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https://www.readbyqxmd.com/read/29452577/polymerase-delta-interacting-protein-2-deficiency-protects-against-blood-brain-barrier-permeability-in-the-ischemic-brain
#1
Marina S Hernandes, Bernard Lassègue, Lula L Hilenski, Jonathan Adams, Ning Gao, Chia-Yi Kuan, Yu-Yo Sun, Lihong Cheng, Daniel S Kikuchi, Manuel Yepes, Kathy K Griendling
BACKGROUND: Polymerase δ-interacting protein 2 (Poldip2) is a multifunctional protein that regulates vascular extracellular matrix composition and matrix metalloproteinase (MMP) activity. The blood-brain barrier (BBB) is a dynamic system assembled by endothelial cells, basal lamina, and perivascular astrocytes, raising the possibility that Poldip2 may be involved in maintaining its structure. We investigated the role of Poldip2 in the late BBB permeability induced by cerebral ischemia...
February 17, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29449802/sparc-and-glua1-containing-ampa-receptors-promote-neuronal-health-following-cns-injury
#2
Emma V Jones, Yann Bernardinelli, Juan G Zarruk, Sabrina Chierzi, Keith K Murai
The proper formation and maintenance of functional synapses in the central nervous system (CNS) requires communication between neurons and astrocytes and the ability of astrocytes to release neuromodulatory molecules. Previously, we described a novel role for the astrocyte-secreted matricellular protein SPARC (Secreted Protein, Acidic and Rich in Cysteine) in regulating α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) and plasticity at developing synapses. SPARC is highly expressed by astrocytes and microglia during CNS development but its level is reduced in adulthood...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29449542/long-non-coding-rnas-in-ischemic-stroke
#3
REVIEW
Mei-Hua Bao, Vivian Szeto, Burton B Yang, Shu-Zhen Zhu, Hong-Shuo Sun, Zhong-Ping Feng
Stroke is one of the leading causes of mortality and disability worldwide. Uncovering the cellular and molecular pathophysiological processes in stroke have been a top priority. Long non-coding (lnc) RNAs play critical roles in different kinds of diseases. In recent years, a bulk of aberrantly expressed lncRNAs have been screened out in ischemic stroke patients or ischemia insulted animals using new technologies such as RNA-seq, deep sequencing, and microarrays. Nine specific lncRNAs, antisense non-coding RNA in the INK4 locus (ANRIL), metastasis-associate lung adenocarcinoma transcript 1 (MALAT1), N1LR, maternally expressed gene 3 (MEG3), H19, CaMK2D-associated transcript 1 (C2dat1), Fos downstream transcript (FosDT), small nucleolar RNA host gene 14 (SNHG14), and taurine-upregulated gene 1 (TUG1), were found increased in cerebral ischemic animals and/or oxygen-glucose deprived (OGD) cells...
February 15, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29445227/novel-ubiquitin-independent-nucleolar-c-myc-degradation-pathway-mediated-by-antizyme-2
#4
Noriyuki Murai, Yasuko Murakami, Ayasa Tajima, Senya Matsufuji
The proto-oncogene c-Myc encodes a short-lived protein c-Myc that regulates various cellular processes including cell growth, differentiation and apoptosis. Degradation of c-Myc is catalyzed by the proteasome and requires phosphorylation of Thr-58 for ubiquitination by E3 ubiquitin ligase, Fbxw7/ FBW7. Here we show that a polyamine regulatory protein, antizyme 2 (AZ2), interacts with c-Myc in the nucleus and nucleolus, to accelerate proteasome-mediated c-Myc degradation without ubiquitination or Thr-58 phosphorylation...
February 14, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29442011/acetylpuerarin-protects-against-ogd-induced-cell-injury-in-bv2-microglia-by-inhibiting-hmgb1-release
#5
Deqing Sun, Aiying Xue, Xia Xue, Manru Ren, Jing Wu, Rongmei Wang
High mobility group box 1 (HMGB1), a non-histone DNA-binding protein, is massively released into the extracellular space from neuronal cells after ischemic injury, initiates inflammatory response and aggravates brain tissue damage. Acetylpuerarin (AP), an acetylated derivative of puerarin, was reported to protect against cerebrovascular ischemia-reperfusion injury in rats through anti-inflammation. In the present study, we aim to investigate whether AP inhibited HMGB1 release in oxygen-glucose deprivation (OGD)-treated BV2 microglia...
