A protective role of heme-regulated eIF2α kinase in cadmium-induced toxicity in erythroid cells

Wang, Lixin; Wang, Xiaoyan; Zhang, Shuping; Qu, Guangbo; Liu, Sijin

doi:10.1016/j.fct.2013.10.017

Cited by 17 publications

(26 citation statements)

References 45 publications

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“…S7B). In agreement with previous reports [22,24,25], As treatment greatly enhanced ATF4 protein level in MEL cells and ex vivo cultured fetal liver cells (Fig. 4A and Supplementary Fig.…”

Section: Nrf2-mir-214 Targets Atf4 To Protect Cells Against As Toxicitysupporting

confidence: 93%

“…Our recent studies demonstrated that ATF4 plays a crucial role against oxidative stress including As-and cadmium-induced impairments to erythroid cells [22,24]. The important role of Nrf2 in anti-stress responses has also been documented in erythroid cells [14,71].…”

Section: Discussionmentioning

confidence: 88%

“…Cells were treated with various reagents including tertiary butylhydroquinone (TBHQ) and ferric nitrilotriacetate (Fe-NTA) (SigmaAldrich, St. Louis, MO, USA). Cell death was determined with a kit from BD Biosciences (San Diego, CA, USA), according to an established method [24].…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

“…Thereafter, FACS analysis was performed on a BD FACSCalibur™ (BD Biosciences), according to the established method as described previously [24].…”

Section: Flow Cytometry (Facs) Analysismentioning

confidence: 99%

“…The increased demand of iron for hemoglobin synthesis in erythroblast results in enhanced formation of labile iron and consequently generation of free radicals, oxidative stress and cytotoxicity [19][20][21]. In addition, erythroid precursors may be also subjected to diverse stresses in bone marrow, such as hypoxia, mechanical stress, radiation, foreign chemicals and environmental toxicants [23][24][25][26]. Thus, an elegant network has evolved to protect erythroid cells during differentiation, including translation control to prevent hemoglobin aggregating by heme-regulated eIF2α kinase (HRI), ATF4 signaling against oxidative stress and Nrf2 signaling-mediated protection, etc [22,27].…”

Section: Introductionmentioning

confidence: 99%

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miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

Gao

Liu

Chen

et al. 2016

Free Radical Biology and Medicine

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“…S7B). In agreement with previous reports [22,24,25], As treatment greatly enhanced ATF4 protein level in MEL cells and ex vivo cultured fetal liver cells (Fig. 4A and Supplementary Fig.…”

Section: Nrf2-mir-214 Targets Atf4 To Protect Cells Against As Toxicitysupporting

confidence: 93%

Section: Discussionmentioning

confidence: 88%

Section: Cell Culture and Treatmentmentioning

confidence: 99%

“…Thereafter, FACS analysis was performed on a BD FACSCalibur™ (BD Biosciences), according to the established method as described previously [24].…”

Section: Flow Cytometry (Facs) Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

Gao

Liu

Chen

et al. 2016

Free Radical Biology and Medicine

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An Important Function of Petrosiol E in Inducing the Differentiation of Neuronal Progenitors and in Protecting Them against Oxidative Stress

Liu

Wang

et al. 2017

Advanced Science

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Insufficient endogenous neurotrophin supply contributes to neurodegeneration. Meanwhile, neuronal injuries are also attributed to oxidative stress upon toxin exposure. Thus, reconstruction neurite extension and antioxidative stress are the potential strategies for ameliorating neuronal injuries. However, there is no well‐defined therapeutic developed in this regard. In search of such therapeutics, Petrosiol E is identified here as a potent inducer to guide the differentiation of neuronal progenitor cells. Petrosiol E also considerably promotes embryonic stem cell differentiation into neural ectoderm features. Moreover, Petrosiol E reveals an antioxidant function to protect cells from oxidative stress induced by arsenic. Moreover, the molecular mechanism underlying Petrosiol E‐induced neuronal differentiation is uncovered: (a) enhancement of NF‐E2‐related factor 2 (Nrf 2) activity in driving neuronal differentiation; (b) diminishment of oxidative stress. Petrosiol E activates the mitogen‐activated protein kinase and serine/threonine kinase signaling to enhance the activity of Nrf 2. As a result of enhanced Nrf 2 activity, neuronal differentiation is accelerated, and the cellular antioxidation responses are also enforced, even under arsenic‐induced neurotoxicity. Together, the combined results unveil a desirable role of Petrosiol E in driving neuronal differentiation and in combating oxidative stress. This study would open an avenue to develop new therapeutics based on Petrosiol compounds to treat neurodegenerative diseases.

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Adverse Impact of Heavy Metals on Bone Cells and Bone Metabolism Dependently and Independently through Anemia

Zhang

Sun²,

Zhang

et al. 2020

Advanced Science

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Mounting evidence is revealing that heavy metals can incur disordered bone homeostasis, leading to the development of degenerative bone diseases, including osteoporosis, osteoarthritis, degenerative disk disease, and osteomalacia. Meanwhile, heavy metal-induced anemia has been found to be intertwined with degenerative bone diseases. However, the relationship and interplay among these adverse outcomes remain elusive. Thus, it is of importance to shed light on the modes of action (MOAs) and adverse outcome pathways (AOPs) responsible for degenerative bone diseases and anemia under exposure to heavy metals. In the current Review, the epidemiological and experimental findings are recapitulated to interrogate the contributions of heavy metals to degenerative bone disease development which may be attributable dependently and independently to anemia. A few likely mechanisms are postulated for anemia-independent degenerative bone diseases, including dysregulated osteogenesis and osteoblastogenesis, imbalanced bone formation and resorption, and disturbed homeostasis of essential trace elements. By contrast, remodeled bone microarchitecture, inhibited erythropoietin production, and disordered iron homeostasis are speculated to account for anemia-associated degenerative bone disorders upon heavy metal exposure. Together, this Review aims to elaborate available literature to fill in the knowledge gaps in understanding the detrimental effects of heavy metals on bone cells and bone homeostasis through different perspectives.

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A protective role of heme-regulated eIF2α kinase in cadmium-induced toxicity in erythroid cells

Cited by 17 publications

References 45 publications

miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

miR-214 protects erythroid cells against oxidative stress by targeting ATF4 and EZH2

An Important Function of Petrosiol E in Inducing the Differentiation of Neuronal Progenitors and in Protecting Them against Oxidative Stress

Adverse Impact of Heavy Metals on Bone Cells and Bone Metabolism Dependently and Independently through Anemia

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