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parkinson's disease and endoplasmic reticulum stress

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https://www.readbyqxmd.com/read/28444413/cerebral-dopamine-neurotrophic-factor-protects-h9c2-cardiomyocytes-from-apoptosis
#1
H Liu, C Yu, H Yu, L Zhong, Y Wang, J Liu, S Zhang, J Sun, L Duan, L Gong, J Yang
BACKGROUND: Cerebral dopamine neurotrophic factor (CDNF) has been studied in animal models of Parkinson's disease, where it was shown to repair and protect dopamine neurons. Alongside its neurotrophic activity, it can also localize in the endoplasmic reticulum (ER) acting as an ER stress response (ERSR) protein to maintain ER homeostasis. Since ER stress plays a major role in the development and progression of cardiovascular diseases, we investigated the role of CDNF in cardiomyocytes during ER stress...
April 25, 2017: Herz
https://www.readbyqxmd.com/read/28367977/riboflavin-deficiency-induces-a-significant-change-in-proteomic-profiles-in-hepg2-cells
#2
Zhonghao Xin, Lingling Pu, Weina Gao, Yawen Wang, Jingyu Wei, Tala Shi, Zhanxin Yao, Changjiang Guo
Riboflavin deficiency is widespread in many regions over the world, especially in underdeveloped countries. In this study, we investigated the effects of riboflavin deficiency on protein expression profiles in HepG2 cells in order to provide molecular information for the abnormalities induced by riboflavin deficiency. HepG2 cells were cultured in media containing different concentrations of riboflavin. Changes of cell viability and apoptosis were assessed. A comparative proteomic analysis was performed using a label-free shotgun method with LC-MS/MS to investigate the global changes of proteomic profiles in response to riboflavin deficiency...
April 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28366931/hydrocortisone-induced-parkin-prevents-dopaminergic-cell-death-via-creb-pathway-in-parkinson-s-disease-model
#3
Sangwoo Ham, Yun-Il Lee, Minkyung Jo, Hyojung Kim, Hojin Kang, Areum Jo, Gum Hwa Lee, Yun Jeong Mo, Sang Chul Park, Yun Song Lee, Joo-Ho Shin, Yunjong Lee
Dysfunctional parkin due to mutations or post-translational modifications contributes to dopaminergic neurodegeneration in Parkinson's disease (PD). Overexpression of parkin provides protection against cellular stresses and prevents dopamine cell loss in several PD animal models. Here we performed an unbiased high-throughput luciferase screening to identify chemicals that can increase parkin expression. Among promising parkin inducers, hydrocortisone possessed the most favorable profiles including parkin induction ability, cell protection ability, and physicochemical property of absorption, distribution, metabolism, and excretion (ADME) without inducing endoplasmic reticulum stress...
April 3, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28359145/neuroprotective-effects-of-protein-tyrosine-phosphatase-1b-inhibition-against-er-stress-induced-toxicity
#4
Yu-Mi Jeon, Shinrye Lee, Seyeon Kim, Younghwi Kwon, Kiyoung Kim, Chang Geon Chung, Seongsoo Lee, Sung Bae Lee, Hyung-Jun Kim
Several lines of evidence suggest that endoplasmic reticulum (ER) stress plays a critical role in the pathogenesis of many neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Protein tyrosine phosphatase 1B (PTP1B) is known to regulate the ER stress signaling pathway, but its role in neuronal systems in terms of ER stress remains largely unknown. Here, we showed that rotenone-induced toxicity in human neuroblastoma cell lines and mouse primary cortical neurons was ameliorated by PTP1B inhibition...
March 28, 2017: Molecules and Cells
https://www.readbyqxmd.com/read/28337696/cerebral-dopamine-neurotrophic-factor-a-potential-therapeutic-agent-for-parkinson-s-disease
#5
REVIEW
Tingting Tang, Yong Li, Qian Jiao, Xixun Du, Hong Jiang
The application of neurotrophic factors (NTFs) is a promising therapeutic strategy for neurodegenerative disorders such as Parkinson's disease (PD). Many NTFs have been reported to enhance the survival, regeneration, and differentiation of neurons and to induce synaptic plasticity. However, because of their potential side-effects and low efficacy after clinical administration, more potent treatments for neurodegenerative disorders are being sought. Cerebral dopamine neurotrophic factor (CDNF), a newly-identified NTF homologous to mesencephalic astrocyte-derived NTF, is structurally and functionally different from other NTFs, providing new hope especially for PD patients...