February 1, 2018: Die Pharmazie
https://www.readbyqxmd.com/read/29438499/ksp1-dependent-phosphorylation-of-eif4g-modulates-post-transcriptional-regulation-of-specific-mrnas-under-glucose-deprivation-conditions
#6
Yeonji Chang, Won-Ki Huh
Post-transcriptional regulation is an important mechanism for modulating gene expression and is performed by numerous mRNA-binding proteins. To understand the mechanisms underlying post-transcriptional regulation, we investigated the phosphorylation status of 32 mRNA-binding proteins under glucose deprivation conditions in Saccharomyces cerevisiae. We identified 17 glucose-sensitive phosphoproteins and signal pathways implicated in their phosphorylation. Notably, phosphorylation of the eukaryotic translation initiation factor 4G (eIF4G) was regulated by both the Snf1/AMPK pathway and the target of rapamycin complex 1 (TORC1) pathway...
February 9, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29436589/ferroptosis-is-associated-with-oxygen-glucose-deprivation-reoxygenation-induced-sertoli-cell-death
#7
Li Li, Yu Hao, Yu Zhao, Huijuan Wang, Xiujun Zhao, Yan Jiang, Fulu Gao
Sertoli cell death contributes to spermatogenesis impairment, which is associated with male infertility. Testicular ischemia‑reperfusion (I/R) injury induces the cell death of germ cells and Sertoli cells, whereas inhibition of cell death ameliorates acute testicular I/R damage. The aim of the present study was to investigate the mechanism of I/R stress-induced cell death in TM4 cells. Oxygen‑glucose deprivation and reoxygenation (OGD/R) was demonstrated to induce I/R injury and cell death in TM4 cells...
February 7, 2018: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29436577/rp105-protects-pc12-cells-from-oxygen%C3%A2-glucose-deprivation-reoxygenation-injury-via-activation-of-the-pi3k-akt-signaling-pathway
#8
Yanpeng Sun, Lu Liu, Jiang Yuan, Qiang Sun, Na Wang, Yunfu Wang
Radioprotective 105 kDa protein (RP105) has been reported to produce favorable outcomes in various cardiovascular disorders via a toll‑like receptor 4‑dependent or ‑independent manner. However, whether RP105 exerts neuroprotective effects against oxygen‑glucose deprivation (OGD)/reoxygenation (OGD/R) injury remains to be elucidated. In the present study, the PC12 neuronal cell line was exposed to 4 h of OGD followed by 24 h of reoxygenation. Adenoviral vectors encoding RP105 were utilized to upregulate the level of RP105 in PC12 cells prior to OGD/R induction...
February 12, 2018: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29436167/sestrin2-facilitates-glutamine-dependent-transcription-of-pgc-1%C3%AE-and-survival-of-liver-cancer-cells-under-glucose-limitation
#9
Ashish Kumar, Sagnik Giri, Chandrima Shaha
Differential utilization of metabolites and metabolic plasticity can confer adaptation to cancer cells under metabolic stress. Glutamine is one of the vital and versatile nutrients which cancer cells consume avidly for their proliferation, therefore, mechanisms related to glutamine metabolism has been identified as targets. Recently, SESN2 (sestrin2), a stress inducible protein has been reported to regulate survival in glutamine depleted cancer cells, based on this, we explored if SESN2 could regulate glutamine metabolism during glucose starvation...
February 12, 2018: FEBS Journal
https://www.readbyqxmd.com/read/29435120/ampk-activation-by-tanshinone-iia-protects-neuronal-cells-from-oxygen-glucose-deprivation
#10
Yingfeng Weng, Jixian Lin, Hui Liu, Hui Wu, Zhimin Yan, Jing Zhao
The current study tested the potential neuroprotective function of Tanshinone IIA (ThIIA) in neuronal cells with oxygen-glucose deprivation (ODG) and re-oxygenation (OGDR). In SH-SY5Y neuronal cells and primary murine cortical neurons, ThIIA pre-treatment attenuated OGDR-induced viability reduction and apoptosis. Further, OGDR-induced mitochondrial depolarization, reactive oxygen species production, lipid peroxidation and DNA damages in neuronal cells were significantly attenuated by ThIIA. ThIIA activated AMP-activated protein kinase (AMPK) signaling, which was essential for neuroprotection against OGDR...
