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https://www.readbyqxmd.com/read/28620835/twenty-years-since-the-discovery-of-the-parkin-gene
#1
REVIEW
Nobutaka Hattori, Yoshikuni Mizuno
Nearly 20 years have passed since we identified the causative gene for a familial Parkinson's disease, parkin (now known as PARK2), in 1998. PARK2 is the most common gene responsible for young-onset Parkinson's disease. It codes for the protein Parkin RBR E3 ubiquitin-protein ligase (PARK2), which directly links to the ubiquitin-proteasome as a ubiquitin ligase. PARK2 is involved in mitophagy, which is a type of autophagy, in collaboration with PTEN-induced putative kinase 1 (PINK1). The PINK1 gene (previously known as PARK6) is also a causative gene for young-onset Parkinson's disease...
June 15, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/28618992/modulating-mitophagy-in-mitochondrial-disease
#2
Eszter Dombi, Heather Mortiboys, Joanna Poulton
Mitochondrial diseases may result from mutations in the maternally-inherited mitochondrial DNA (mtDNA) or from mutations in nuclear genes encoding mitochondrial proteins. Their bi-genomic nature makes mitochondrial diseases a very heterogeneous group of disorders that can present at any age and can affect any type of tissue. The autophagic-lysosomal degradation pathway plays an important role in clearing dysfunctional and redundant mitochondria through a specific quality control mechanism termed mitophagy. Mitochondria could be targeted for autophagic degradation for a variety of reasons including basal turnover for recycling, starvation induced degradation, and degradation due to damage...
June 16, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28615325/calcium-calmodulin-dependent-protein-kinase-regulates-the-pink1-parkin-and-dj-1-pathways-of-mitophagy-during-sepsis
#3
Xianghong Zhang, Du Yuan, Qian Sun, Li Xu, Emma Lee, Anthony J Lewis, Brian S Zuckerbraun, Matthew R Rosengart
During sepsis and shock states, mitochondrial dysfunction occurs. Consequently, adaptive mechanisms, such as fission, fusion, and mitophagy, are induced to eliminate damaged portions or entire dysfunctional mitochondria. The regulatory PINK1/Parkin and DJ-1 pathways are strongly induced by mitochondrial depolarization, although a direct link between loss of mitochondrial membrane potential (ΔΨ) and mitophagy has not been identified. Mitochondria also buffer Ca(2+), and their buffering capacity is dependent on ΔΨ...
June 14, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28608965/hydrogen-sulphide-modulating-mitochondrial-morphology-to-promote-mitophagy-in-endothelial-cells-under-high-glucose-and-high-palmitate
#4
Ning Liu, Jichao Wu, Linxue Zhang, Zhaopeng Gao, Yu Sun, Miao Yu, Yajun Zhao, Shiyun Dong, Fanghao Lu, Weihua Zhang
Endothelial cell dysfunction is one of the main reasons for type II diabetes vascular complications. Hydrogen sulphide (H2 S) has antioxidative effect, but its regulation on mitochondrial dynamics and mitophagy in aortic endothelial cells under hyperglycaemia and hyperlipidaemia is unclear. Rat aortic endothelial cells (RAECs) were treated with 40 mM glucose and 200 μM palmitate to imitate endothelium under hyperglycaemia and hyperlipidaemia, and 100 μM NaHS was used as an exogenous H2 S donor. Firstly, we demonstrated that high glucose and palmitate decreased H2 S production and CSE expression in RAECs...
June 13, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28602540/deficiencies-in-mitochondrial-dynamics-sensitize-caenorhabditis-elegans-to-arsenite-and-other-mitochondrial-toxicants-by-reducing-mitochondrial-adaptability
#5
Anthony L Luz, Tewodros R Godebo, Latasha L Smith, Tess C Leuthner, Laura L Maurer, Joel N Meyer
Mitochondrial fission, fusion, and mitophagy are interlinked processes that regulate mitochondrial shape, number, and size, as well as metabolic activity and stress response. The fundamental importance of these processes is evident in the fact that mutations in fission (DRP1), fusion (MFN2, OPA1), and mitophagy (PINK1, PARK2) genes can cause human disease (collectively >1/10,000). Interestingly, however, the age of onset and severity of clinical manifestations varies greatly between patients with these diseases (even those harboring identical mutations), suggesting a role for environmental factors in the development and progression of certain mitochondrial diseases...