March 23, 2017: Neuroscience Bulletin
https://www.readbyqxmd.com/read/28316566/blockade-of-ryrs-in-the-er-attenuates-6-ohda-induced-calcium-overload-cellular-hypo-excitability-and-apoptosis-in-dopaminergic-neurons
#6
Lu Huang, Ying Xue, DaYun Feng, RuiXin Yang, Tiejian Nie, Gang Zhu, Kai Tao, GuoDong Gao, Qian Yang
Calcium (Ca(2+)) dyshomeostasis induced by endoplasmic reticulum (ER) stress is an important molecular mechanism of selective dopaminergic (DA) neuron loss in Parkinson's disease (PD). Inositol 1,4,5-triphosphate receptors (IP3Rs) and ryanodine receptors (RyRs), which are located on the ER surface, are the main endogenous Ca(2+) release channels and play crucial roles in regulating Ca(2+) homeostasis. However, the roles of these endogenous Ca(2+) release channels in PD and their effects on the function and survival of DA neurons remain unknown...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28315279/the-role-of-sigma-1-receptor-as-a-neuroprotective-target-in-glaucoma
#7
Barbara Mysona, Neil Kansara, Jing Zhao, Kathryn Bollinger
The role of sigma 1 receptor (S1R) in glaucoma is emerging as a promising field of study. Glaucoma is an optic neuropathy that shares common pathogenic mechanisms with other neurodegenerative diseases such as Alzheimer's and Parkinson's disease . S1R modulates multiple cellular functions associated with neurodegeneration . These include Ca(2+) ion homeostasis, endoplasmic reticulum (ER) and oxidative stress , survival signaling pathways, neurotrophin secretion, and glial activation. S1R may also have neurorestorative properties including enhancement of neuronal plasticity and neurite outgrowth...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28273718/mechanisms-of-parkinson-s-disease-related-proteins-in-mediating-secondary-brain-damage-after-cerebral-ischemia
#8
TaeHee Kim, Raghu Vemuganti
Both Parkinson's disease (PD) and stroke are debilitating conditions that result in neuronal death and loss of neurological functions. These two conditions predominantly affect aging populations with the deterioration of the quality of life for the patients themselves and a tremendous burden to families. While the neurodegeneration and symptomology of PD develop chronically over the years, post-stroke neuronal death and dysfunction develop rapidly in days. Despite the discrepancy in the pathophysiological time frame and severity, both conditions share common molecular mechanisms that include oxidative stress, mitochondrial dysfunction, inflammation, endoplasmic reticulum stress, and activation of various cell death pathways (apoptosis/necrosis/autophagy) that synergistically modulate the neuronal death...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/28243526/bax-inhibitor-1-knockdown-phenotypes-are-suppressed-by-buffy-and-exacerbate-degeneration-in-a-drosophila-model-of-parkinson-disease
#9
P Githure M'Angale, Brian E Staveley
BACKGROUND: Bax inhibitor-1 (BI-1) is an evolutionarily conserved cytoprotective transmembrane protein that acts as a suppressor of Bax-induced apoptosis by regulation of endoplasmic reticulum stress-induced cell death. We knocked down BI-1 in the sensitive dopa decarboxylase (Ddc) expressing neurons of Drosophila melanogaster to investigate its neuroprotective functions. We additionally sought to rescue the BI-1-induced phenotypes by co-expression with the pro-survival Buffy and determined the effect of BI-1 knockdown on the neurodegenerative α-synuclein-induced Parkinson disease (PD) model...
2017: PeerJ
https://www.readbyqxmd.com/read/28193519/thiamine-deficiency-induces-endoplasmic-reticulum-stress-and-oxidative-stress-in-human-neurons-derived-from-induced-pluripotent-stem-cells
#10
Xin Wang, Mei Xu, Jacqueline A Frank, Zun-Ji Ke, Jia Luo
Thiamine (vitamin B1) deficiency (TD) plays a major role in the etiology of Wernicke's encephalopathy (WE) which is a severe neurological disorder. TD induces selective neuronal cell death, neuroinflammation, endoplasmic reticulum (ER) stress and oxidative stress in the brain which are commonly observed in many aging-related neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and progressive supranuclear palsy (PSP). However, the underlying cellular and molecular mechanisms remain unclear...
