Ochratoxin A-Induced Apoptosis of IPEC-J2 Cells through ROS-Mediated Mitochondrial Permeability Transition Pore Opening Pathway

Wang, Hong; Chen, Ying; Zhai, Nianhui; Chen, Xingxiang; Gan, Fang; Hu, Li; Huang, Kehe

doi:10.1021/acs.jafc.7b04434

Cited by 86 publications

(50 citation statements)

References 46 publications

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“…Caspase 9, the initiator caspase in the mitochondria-dependent apoptosis pathway, activates the downstream effector Caspase 3, and active Caspase 3 impairs DNA repair through the cleavage of poly ADP-ribose polymerase (PARP). Excess ROS upregulate autophagy to remove proteins and organelles with oxidative damage in the cytoplasm [18][19][20][21]. LC3-phosphatidylethanolamine conjugate (LC3-II), a marker for autophagy, is involved in the formation of autophagosome membranes, and autophagosomes might fuse with lysosomes to degrade damaged cytosolic components [22][23][24][25].…”

Section: Introductionmentioning

confidence: 99%

2,3,4′,5-Tetrahydroxystilbene-2-O-β-D-Glucoside (THSG) Activates the Nrf2 Antioxidant Pathway and Attenuates Oxidative Stress-Induced Cell Death in Mouse Cochlear UB/OC-2 Cells

Lin

Luo

et al. 2020

Biomolecules

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Oxidative stress plays a critical role in the pathogenesis of hearing loss, and 2,3,4 ,5-tetrahydroxystilbene-2-O-β-D-glucoside (THSG) exerts antioxidant effects by inhibiting reactive oxygen species (ROS) generation. With the aim of developing new therapeutic strategies for oxidative stress, this study investigated the protective mechanism of THSG in vitro using a normal mouse cochlear cell line (UB/OC-2). The THSG and ascorbic acid have similar free radical scavenger capacities. H 2 O 2 , but not THSG, reduced the UB/OC-2 cell viability. Moreover, H 2 O 2 might induce apoptosis and autophagy by inducing morphological changes, as visualized by microscopy. As evidenced by Western blot analysis and monodansylcadaverine (MDC) staining, THSG might decrease H 2 O 2 -induced autophagy. According to a Western blotting analysis and Annexin V/PI and JC-1 staining, THSG might protect cells from H 2 O 2 -induced apoptosis and stabilize the mitochondrial membrane potential. Furthermore, THSG enhanced the translocation of nucleus factor erythroid 2-related factor 2 (Nrf2) into the nucleus and increased the mRNA and protein expression of antioxidant/detoxifying enzymes under H 2 O 2 -induced oxidative stress conditions. Collectively, our findings demonstrate that THSG, as a scavenging agent, can directly attenuate free radicals and upregulate antioxidant/detoxifying enzymes to protect against oxidative damage and show that THSG protects UB/OC-2 cells from H 2 O 2 -induced autophagy and apoptosis in vitro.

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Section: Introductionmentioning

confidence: 99%

2,3,4′,5-Tetrahydroxystilbene-2-O-β-D-Glucoside (THSG) Activates the Nrf2 Antioxidant Pathway and Attenuates Oxidative Stress-Induced Cell Death in Mouse Cochlear UB/OC-2 Cells

Lin

Luo

et al. 2020

Biomolecules

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“…A wide range of chemical entities possesses ·OH‐scavenging abilities, for instance isopropyl alcohol, cytosine, uracil, Tempo, GSH, and DMSO, among which a great proportion are biologically relevant . However, a reliable and robust method to quantify their reactivity is currently lacking, impeding the understanding of various fundamental processes in chemical and biological systems.…”

Section: Resultsmentioning

confidence: 99%

Synthesis and activity of a coumarin‐based fluorescent probe for hydroxyl radical detection