June 8, 2017: Toxicology
https://www.readbyqxmd.com/read/28600493/adiponectin-modulates-oxidative-stress-induced-mitophagy-and-protects-c2c12-myoblasts-against-apoptosis
#6
Yinghui Ren, Yan Li, Jun Yan, Mingkun Ma, Dongmei Zhou, Zhenyi Xue, Zimu Zhang, Hongkun Liu, Huipeng Yang, Long Jia, Lijuan Zhang, Qi Zhang, Shuqin Mu, Rongxin Zhang, Yurong Da
Adiponectin (APN), also known as apM1, Acrp30, GBP28 and adipoQ, is a circulating hormone that is predominantly produced by adipose tissue. Many pharmacological studies have demonstrated that this protein possesses potent anti-diabetic, anti-atherogenic and anti-inflammatory properties. Although several studies have demonstrated the antioxidative activity of this protein, the regulatory mechanisms have not yet been defined in skeletal muscles. The aim of the present study was to examine the cytoprotective effects of APN against damage induced by oxidative stress in mouse-derived C2C12 myoblasts...
June 9, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28598236/destructive-cellular-paths-underlying-familial-and-sporadic-parkinson-disease-converge-on-mitophagy
#7
Xinnan Wang
The knowledge gap separating the molecular and cellular underpinnings of Parkinson disease (PD) and its pathology hinders treatment innovation. Adding to this difficulty is the lack of a reliable biomarker for PD. Our previous studies identify a link of 2 PD proteins, PINK1 and PRKN/Parkin to a mitochondrial motor/adaptor RHOT1/Miro-1, which mediates mitochondrial motility and mitophagy. Here we review our recent paper showing that a third PD protein, LRRK2, also targets RHOT1 and regulates mitophagy, and pathogenic LRRK2 disrupts this function...
June 9, 2017: Autophagy
https://www.readbyqxmd.com/read/28580603/enhancement-of-high-glucose-induced-pink1-expression-by-melatonin-stimulates-neuronal-cell-survival-involvement-of-mt2-akt-nf-%C3%AE%C2%BAb-pathway
#8
Xaykham Onphachanh, Hyun Jik Lee, Jae Ryong Lim, Young Hyun Jung, Jun Sung Kim, Chang Woo Chae, Sei-Jung Lee, Amr Ahmed Gabr, Ho Jae Han
Hyperglycemia is a representative hallmark and risk factor for diabetes mellitus (DM) and is closely linked to DM-associated neuronal cell death. Previous investigators reported on a genome-wide association study and showed relationships between DM and melatonin receptor (MT), highlighting the role of MT signaling by assessing melatonin in DM. However, the role of MT signaling in DM pathogenesis is unclear. Therefore, we investigated the role of mitophagy regulators in high glucose-induced neuronal cell death and the effect of melatonin against high glucose-induced mitophagy regulators in neuronal cells...
June 5, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28573163/non-radioactive-in-vitro-pink1-kinase-assays-using-ubiquitin-or-parkin-as-substrate
#9
Fabienne C Fiesel, Roman Hudec, Wolfdieter Springer
This protocol describes the in vitro phosphorylation of ubiquitin and Parkin by the kinase PINK1 using recombinant proteins. Both substrates, ubiquitin and Parkin, are phosphorylated at the conserved serine 65 residue (pS65-ubiquitin and pS65-Parkin). The protocol also includes the use of monomeric and K48- and K63-linked poly-ubiquitin chains as alternative substrates. Although there are commercially available antibodies, we have not tested their performance in this assay since, but used validated antibodies from our laboratory...
October 5, 2016: Bio-protocol
https://www.readbyqxmd.com/read/28556983/pink1-regulates-mitochondrial-trafficking-in-dendrites-of-cortical-neurons-through-mitochondrial-pka
#10
Tania DasBanerjee, Raul Y Dagda, Marisela Dagda, Charleen T Chu, Monica Rice, Emmanuel Vazquez-Mayorga, Ruben K Dagda
Mitochondrial Protein Kinase A (PKA) and PTEN-induced kinase 1 (PINK1), which is linked to Parkinson's disease, are two neuroprotective serine/threonine kinases that regulate dendrite remodeling, and mitochondrial function. We have previously shown that PINK1 regulates dendrite morphology by enhancing PKA activity. Here, we show the molecular mechanisms by which PINK1 and PKA in the mitochondrion interact to regulate dendrite remodeling, mitochondrial morphology, content, and trafficking in dendrites. PINK1-deficient cortical neurons exhibit impaired mitochondrial trafficking, reduced mitochondrial content, fragmented mitochondria, and a reduction in dendrite outgrowth compared to wild-type neurons...