January 12, 2018: Oncotarget
https://www.readbyqxmd.com/read/29431851/stress-induced-trna-cleavage-and-tirna-generation-in-rat-neuronal-pc12-cells
#11
Elkordy Alaa, Eikan Mishima, Kuniyasu Niizuma, Yasutoshi Akiyama, Miki Fujimura, Teiji Tominaga, Takaaki Abe
Transfer RNA (tRNA) plays a role in stress response programs involved in various pathological conditions including neurological diseases. Under cell stress conditions, intracellular tRNA is cleaved by a specific ribonuclease, angiogenin, generating tRNA-derived fragments or tRNA-derived stress-induced RNA (tiRNA). Generated tiRNA contributes to the cell stress response and has potential cell protective effects. However, tiRNA generation under stress conditions in neuronal cells has not been fully elucidated...
February 12, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29426336/salidroside-provides-neuroprotection-by-modulating-microglial-polarization-after-cerebral-ischemia
#12
Xiangrong Liu, Shaohong Wen, Feng Yan, Kuan Liu, Liqiang Liu, Lei Wang, Shangfeng Zhao, Xunming Ji
BACKGROUND: Following stroke, microglia can be driven to the "classically activated" pro-inflammatory (M1) phenotype and the "alternatively activated" anti-inflammatory (M2) phenotype. Salidroside (SLDS) is known to inhibit inflammation and to possess protective effects in neurological diseases, but to date, the exact mechanisms involved in these processes after stroke have yet to be elucidated. The purpose of this study was to determine the effects of SLDS on neuroprotection and microglial polarization after stroke...
February 9, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29425821/mmp9-is-involved-in-ho-1-mediated-upregulation-of-apical-junctional-complex-in-caco-2-cells-under-oxygen-glucose-deprivation
#13
Yongqu Lu, Jie An, Yulin Liu, Lehao Ren, Li Zhang
Ischemia reperfusion injury is a critical factor in the recovery process after intestine trauma and the functional restoration of intestinal reconstruction. This study was the first to explore the expression of apical junctional complex (AJC) induced by heme oxygenase-1 (HO-1) in Caco-2 cells in oxygen-glucose deprivation (OGD) models. Here we showed that HO-1 was upregulated after OGD. Notably, activation of HO-1 largely enhanced the expression of AJC proteins including Claudin-4, E-cadherin and β-catenin in Caco-2 cells, but decreased the expression of matrix metalloproteinase 9 (MMP9)...
February 6, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29424914/microrna-298-regulates-apoptosis-of-cardiomyocytes-after-myocardial-infarction
#14
Q Zhang, N Yu, B-T Yu
OBJECTIVE: To investigate the role and mechanism of micro ribonucleic acid (miR)-298 in myocardial apoptosis after myocardial infarction. MATERIALS AND METHODS: In vivo experiments, the rat model of myocardial infarction was established, and miR-298 was up-regulated via lentivirus with miR-298 overexpression. Cardiac function of rats was detected via echocardiography, Bcl-2 associated X protein (BAX) expressions in infarction border zone were detected via Real-time Quantitative PCR (qT-PCR) and Western blot, and TUNEL assay was used to detect the myocardial apoptosis...
January 2018: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/29424909/mir-124-affects-the-apoptosis-of-brain-vascular-endothelial-cells-and-ros-production-through-regulating-pi3k-akt-signaling-pathway
#15
S-W Wang, L-X Deng, H-Y Chen, Z-Q Su, S-L Ye, W-Y Xu
OBJECTIVE: The apoptosis of vascular endothelial cells (VEC) is related to ischemic stroke. Phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT/PKB) signaling pathway can upregulate Bcl-2 expression, reduce reactive oxygen species (ROS) production, and induce apoptosis. The level of miR-124 was significantly increased after cerebral ischemia. This study aimed to investigate the role of miR-124 in regulating PI3K expression, brain VEC apoptosis, and ROS production. MATERIALS AND METHODS: The expressions of miR-124, PI3K, p-AKT, and Bcl-2 in brain VEC of rats from the sham group and middle cerebral artery occlusion (MCAO) group were tested...