Zhang

Zhou

et al. 2019

Luminescence

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As a type of reactive oxygen species (ROS), hydroxyl radical (·OH) is closely associated with many kinds of diseases. The present study aimed to develo p a novel OH fluorescent probe based on coumarin, a new compound that has not been previously reported. This probe exhibited good linear range and selectivity for ·OHl, and is able to avoid interference from some metal ions and other kinds of ROS (H2O2, O2.‐, 1O2, and HClO). Meanwhile, this probe has been used to evaluate the ·OH‐scavenging efficiency of different compounds, such as isopropyl alcohol, cytosine, uracil, Tempo, Glutathione (GSH), and dimethyl sulfoxide (DMSO). Therefore, the present study shows that this probe not only can effectively measure the level of ·OH, but also can assess the ·OH‐scavenging efficiency of different compounds. Furthermore this current study suggested that following further optimization, this probe may be potentially applied in the diagnosis of oxidative stress in human body.

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“…mPTP is a channel that spans from the outer mitochondrial membrane to the mitochondrial matrix and controls the migration of molecules into and out of mitochondria [40]. Persistent opening of mPTP in response to high concentration of Ca 2+ can lead to decrease of the mitochondrial membrane potential (△ψm) and makes mitochondria become permeable to molecules less than 1.5 kDa and water [11,12,41,42]. Therefore, the opening of mPTP is the key link of mitochondrial damage.…”

Section: Discussionmentioning

confidence: 99%

“…TGEV-induced mitochondrial damage is a key factor of inflammation and is caused by abnormal opening of mitochondrial permeability transmission pore (mPTP) [10]. Persistent opening of mPTP can lead to decrease of the mitochondrial membrane potential (△ψm), reduction Ivyspring International Publisher of ATP production, release of ROS from mitochondria, finally mitochondrial damage [11][12][13][14]. Viral infection is one of the important factors for mitochondrial injury [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2

Zhao¹,

Ma²,

Guo³

et al. 2019

Int. J. Biol. Sci.

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Transmissible gastroenteritis (TGE) is a contagious and infectious disease that is characterized by severe vomiting and diarrhea of swine , especially piglet, and caused by transmissible gastroenteritis coronavirus (TGEV) . TGEV infection provokes mitochondrial damage of porcine intestinal epthelial cell (IPEC), which is responsible for inflammation and cell death. In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2). Activation of NF-κB is an important factor for mitochondrial damage. Mitochondrial permeability transition pore (mPTP) opening is a key reason for mitochondrial damage. So, we speculate that circEZH2 may regulate TGEV-induced mPTP opening via NF-kB pathway. In the present study, we found that mPTP opening of IPEC-J2 was occured during TGEV infection and suppressed by circEZH2 via attaching miR-22. Hexokinase 2 (HK2) and interleukin 6 (IL-6) were identified as the targets of miR-22. Silencing HK2 enhanced TGEV-induced mPTP opening, while no effect on NF-κB pathway. Silencing IL-6 promoted TGEV-induced mPTP opening and inhibited NF-κB pathway. Inhibitor of NF-κB increased TGEV-induced mPTP opening. The data revealed that TGEV-induced mPTP opening was regulated via two pathways: circEZH2/miR-22/HK2 axis and circEZH2/miR-22/IL-6/NF-κB axis.

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Ochratoxin A-Induced Apoptosis of IPEC-J2 Cells through ROS-Mediated Mitochondrial Permeability Transition Pore Opening Pathway

Cited by 86 publications

References 46 publications

2,3,4′,5-Tetrahydroxystilbene-2-O-β-D-Glucoside (THSG) Activates the Nrf2 Antioxidant Pathway and Attenuates Oxidative Stress-Induced Cell Death in Mouse Cochlear UB/OC-2 Cells

2,3,4′,5-Tetrahydroxystilbene-2-O-β-D-Glucoside (THSG) Activates the Nrf2 Antioxidant Pathway and Attenuates Oxidative Stress-Induced Cell Death in Mouse Cochlear UB/OC-2 Cells

Synthesis and activity of a coumarin‐based fluorescent probe for hydroxyl radical detection

Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2

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