Glial dysfunction in parkin null mice: effects of aging

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
Rosa M SolanoMaría A Mena

Abstract

Parkin mutations in humans produce parkinsonism whose pathogenesis is related to impaired protein degradation, increased free radicals, and abnormal neurotransmitter release. The role of glia in parkin deficiency is little known. We cultured midbrain glia from wild-type (WT) and parkin knock-out (PK-KO) mice. After 18-20 d in vitro, PK-KO glial cultures had less astrocytes, more microglia, reduced proliferation, and increased proapoptotic protein expression. PK-KO glia had greater levels of intracellular glutathione (GSH), increased mRNA expression of the GSH-synthesizing enzyme gamma-glutamylcysteine synthetase, and greater glutathione S-transferase and lower glutathione peroxidase activities than WT. The reverse happened in glia cultured in serum-free defined medium (EF12) or in old cultures. PK-KO glia was more susceptible than WT to transference to EF12 or neurotoxins (1-methyl-4-phenylpyridinium, blockers of GSH synthesis or catalase, inhibitors of extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3 kinases), aging of the culture, or combination of these insults. PK-KO glia was less susceptible than WT to Fe2+ plus H2O2 and less responsive to protection by deferoxamine. Old WT glia increased the expression...Continue Reading

Citations

Sep 25, 2009·Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]·Agnieszka CiesielskaA Członkowski
Jul 30, 2011·Neurogenetics·Gregory J MichaelManuel B Graeber
Jan 24, 2009·Apoptosis : an International Journal on Programmed Cell Death·Oren A LevyLloyd A Greene
Oct 1, 2010·Neurotherapeutics : the Journal of the American Society for Experimental NeuroTherapeutics·Phillip M Rappold, Kim Tieu
Jan 8, 2011·Human Molecular Genetics·Saskia SchmidtHermann Lübbert
Aug 25, 2012·PLoS Currents·Carolina RuizMaria Angeles Mena
Jan 27, 2009·Biological Chemistry·Nazzareno BallatoriChristine L Hammond
Jan 19, 2012·Drugs & Aging·José Luis López-SendónJusto García de Yébenes
Sep 5, 2008·Neurochemical Research·Ikuko Miyazaki, Masato Asanuma
Nov 18, 2009·Journal of Neuropathology and Experimental Neurology·Yun Ju C SongTamas R Revesz
Sep 19, 2014·Biochemical Society Transactions·Terri-Leigh StephenJosef T Kittler
Oct 27, 2010·Parkinson's Disease·Sonja MendritzkiHermann Lübbert
Aug 26, 2014·Frontiers in Molecular Neuroscience·Anne H P JansenElly M Hol
Sep 27, 2014·PloS One·Maria Jose CasarejosMaria Angeles Mena
Jun 13, 2012·Free Radical Biology & Medicine·Micha M M WilhelmusJack van Horssen
Oct 7, 2016·Frontiers in Molecular Neuroscience·Weidong LeYu Tang
Nov 26, 2008·The Neuroscientist : a Review Journal Bringing Neurobiology, Neurology and Psychiatry·Maria A Mena, Justo García de Yébenes
Jan 20, 2018·Molecular Neurobiology·Khushnuma WahabiMoshahid A Rizvi
Apr 5, 2013·Journal of Neuroscience Research·Qiong LiYong Zhao
Nov 8, 2013·Diabetes & Metabolism Journal·Jong-Ok PyoYong-Keun Jung
Mar 13, 2010·Annals of Neurology·Masato AsanumaMiho Murata
Jan 25, 2014·CNS Neuroscience & Therapeutics·Albert J FenoyYing Xia
Sep 1, 2019·Current Alzheimer Research·Laura Trujillo-EstradaFrank M LaFerla
Jun 3, 2009·Physical Therapy·James H Cauraugh, Jeffery J Summers
Mar 25, 2015·Movement Disorders : Official Journal of the Movement Disorder Society·Roberto ErroMichele Tinazzi
May 8, 2018·Experimental Neurobiology·Eun-Hye JoeSangmyun Park
Jul 4, 2020·Cellular and Molecular Life Sciences : CMLS·Ana V DominguesFábio G Teixeira
Feb 2, 2019·International Journal of Molecular Sciences·Masato AsanumaToshiaki Sendo
Jul 3, 2019·Frontiers in Cellular Neuroscience·Violetta Refolo, Nadia Stefanova
Sep 26, 2020·Frontiers in Cellular Neuroscience·Rebecca StevensonYossi Buskila
Nov 6, 2020·Cells·Alba Navarro-RomeroMarta Martinez-Vicente
Jan 5, 2021·Nihon yakurigaku zasshi. Folia pharmacologica Japonica·Masato Asanuma, Ikuko Miyazaki
Sep 9, 2020·Neuron·Mathias LinnerbauerFrancisco J Quintana

❮ Previous
Next ❯

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.

Astrocytes

Astrocytes are glial cells that support the blood-brain barrier, facilitate neurotransmission, provide nutrients to neurons, and help repair damaged nervous tissues. Here is the latest research.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Astrocytes & Neurodegeneration

Astrocytes are important for the health and function of the central nervous system. When these cells stop functioning properly, either through gain of function or loss of homeostatic controls, neurodegenerative diseases can occur. Here is the latest research on astrocytes and neurodegeneration.