January 2018: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/29424025/nrf2-mediated-neuroprotection-against-oxygen-glucose-deprivation-reperfusion-injury-by-emodin-via-ampk-dependent-inhibition-of-gsk-3%C3%AE
#16
Sun Young Park, Young-Whan Choi, Geuntae Park
OBJECTIVES: Our study verified the neuroprotective properties of emodin against oxygen-glucose deprivation/reoxygenation (OGD/R) and demonstrated its mechanism. METHODS: Human neuronal SH-SY5Y cells were investigated by analysing cell viability, lactate dehydrogenase levels, expression of molecules related to apoptotic cell death, and using biochemical techniques, flow cytometry and Western blot assays. KEY FINDINGS: Emodin reduced OGD/R-lead to neurotoxicity in SH-SY5Y cells...
February 9, 2018: Journal of Pharmacy and Pharmacology
https://www.readbyqxmd.com/read/29421654/extracellular-acidification-by-lactic-acid-suppresses-glucose-deprivation-induced-cell-death-and-autophagy-in-b16-melanoma-cells
#17
Taisuke Matsuo, Yasuyuki Sadzuka
In solid tumors, cancer cells survive and proliferate under conditions of microenvironment stress such as poor nutrients and hypoxia due to inadequate vascularization. These stress conditions in turn activate autophagy, which is important for cancer cell survival. However, autophagy has a contrary effect of inducing cell death in cancer cells cultured in vitro under conditions of glucose deprivation. In this study, we hypothesized that supplementation of lactic acid serves as a means of cell survival under glucose-deprived conditions...
February 5, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29419806/neuroprotective-effects-of-bioactive-compounds-and-mapk-pathway-modulation-in-ischemia-stressed-pc12-pheochromocytoma-cells
#18
REVIEW
Adi Lahiani, Annette Brand-Yavin, Ephraim Yavin, Philip Lazarovici
This review surveys the efforts taken to investigate in vitro neuroprotective features of synthetic compounds and cell-released growth factors on PC12 clonal cell line temporarily deprived of oxygen and glucose followed by reoxygenation (OGD/R). These cells have been used previously to mimic some of the properties of in vivo brain ischemia-reperfusion-injury (IRI) and have been instrumental in identifying common mechanisms such as calcium overload, redox potential, lipid peroxidation and MAPKs modulation. In addition, they were useful for establishing the role of certain membrane penetrable cocktails of antioxidants as well as potential growth factors which may act in neuroprotection...
February 8, 2018: Brain Sciences
https://www.readbyqxmd.com/read/29416745/itraq-analysis-of-a-mouse-acute-myocardial-infarction-model-reveals-that-vitamin-d-binding-protein-promotes-cardiomyocyte-apoptosis-after-hypoxia
#19
Yun Wu, Fen Liu, Xiang Ma, Dilare Adi, Ming-Tao Gai, Xiang Jin, Yi-Ning Yang, Ying Huang, Xiang Xie, Xiao-Mei Li, Zhen-Yan Fu, Bang-Dang Chen, Yi-Tong Ma
The proteome profile changes after acute myocardial infarction (AMI) and the roles played by important protein species remain poorly understood. Here, we constructed a mouse AMI model by ligating the left coronary artery of male C57B/6J mice to investigate the molecular changes after AMI on the protein level. Total proteins of the left ventricle were extracted and quantitatively analyzed by isobaric tags using relative and absolute quantitation (iTRAQ) technologies. The transcript and protein levels of important genes were further validated using quantitative polymerase chain reaction and western blot...
January 5, 2018: Oncotarget
https://www.readbyqxmd.com/read/29416029/neuroglobin-boosts-axon-regeneration-during-ischemic-reperfusion-via-p38-binding-and-activation-depending-on-oxygen-signal
#20
Xin Xin Xiong, Feng Pan, Ruo Qiao Chen, Dian Xing Hu, Xin Yao Qiu, Chun Yang Li, Xiao Qiang Xie, Bo Tian, Xiao Qian Chen
Cerebral ischemia causes severe cell death or injury including axon breakdown or retraction in the brain. Axon regeneration is crucial for the functional recovery of injured neurons or brains after ischemia/reperfusion (I/R); however, this process has been proved extremely difficult in adult brains and there is still no effective therapy for it. Here we reported that neuroglobin (Ngb), a novel oxygen-binding or sensor protein existing predominantly in neurons or brains, functions as a driving factor for axon regeneration during I/R...
February 7, 2018: Cell Death & Disease
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