April 1, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/28131727/long-term-protective-effects-of-aav9-mesencephalic-astrocyte-derived-neurotrophic-factor-gene-transfer-in-parkinsonian-rats
#11
Fei Hao, Chun Yang, Sha-Sha Chen, Yan-Yan Wang, Wei Zhou, Qiang Hao, Tao Lu, Barry Hoffer, Li-Ru Zhao, Wei-Ming Duan, Qun-Yuan Xu
Intrastriatal injection of mesencephalic astrocyte-derived neurotrophic factor (MANF) protein has been shown to provide neuroprotective and neurorestorative effects in a 6-hydroxydopamine (6-OHDA) - lesioned rat model of Parkinson's disease. Here, we used an adeno-associated virus serotype 9 (AAV9) vector to deliver the human MANF (hMANF) gene into the rat striatum 10days after a 6-OHDA lesion to examine long-term effects of hMANF on nigral dopaminergic neurons and mechanisms underlying MANF neuroprotection...
January 25, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28116245/7-ketocholesterol-induces-apoptosis-of-mc3t3-e1-cells-associated-with-reactive-oxygen-species-generation-endoplasmic-reticulum-stress-and-caspase-3-7-dependent-pathway
#12
Yuta Sato, Noriko Ishihara, Daiji Nagayama, Atsuhito Saiki, Ichiro Tatsuno
Type 2 diabetes mellitus (T2DM) is associated with an increased risk of bone fractures without reduction of bone mineral density. The cholesterol oxide 7-ketocholesterol (7KCHO) has been implicated in numerous diseases such as atherosclerosis, Alzheimer's disease, Parkinson's disease, cancer, age-related macular degeneration and T2DM. In the present study, 7KCHO decreased the viability of MC3T3-E1 cells, increased reactive oxygen species (ROS) production and apoptotic rate, and upregulated the caspase-3/7 pathway...
March 2017: Molecular Genetics and Metabolism Reports
https://www.readbyqxmd.com/read/28087337/tunicamycin-impairs-olfactory-learning-and-synaptic-plasticity-in-the-olfactory-bulb
#13
Jia Tong, Fumino Okutani, Yoshihiro Murata, Mutsuo Taniguchi, Toshiharu Namba, Yu-Jie Wang, Hideto Kaba
Tunicamycin (TM) induces endoplasmic reticulum (ER) stress and inhibits N-glycosylation in cells. ER stress is associated with neuronal death in neurodegenerative disorders, such as Parkinson's disease and Alzheimer's disease, and most patients complain of the impairment of olfactory recognition. Here we examined the effects of TM on aversive olfactory learning and the underlying synaptic plasticity in the main olfactory bulb (MOB). Behavioral experiments demonstrated that the intrabulbar infusion of TM disabled aversive olfactory learning without affecting short-term memory...
March 6, 2017: Neuroscience
https://www.readbyqxmd.com/read/28004277/tauroursodeoxycholic-bile-acid-arrests-axonal-degeneration-by-inhibiting-the-unfolded-protein-response-in-x-linked-adrenoleukodystrophy
#14
Nathalie Launay, Montserrat Ruiz, Laia Grau, Francisco J Ortega, Ekaterina V Ilieva, Juan José Martínez, Elena Galea, Isidre Ferrer, Erwin Knecht, Aurora Pujol, Stéphane Fourcade
The activation of the highly conserved unfolded protein response (UPR) is prominent in the pathogenesis of the most prevalent neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), which are classically characterized by an accumulation of aggregated or misfolded proteins. This activation is orchestrated by three endoplasmic reticulum (ER) stress sensors: PERK, ATF6 and IRE1. These sensors transduce signals that induce the expression of the UPR gene programme...
February 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/27939990/apomorphine-prevents-lps-induced-il-23-p19-mrna-expression-via-inhibition-of-jnk-and-atf4-in-hapi-cells
#15
Hirokazu Hara, Dai Kimoto, Miho Kajita, Chisato Takada, Tetsuro Kamiya, Tetsuo Adachi
Inflammation has been reported to be closely related to exaggeration of cerebral ischemia and neurodegenerative diseases. Microglia, resident immune cells in the central nervous system, can be activated in response to neuronal injury and produce proinflammatory cytokines, resulting in further aggravation of neuronal injury. Interleukin (IL)-23, which consists of p19 and IL-12 p40 subunits, has been shown to be involved in brain injury associated with neuroinflammation. Apomorphine (Apo), a nonselective dopamine receptor agonist, has been used for clinical therapy of Parkinson's disease...
