Ultrasmall Prussian blue nanoparticles attenuate UVA-induced cellular senescence in human dermal fibroblasts <i>via</i> inhibiting the ERK/AP-1 pathway

Li, Yueyue; Zeng, Ni; Qin, Zhen; Chen, Yihe; Lü, Qian; Cheng, Yuxin; Xia, Qingyue; Lu, Zhiyu; Gu, Ning; Luo, Dan

doi:10.1039/d1nr04268h

Cited by 9 publications

(6 citation statements)

References 31 publications

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“…Protein kinase Cζ (PKCζ) phosphorylates p47phox and causes membrane-translocation of p47, inducing NOX2 activation [ 32 ]. ROS promotes phosphorylation of extracellular signal-regulated kinases (ERK), a subunit of MAPKs [ 33 , 34 ]. We found that MNNG induced phosphorylation of PKCζ, p47, and ERK, which were all restrained by crocetin pre-treatment in a concentration-dependent manner (Fig.…”

Section: Resultsmentioning

confidence: 99%

Crocetin antagonizes parthanatos in ischemic stroke via inhibiting NOX2 and preserving mitochondrial hexokinase-I

Liu

Zhang

et al. 2023

Cell Death Dis

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Parthanatos is one of the major pathways of programmed cell death in ischemic stroke characterized by DNA damage, poly (ADP-ribose) polymerases (PARP) activation, and poly (ADP-ribose) (PAR) formation. Here we demonstrate that crocetin, a natural potent antioxidant compound from Crocus sativus, antagonizes parthanatos in ischemic stroke. We reveal that mechanistically, crocetin inhibits NADPH oxidase 2 (NOX2) activation to reduce reactive oxygen species (ROS) and PAR production at the early stage of parthanatos. Meanwhile we demonstrate that PARylated hexokinase-I (HK-I) is a novel substrate of E3 ligase RNF146 and that crocetin interacts with HK-I to suppress RNF146-mediated HK-I degradation at the later stage of parthanatos, preventing mitochondrial dysfunction and DNA damage that ultimately trigger the irreversible cell death. Our study supports further development of crocetin as a potential drug candidate for preventing and/or treating ischemic stroke.

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Section: Resultsmentioning

confidence: 99%

Crocetin antagonizes parthanatos in ischemic stroke via inhibiting NOX2 and preserving mitochondrial hexokinase-I

Liu

Zhang

et al. 2023

Cell Death Dis

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“…Further research and exploration of the unique properties of USPBNZs in the context of skin health are warranted and may contribute to the development of innovative strategies for skin care and anti-aging interventions. 15 2.2.2 The significance of PBNZ crystallinity. The degree of crystallization significantly influences both the size and catalytic selectivity of the enzyme activity of nanomaterials such as PBNZs.…”

Section: Ning Gumentioning

confidence: 99%

Section: The Discovery and Modulation Of The Ros-scavenging Activity ...mentioning

confidence: 99%

Prussian blue nanozymes: progress, challenges, and opportunities

Long

Duan

et al. 2023

Nanoscale

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“…Protein kinase Cζ (PKCζ) phosphorylates p47phox and causes membrane-translocation of p47, inducing NOX2 activation 31 . ROS promotes phosphorylation of extracellular signal-regulated kinases (ERK), a subunit of MAPKs 32,33 . We found that MNNG induced phosphorylation of PKCζ, p47, and ERK, which were all restrained by crocetin pre-treatment in a concentration-dependent manner (Fig.…”

Section: Crocetin Reduces the Mnng-induced Early Phase Of Oxidative S...mentioning

confidence: 99%

Crocetin antagonizes parthanatos in ischemic stroke via inhibiting NOX2 and preserving mitochondrial hexokinase-I

Liu

Zhang

et al. 2022

Preprint

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Parthanatos is one of the major types of programmed cell death in ischemic stroke characterized by DNA damage, poly (ADP-ribose) polymerases (PARP) activation, and poly (ADP-ribose) (PAR) formation. Here we demonstrate that crocetin, a natural potent antioxidant compound from Crocus sativus, antagonizes parthanatos in ischemic stroke. We reveal that mechanistically, crocetin inhibits NADPH oxidase 2 (NOX2) activation to reduce reactive oxygen species (ROS) and PAR production at the early stage of parthanatos. Meanwhile we demonstrate that PARylated hexokinase-I (HK-I) is a novel substrate of E3 ligase RNF146 and that crocetin interact with HK-I to suppresses RNF146-mediated HK-I degradation at the late stage of parthanatos, preventing mitochondrial dysfunction and DNA damage that ultimately triggers the irreversible cell death. Our study supports further development of crocetin as a potential drug candidate for preventing and/or treating ischemic stroke.

show abstract

Ultrasmall Prussian blue nanoparticles attenuate UVA-induced cellular senescence in human dermal fibroblasts via inhibiting the ERK/AP-1 pathway

Abstract: Ultraviolet A (UVA) irradiation can induce cellular senescence and cause skin photoaging, which is mainly driven by excessive production of reactive oxygen species (ROS). Emerging studies have focused on new...

Cited by 9 publications

References 31 publications

Crocetin antagonizes parthanatos in ischemic stroke via inhibiting NOX2 and preserving mitochondrial hexokinase-I

Crocetin antagonizes parthanatos in ischemic stroke via inhibiting NOX2 and preserving mitochondrial hexokinase-I

Prussian blue nanozymes: progress, challenges, and opportunities

Crocetin antagonizes parthanatos in ischemic stroke via inhibiting NOX2 and preserving mitochondrial hexokinase-I

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