Down-regulation of Homer1 attenuates t-BHP-induced oxidative stress through regulating calcium homeostasis and ER stress in brain endothelial cells

Guo, Zhenyu; Zhang, Yahong; Xie, Guoqiang; Liu, Chong-Xiao; Ren, Zhimin; Shi, Wei

doi:10.1016/j.bbrc.2016.07.012

Cited by 9 publications

(4 citation statements)

References 21 publications

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“…In this study, next-generation deep sequencing of differentially expressed microRNAs in the cerebellum of Ndufa4 -KO mice was performed to characterize the miR-145a-5p target genes in neurons, combined with bioinformatic prediction. Homer1, a postsynaptic density protein, is a key regulator of neuronal synaptic activity and neurological disease pathogenesis [ 37 , 38 ]. In contrast, Ccnd2 is a member of the highly conserved cyclin family that regulates cell cycle progression, cell proliferation, and apoptosis in distinct contexts whose expression is considerably regulated by microRNAs [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

Ndufa4 Regulates the Proliferation and Apoptosis of Neurons via miR-145a-5p/Homer1/Ccnd2

Chen

et al. 2023

Mol Neurobiol

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The Dandy–Walker malformation (DWM) is characterized by neuron dysregulation in embryonic development; however, the regulatory mechanisms associated with it are unclear. This study aimed to investigate the role of NADH dehydrogenase 1 alpha subcomplex 4 (NDUFA4) in regulating downstream signaling cascades and neuronal proliferation and apoptosis. Ndufa4 overexpression promoted the proliferation of neurons and inhibited their apoptosis in vitro, which underwent reverse regulation by the Ndufa4 short hairpin RNAs. Ndufa4-knockout (KO) mice showed abnormal histological alterations in the brain tissue, in addition to impaired spatial learning capacity and exploratory activity. Ndufa4 depletion altered the microRNA expressional profiles of the cerebellum: Ndufa4 inhibited miR-145a-5p expression both in the cerebellum and neurons. miR-145a-5p inhibited the proliferation of neurons and promoted their apoptosis. Ndufa4 promoted and miR-145a-5p inhibited the expression of human homer protein homolog 1 and cyclin D2 in neurons. Thus, Ndufa4 promotes the proliferation of neurons and inhibits their apoptosis by inhibiting miR-145a-5p, which directly targets and inhibits the untranslated regions of Homer1 and Ccnd2 expression.

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Section: Discussionmentioning

confidence: 99%

Ndufa4 Regulates the Proliferation and Apoptosis of Neurons via miR-145a-5p/Homer1/Ccnd2

Chen

et al. 2023

Mol Neurobiol

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“…These two pathways usually occur together. Their data revealed that polymers of AAT that accumulate in a spheric manner produce a loss of the normal tubule ER network, forming a vesiculated ER, which leads to impairment of luminal protein mobility [87]. ER vesiculation is associated with other cellular stresses, including mechanical injury and elevated cytosolic calcium concentration [101,102].…”

Section: Litopenaeus Vannameimentioning

confidence: 99%

Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases

Magallón

Carrión

Bañuls

et al. 2021

JCM

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Several studies have shown that some rare respiratory diseases, such as alpha-1 antitrypsin deficiency (AATD), idiopathic pulmonary fibrosis (IPF), cystic fibrosis (CF), and primary ciliary dyskinesia (PCD) present oxidative stress (OS) and endoplasmic reticulum (ER) stress. Their involvement in these pathologies and the use of antioxidants as therapeutic agents to minimize the effects of OS are discussed in this review.

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“…ERp57/PDIA3 might also participate in the modulation of mitochondrial Ca 2+ indirectly through the interaction with calnexin [37]. The t-BHP-mediated intracellular Ca 2+ increase could induce ROS generation and mitochondrial dysfunction [38]. Our previous study has found that DT-010 could reduce t-BHP-induced intracellular free radical production, including hydroxyl radical (•OH), superoxide anion(•O 2− ), and peroxynitrite radical (ONOO − ).…”

Section: Discussionmentioning

confidence: 99%

DT-010 Exerts Cardioprotective Effects by Regulating the Crosstalk between the AMPK/PGC-1α Pathway and ERp57

Zhang

et al. 2023

Cardiovascular Therapeutics

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The AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) pathway performs a crucial role in energy metabolism and mitochondrial network. Our previous study found that DT-010, a novel danshensu (DSS) and tetramethylpyrazine (TMP) conjugate, had significant cardioprotective properties in vitro and in vivo. We also reported that ERp57 served as a major target of DSS using the chemical proteomics approach. In this article, we focus on exploring the interrelationship between the regulation of the AMPK/PGC-1α pathway and promoting ERp57 expression induced by DT-010 in tert-butylhydroperoxide- (t-BHP-) induced H9c2 cell injury. The results showed that DT-010 activated the AMPK/PGC-1α pathway and increased ERp57 protein expression. Importantly, the above phenomenon as well as the mitochondrial function can be partially reversed by siRNA-mediated ERp57 suppression. Meanwhile, silencing AMPK significantly inhibited the ERp57 expression induced by DT-010. In addition, molecular docking and kinase assay in vitro revealed that DT-010 had no direct regulation effects on AMPK activity. Taken together, DT-010 exerted cardioprotective effects by regulating the crosstalk of AMPK/PGC-1α pathway and ERp57, representing a potential therapeutic agent for ischemic heart disease.

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Down-regulation of Homer1 attenuates t-BHP-induced oxidative stress through regulating calcium homeostasis and ER stress in brain endothelial cells

Cited by 9 publications

References 21 publications

Ndufa4 Regulates the Proliferation and Apoptosis of Neurons via miR-145a-5p/Homer1/Ccnd2

Ndufa4 Regulates the Proliferation and Apoptosis of Neurons via miR-145a-5p/Homer1/Ccnd2

Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases

DT-010 Exerts Cardioprotective Effects by Regulating the Crosstalk between the AMPK/PGC-1α Pathway and ERp57

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