NDLI: Phosphorylation of GFAP is Associated with Injury in the Neonatal Pig Hypoxic-Ischemic Brain

Content Provider	Springer Nature Link
Author	Sullivan, Susan M. Sullivan, Robert K. P. Miller, Stephanie M. Ireland, Zoe Björkman, S. Tracey Pow, David V. Colditz, Paul B.
Copyright Year	2012
Abstract	Glial fibrillary acidic protein (GFAP) is an intermediate filament protein expressed in the astrocyte cytoskeleton that plays an important role in the structure and function of the cell. GFAP can be phosphorylated at six serine (Ser) or threonine (Thr) residues but little is known about the role of GFAP phosphorylation in physiological and pathophysiological states. We have generated antibodies against two phosphorylated GFAP (pGFAP) proteins: p8GFAP, where GFAP is phosphorylated at Ser-8 and p13GFAP, where GFAP is phosphorylated at Ser-13. We examined p8GFAP and p13GFAP expression in the control neonatal pig brain and at 24 and 72 h after an hypoxic-ischemic (HI) insult. Immunohistochemistry demonstrated pGFAP expression in astrocytes with an atypical cytoskeletal morphology, even in control brains. Semi-quantitative western blotting revealed that p8GFAP expression was significantly increased at 24 h post-insult in HI animals with seizures in frontal, parietal, temporal and occipital cortices. At 72 h post-insult, p8GFAP and p13GFAP expression were significantly increased in HI animals with seizures in brain regions that are vulnerable to cellular damage (cortex and basal ganglia), but no changes were observed in brain regions that are relatively spared following an HI insult (brain stem and cerebellum). Increased pGFAP expression was associated with poor neurological outcomes such as abnormal encephalography and neurobehaviour, and increased histological brain damage. Phosphorylation of GFAP may play an important role in astrocyte remodelling during development and disease and could potentially contribute to the plasticity of the central nervous system.
Starting Page	2364
Ending Page	2378
Page Count	15
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	37
Issue Number	11
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2012-04-19
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Astrocyte Central nervous system Cytoskeleton Glia Plasticity Seizure Biochemistry Neurochemistry Neurosciences Neurology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Neuroprotective effect of astrocyte-derived IL-33 in neonatal hypoxic-ischemic brain injury

Plasticity of Neurons and Glia Following Neonatal Hypoxic-Ischemic Brain Injury in Rats

Neuroprotective Effects of a PSD-95 Inhibitor in Neonatal Hypoxic-Ischemic Brain Injury

Comprehensive Gene Expression Analysis of Cerebral Cortices from Mature Rats After Neonatal Hypoxic–Ischemic Brain Injury

TRPM7 inhibitor carvacrol protects brain from neonatal hypoxic-ischemic injury

Aggravated brain injury after neonatal hypoxic ischemia in microglia-depleted mice

Changes in Hypoxia-Inducible Factor-1 (HIF-1) and Regulatory Prolyl Hydroxylase (PHD) Enzymes Following Hypoxic–Ischemic Injury in the Neonatal Rat

Neuron–Astroglial Interactions in Cell-Fate Commitment and Maturation in the Central Nervous System

Astrocyte Mitochondrial Mechanisms of Ischemic Brain Injury and Neuroprotection

Phosphorylation of GFAP is Associated with Injury in the Neonatal Pig Hypoxic-Ischemic Brain

Similar Documents

Neuroprotective effect of astrocyte-derived IL-33 in neonatal hypoxic-ischemic brain injury

Plasticity of Neurons and Glia Following Neonatal Hypoxic-Ischemic Brain Injury in Rats

Neuroprotective Effects of a PSD-95 Inhibitor in Neonatal Hypoxic-Ischemic Brain Injury

Comprehensive Gene Expression Analysis of Cerebral Cortices from Mature Rats After Neonatal Hypoxic–Ischemic Brain Injury

TRPM7 inhibitor carvacrol protects brain from neonatal hypoxic-ischemic injury

Aggravated brain injury after neonatal hypoxic ischemia in microglia-depleted mice

Changes in Hypoxia-Inducible Factor-1 (HIF-1) and Regulatory Prolyl Hydroxylase (PHD) Enzymes Following Hypoxic–Ischemic Injury in the Neonatal Rat

Neuron–Astroglial Interactions in Cell-Fate Commitment and Maturation in the Central Nervous System

Astrocyte Mitochondrial Mechanisms of Ischemic Brain Injury and Neuroprotection

Phosphorylation of GFAP is Associated with Injury in the Neonatal Pig Hypoxic-Ischemic Brain