NDLI: Aβ Potentiates Inflammatory Activation of Glial Cells Induced by Scavenger Receptor Ligands and Inflammatory Mediators in Culture

Content Provider	Springer Nature Link
Author	Murgas, P. Godoy, B. von Bernhardi, R.
Copyright Year	2012
Abstract	Alzheimer disease (AD) is a neurodegenerative disorder characterized by the accumulation of β amyloid (Aβ) aggregates. Aβ induces the inflammatory activation of glia, inducing secretion of Interleukin 1β (IL1β), nitric oxide (NO) and superoxide radicals. The specific receptor responsible for the induction of inflammatory activation by Aβ, is still an open question. We propose that scavenger receptors (SR) participate in the activation of glia by Aβ. We assessed production of NO, synthesis of IL1β and activation of ERK, JNK and NF-κB signaling pathways by Western blot, in primary rat glial cultures exposed to SR ligands (fucoidan and Poly I), LPS + IFNγ (LI), and Aβ. Poly I but not fucoidan nor fibrillar Aβ increased threefold NO production by astrocytes in a time-dependent manner. Fucoidan and Poly I increased 5.5- and 3.5-fold NO production by microglia, and co-stimulation with Aβ increased an additional 60% NO induced by SR ligands. Potentiation by Aβ was observed later for astrocytes than for microglia. In astrocytes, co-stimulation with Aβ potentiated ERK and JNK activation in response to Fucoidan and Poly I, whereas it reduced induction of JNK activation by LI and left unaffected NF-κB activation induced by LI. Levels of pro-IL1β in astrocytes increased with Aβ, SR ligands and LI, and were potentiated by co-stimulation with Aβ. Our results suggest that SRs play a role on inflammatory activation, inducing production of NO and IL1β, and show potentiation by Aβ. Potentiation of the inflammatory response of Aβ could be meaningful for the activation of glia observed in AD.
Starting Page	69
Ending Page	78
Page Count	10
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	22
Issue Number	1
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2012-01-12
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Alzheimer disease Astrocytes MAPKs Interleukin-1β Nitric oxide Inflammation Neurology Neurochemistry Neurobiology Pharmacology/Toxicology Cell Biology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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

SR-A Regulates the Inflammatory Activation of Astrocytes

Effect of Microglia Activation on Dopaminergic Neuronal Injury Induced by Manganese, and Its Possible Mechanism

Inhibition of microglial inflammatory responses by norepinephrine: effects on nitric oxide and interleukin-1β production

Role of activated astrocytes in neuronal damage: Potential links to HIV-1-associated dementia

Amplification and propagation of interleukin-1β signaling by murine brain endothelial and glial cells

Nitric Oxide as an Initiator of Brain Lesions During the Development of Alzheimer Disease

Glial cell dysregulation: a new perspective on Alzheimer disease

5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) attenuates the expression of LPS- and Aβ peptide-induced inflammatory mediators in astroglia

Mechanism for Quinolinic Acid Cytotoxicity in Human Astrocytes and Neurons

Aβ Potentiates Inflammatory Activation of Glial Cells Induced by Scavenger Receptor Ligands and Inflammatory Mediators in Culture

Similar Documents

SR-A Regulates the Inflammatory Activation of Astrocytes

Effect of Microglia Activation on Dopaminergic Neuronal Injury Induced by Manganese, and Its Possible Mechanism

Inhibition of microglial inflammatory responses by norepinephrine: effects on nitric oxide and interleukin-1β production

Role of activated astrocytes in neuronal damage: Potential links to HIV-1-associated dementia

Amplification and propagation of interleukin-1β signaling by murine brain endothelial and glial cells

Nitric Oxide as an Initiator of Brain Lesions During the Development of Alzheimer Disease

Glial cell dysregulation: a new perspective on Alzheimer disease

5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) attenuates the expression of LPS- and Aβ peptide-induced inflammatory mediators in astroglia

Mechanism for Quinolinic Acid Cytotoxicity in Human Astrocytes and Neurons

Aβ Potentiates Inflammatory Activation of Glial Cells Induced by Scavenger Receptor Ligands and Inflammatory Mediators in Culture