May 30, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28541509/evidence-that-phosphorylated-ubiquitin-signaling-is-involved-in-the-etiology-of-parkinson-s-disease
#11
Kahori Shiba-Fukushima, Kei-Ichi Ishikawa, Tsuyoshi Inoshita, Nana Izawa, Masashi Takanashi, Shigeto Sato, Osamu Onodera, Wado Akamatsu, Hideyuki Okano, Yuzuru Imai, Nobutaka Hattori
The ubiquitin (Ub) kinase PINK1 and the E3 Ub ligase Parkin, two gene products associated with young-onset Parkinson's disease (PD), participate in mitochondrial quality control. The phosphorylation of mitochondrial polyUb by PINK1, which is activated in a mitochondrial membrane potential (ΔΨm)-dependent manner, facilitates the mitochondrial translocation and concomitant enzymatic activation of Parkin, leading to the clearance of phospho-polyUb-tagged mitochondria via mitophagy. Thus, Ub phosphorylation is a key event in PINK1-Parkin-mediated mitophagy...
May 25, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28536949/exercise-and-doxorubicin-treatment-modulate-cardiac-mitochondrial-quality-control-signaling
#12
I Marques-Aleixo, E Santos-Alves, J R Torrella, P J Oliveira, J Magalhães, A Ascensão
The cross-tolerance effect of exercise against heart mitochondrial-mediated quality control, remodeling and death-related mechanisms associated with sub-chronic Doxorubicin (DOX) treatment is yet unknown. We therefore analyzed the effects of two distinct chronic exercise models (endurance treadmill training-TM and voluntary free wheel activity-FW) performed during the course of the sub-chronic DOX treatment on mitochondrial susceptibility to permeability transition pore (mPTP), apoptotic and autophagic signaling and mitochondrial dynamics...
May 23, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28535644/-effect-of-neuroglobin-on-oxygen-glucose-deprivation-and-reoxygenation-induced-autophagy-in-a-human-neuroblastoma-cell-line
#13
S Y Deng, Y H Ai, H Gong, L Wu, C X Chen, Y M Wang, Z Y Liu, L Huang, Q Y Peng, L N Zhang
Objective: To investigate the effect of neuroglobin on oxygen-glucose deprivation and reoxygenation (OGD/R) induced autophagy in a human neuroblastoma cell line (SH-SY5Y). Methods: SH-SY5Y cells were transfected with plasmids (or vector) to establish a stable cell line of NGB overexpression (OE). After treated with OGD/R, cells were collected for the analyses of mRNA (Atg5, Atg7, BECN1 and FUNDC1) and protein levels of LC3. Furthermore, mitochondrial and cytosolic fractions were isolated for protein levels of PINK1 and Parkin...
May 23, 2017: Zhonghua Yi Xue za Zhi [Chinese medical journal]
https://www.readbyqxmd.com/read/28515082/parkin-independent-mitophagy-fkbp8-takes-the-stage
#14
Grace Gy Lim, Kah-Leong Lim
Although the Parkin/PINK1 pathway has received considerable attention in recent years as a key regulator of mitophagy in mammals, it is important to recognize that multiple mitophagy receptors like BNIP3, NIX, and FUNDC1 exist that can promote the selective clearance of mitochondria in the absence of Parkin. In this issue, Bhujabal et al expand the repertoire of Parkin-independent mitophagy receptors to include the anti-apoptotic protein, FKBP8. The authors demonstrate that FKBP8 interacts preferentially with LC3A via its LIR motif to destroy damaged mitochondria...
June 2017: EMBO Reports
https://www.readbyqxmd.com/read/28512249/p62-sqstm1-cooperates-with-hyperactive-mtorc1-to-regulate-glutathione-production-maintain-mitochondrial-integrity-and-promote-tumorigenesis
#15
Hilaire C Lam, Christian V Baglini, Alicia Llorente Lope, Andrey A Parkhitko, Heng-Jia Liu, Nicola Alesi, Izabela A Malinowska, Darius Ebrahimi-Fakhari, Afshin Saffari, Jane J Yu, Ana Pereira, Damir Khabibullin, Barbara Ogorek, Julie Nijmeh, Taylor Kavanagh, Adam Handen, Stephen Y Chan, John M Asara, William M Oldham, Maria T Diaz-Meco, Jorge Moscat, Mustafa Sahin, Carmen Priolo, Elizabeth P Henske
p62/sequestosome-1 (SQSTM1) is a multifunctional adaptor protein and autophagic substrate that accumulates in cells with hyperactive mTORC1, such as kidney cells with mutations in the tumor suppressor genes tuberous sclerosis complex (TSC)1 or TSC2. Here we report that p62 is a critical mediator of TSC2-driven tumorigenesis, as Tsc2(+/-) and Tsc2f/f Ksp-CreERT2(+) mice crossed to p62(-/-) mice were protected from renal tumor development. Metabolic profiling revealed that depletion of p62 in Tsc2-null cells decreased intracellular glutamine, glutamate, and glutathione (GSH)...
