuszczycowe mają zmniejszoną zdolność do apoptozy, co może mieć duże znaczenie dla przerostu naskórka w łuszczycy. Zaburzenia apoptozy w łuszczycy dotyczą również komórek układu immunologicznego. W pracy omó-wiono podstawy procesu apoptozy, a także jej wybrane aspekty w patogenezie łuszczycy. ABStrActApoptosis is a physiological mechanism of programmed cell death, in contrast to necrosis, without eliciting an inflammatory response. It plays the key role in the functioning of different tissues and organs. The balance between proliferation and apoptosis of keratinocytes is important for epidermal maintenance of homeostasis. Dysfunctional apoptosis plays an important role in the development of several skin disorders. Diseases with an increase of apoptosis are usually acute, while those with inhibited apoptosis tend to be chronic. Psoriasis is an immune-mediated chronic inflammatory skin disease. It is characterized by keratinocyte hyperproliferation and abnormal differentiation. Psoriatic keratinocytes are resistant to apoptosis and this phenomenon can be the key event in psoriatic hyperplasia. Apoptosis disturbances can also affect immune cells involved in the pathogenesis of psoriasis. In this review, we describe the basic concept of apoptosis and its relevance in psoriatic pathogenesis.

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“…Also, previous research have demonstrated that Ni can induce apoptosis in B cells [23], human T hybridoma cells [24], HEp-2 and MCF-7 cells [25], CHO cells [26], and normal rat kidney cells [27]. So far, the extrinsic and intrinsic apoptotic pathways are widely explored in the apoptosis [28]. The intrinsic signaling pathways are known as mitochondria- and ER-initiated apoptosis [29, 30].…”

Section: Introductionmentioning

confidence: 99%

Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response

Guo

Cui

Fang

et al. 2016

Aging

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Up to now, the precise mechanism of Ni toxicology is still indistinct. Our aim was to test the apoptosis, cell cycle arrest and inflammatory response mechanism induced by NiCl2 in the liver of broiler chickens. NiCl2 significantly increased hepatic apoptosis. NiCl2 activated mitochondria-mediated apoptotic pathway by decreasing Bcl-2, Bcl-xL, Mcl-1, and increasing Bax, Bak, caspase-3, caspase-9 and PARP mRNA expression. In the Fas-mediated apoptotic pathway, mRNA expression levels of Fas, FasL, caspase-8 were increased. Also, NiCl2 induced ER stress apoptotic pathway by increasing GRP78 and GRP94 mRNA expressions. The ER stress was activated through PERK, IRE1 and ATF6 pathways, which were characterized by increasing eIF2α, ATF4, IRE1, XBP1 and ATF6 mRNA expressions. And, NiCl2 arrested G2/M phase cell cycle by increasing p53, p21 and decreasing cdc2, cyclin B mRNA expressions. Simultaneously, NiCl2 increased TNF-α, IL-1β, IL-6, IL-8 mRNA expressions through NF-κB activation. In conclusion, NiCl2 induces apoptosis through mitochondria, Fas and ER stress-mediated apoptotic pathways and causes cell cycle G2/M phase arrest via p53-dependent pathway and generates inflammatory response by activating NF-κB pathway.

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Research Advances on Pathways of Nickel-Induced Apoptosis

Cited by 66 publications

References 190 publications

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

Selected aspects of apoptosis in psoriasis

Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response

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