December 9, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27866808/combined-beta-glucosylceramide-and-ambroxol-hydrochloride-in-patients-with-gaucher-related-parkinson-disease-from-clinical-observations-to-drug-development
#16
Yuval Ishay, Ari Zimran, Jeffrey Szer, Tama Dinur, Yaron Ilan, David Arkadir
Both patients with non-neuronopathic Gaucher disease (GD) and heterozygous GBA mutation carrier are at increased risk for Parkinson disease (PD). The risk for PD in these groups does not linearly increase with glucosylceramide (GC) accumulation or with acid β-glucocerebrosidase (GCase) activity. This observation, together with other clinical systemic observations raises the possibility that extra-cellular GC actually has beneficial, anti-inflammatory, properties. Based on this hypothesis, we suggest here that the administration of supplementary oral GC to GBA carriers at risk for PD may slow inflammatory-driven secondary neuronal death...
November 12, 2016: Blood Cells, Molecules & Diseases
https://www.readbyqxmd.com/read/27815720/the-role-of-endoplasmic-reticulum-stress-in-neurodegenerative-disease
#17
REVIEW
Chunchen Xiang, Yujia Wang, Han Zhang, Fang Han
The endoplasmic reticulum (ER) is an important organelle involved in cellular homeostasis and control of protein quality. Unfolded protein response (UPR) is a cellular response to ER stress and promotes cell survival. Severe or prolonged stress activates apoptosis signaling to trigger cell death. In mammals, the UPR is initiated by three major ER stress sensors, including inositol-requiring transmembrane kinase 1, double-stranded RNA-activated protein kinase-like ER kinase and activating transcription factor 6...
January 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/27776889/a-new-target-for-parkinson-s-disease-small-molecule-serca-activator-cdn1163-ameliorates-dyskinesia-in-6-ohda-lesioned-rats
#18
Russell Dahl
Endoplasmic reticulum (ER) stress is intimately linked to Parkinson's disease (PD) pathophysiology. Disrupted intracellular calcium homeostasis is a major cause of the ER stress seen in dopaminergic neurons, leading to the cell death and subsequent loss of movement and coordination in patients. Dysfunctional calcium handling proteins play a major role in the promulgation of ER stress in PD. Specifically, compromised sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) has been identified as a major cause of ER stress and neuron loss in PD...
January 1, 2017: Bioorganic & Medicinal Chemistry
https://www.readbyqxmd.com/read/27774335/n-acetylcysteine-in-combination-with-igf-1-enhances-neuroprotection-against-proteasome-dysfunction-induced-neurotoxicity-in-sh-sy5y-cells
#19
Benxu Cheng, Pinki Anand, Anxiu Kuang, Feroz Akhtar, Virginia L Scofield
Ubiquitin proteasome system (UPS) dysfunction has been implicated in the development of many neuronal disorders, including Parkinson's disease (PD). Previous studies focused on individual neuroprotective agents and their respective abilities to prevent neurotoxicity following a variety of toxic insults. However, the effects of the antioxidant N-acetylcysteine (NAC) on proteasome impairment-induced apoptosis have not been well characterized in human neuronal cells. The aim of this study was to determine whether cotreatment of NAC and insulin-like growth factor-1 (IGF-1) efficiently protected against proteasome inhibitor-induced cytotoxicity in SH-SY5Y cells...
2016: Parkinson's Disease
https://www.readbyqxmd.com/read/27748814/neurotoxin-%C3%AE-%C3%A2-n%C3%A2-methylamino%C3%A2-l%C3%A2-alanine-induces-endoplasmic-reticulum-stress%C3%A2-mediated-neuronal-apoptosis
#20
Haiying Shen, Kiyoon Kim, Yoojung Oh, Kyung Sik Yoon, Hyung Hwan Baik, Sung Soo Kim, Joohun Ha, Insug Kang, Wonchae Choe
β-N-methylamino-L-alanine (BMAA) is a neurotoxin that is closely associated with the incidence of amyotrophic lateral sclerosis, Parkinson's disease and Alzheimer's disease. In cultured neuronal cells, BMAA notably induces the upregulation of endoplasmic reticulum (ER) chaperons and activates the unfolded protein response (UPR) receptor pathways of protein kinase RNA‑like endoplasmic reticulum kinase, inositol‑requiring kinase 1 and transcription factor 6. The ER stress‑specific protein CCAAT/‑enhancer‑binding protein homologous protein (CHOP) affords pro‑apoptotic responses that cause mitochondrial damage and caspase activation...
November 2016: Molecular Medicine Reports
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