May 16, 2017: Cancer Research
https://www.readbyqxmd.com/read/28511347/mitochondrial-complex-i-deactivation-is-related-to-superoxide-production-in-acute-hypoxia
#16
Pablo Hernansanz-Agustín, Elena Ramos, Elisa Navarro, Esther Parada, Nuria Sánchez-López, Laura Peláez-Aguado, J Daniel Cabrera-García, Daniel Tello, Izaskun Buendia, Anabel Marina, Javier Egea, Manuela G López, Anna Bogdanova, Antonio Martínez-Ruiz
Mitochondria use oxygen as the final acceptor of the respiratory chain, but its incomplete reduction can also produce reactive oxygen species (ROS), especially superoxide. Acute hypoxia produces a superoxide burst in different cell types, but the triggering mechanism is still unknown. Herein, we show that complex I is involved in this superoxide burst under acute hypoxia in endothelial cells. We have also studied the possible mechanisms by which complex I could be involved in this burst, discarding reverse electron transport in complex I and the implication of PTEN-induced putative kinase 1 (PINK1)...
August 2017: Redox Biology
https://www.readbyqxmd.com/read/28511254/genetic-forms-of-parkinson-s-disease
#17
Christine Y Kim, Roy N Alcalay
One of the greatest advances in Parkinson's disease (PD) research in the past two decades has been a better understanding of PD genetics. Of the many candidate genes investigated, the best studied include LRRK2, SNCA, VPS35, Parkin, PINK1, and DJ1. The authors review the key clinical features of these monogenic forms, as well as for the prevalent risk factor gene, GBA, including the phenotype, clinical course, and treatment response. They also outline areas for future investigation: longitudinal studies of PD's clinical course, the identification of its premotor manifestations, and its specific mechanisms of pathogenicity...
April 2017: Seminars in Neurology
https://www.readbyqxmd.com/read/28507507/pink1-parkin-dependent-mitochondrial-surveillance-from-pleiotropy-to-parkinson-s-disease
#18
REVIEW
Francois Mouton-Liger, Maxime Jacoupy, Jean-Christophe Corvol, Olga Corti
Parkinson's disease (PD) is one of the most frequent neurodegenerative disease caused by the preferential, progressive degeneration of the dopaminergic (DA) neurons of the substantia nigra (SN) pars compacta. PD is characterized by a multifaceted pathological process involving protein misfolding, mitochondrial dysfunction, neuroinflammation and metabolism deregulation. The molecular mechanisms governing the complex interplay between the different facets of this process are still unknown. PARK2/Parkin and PARK6/PINK1, two genes responsible for familial forms of PD, act as a ubiquitous core signaling pathway, coupling mitochondrial stress to mitochondrial surveillance, by regulating mitochondrial dynamics, the removal of damaged mitochondrial components by mitochondria-derived vesicles, mitophagy, and mitochondrial biogenesis...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28505239/foxo1-promotes-mitophagy-in-the-podocytes-of-diabetic-male-mice-via-the-pink1-parkin-pathway
#19
Wen Li, Mengmeng Du, Qingzhu Wang, Xiaojun Ma, Lina Wu, Feng Guo, Hongfei Ji, Fengjuan Huang, Guijun Qin
We recently showed that Forkhead-box class O1 (FoxO1) activation protects against high glucose-induced injury by preventing mitochondrial dysfunction in the rat kidney cortex. In addition, FoxO1 has been reported to mediate PINK1 transcription and promote autophagy in response to mitochondrial oxidative stress in murine cardiomyocytes. In this study, we ascertained whether over-expressing FoxO1 in the kidney cortex reverses pre-established diabetic nephropathy in animal models. The effect of FoxO1 on mitophagy signaling pathways was evaluated in mouse podocytes...
May 12, 2017: Endocrinology
https://www.readbyqxmd.com/read/28504722/thyroid-hormone-protects-hepatocytes-from-hbx-induced-carcinogenesis-by-enhancing-mitochondrial-turnover
#20
H-C Chi, S-L Chen, S-L Lin, C-Y Tsai, W-Y Chuang, Y-H Lin, Y-H Huang, M-M Tsai, C-T Yeh, K-H Lin
Infection by hepatitis B virus (HBV) accounts for 50-80% of hepatocellular carcinoma (HCC) development worldwide, in which the HBV-encoded X protein (HBx) has critical role in the induction of carcinogenesis. Several studies have shown that thyroid hormone (TH) suppresses HCC development and protects hepatocytes from HBx-induced damage, thus it is of interest to examine whether TH can protect hepatocytes from HBx-induced carcinogenesis. By treating HBx- transgenic mice with or without TH, we confirmed the protective effects of TH on HBx-induced hepatocarcinogenesis, which was achieved via reduction of reactive oxygen species (ROS) inflicted DNA damage...
May 15, 2017: Oncogene
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