NDLI: IL-17A Induces MIP-1α Expression in Primary Astrocytes via Src/MAPK/PI3K/NF-kB Pathways: Implications for Multiple Sclerosis

Please wait, while we are loading the content...

The Calcineurin Inhibitor Ascomicin Interferes with the Early Stage of the Epileptogenic Process Induced by Latrunculin A Microperfusion in Rat Hippocampus

P2X4 Receptor Regulates Alcohol-Induced Responses in Microglia

Pro-Inflammatory Interferon Gamma Signaling is Directly Associated with Stroke Induced Neurodegeneration

3,4-Methylenedioxymethamphetamine (MDMA – Ecstasy) Decreases Neutrophil Activity Through the Glucocorticoid Pathway and Impairs Host Resistance to Listeria Monocytogenes Infection in Mice

Cocaine Potentiates Cathepsin B Secretion and Neuronal Apoptosis from HIV-Infected Macrophages

Expression of the Mannose Receptor CD206 in HIV and SIV Encephalitis: A Phenotypic Switch of Brain Perivascular Macrophages with Virus Infection

Domain Structure and Conformational Changes in rat K$_{V}$2.1 ion Channel

Plasma Cytokine Levels are Related to Brain Volumes in HIV-infected Individuals

Journal of Neuroimmune Pharmacology : Volume 9, Issue 4, September 2014

Journal of Neuroimmune Pharmacology : Volume 9, Issue 3, June 2014

Journal of Neuroimmune Pharmacology : Volume 9, Issue 2, March 2014

Journal of Neuroimmune Pharmacology : Volume 9, Issue 1, Supplement,March 2014

Journal of Neuroimmune Pharmacology : Volume 9, Issue 1, March 2014

Journal of Neuroimmune Pharmacology : Volume 8

Journal of Neuroimmune Pharmacology : Volume 7

Journal of Neuroimmune Pharmacology : Volume 6

Journal of Neuroimmune Pharmacology : Volume 5

Journal of Neuroimmune Pharmacology : Volume 4

Journal of Neuroimmune Pharmacology : Volume 3

Journal of Neuroimmune Pharmacology : Volume 2

Journal of Neuroimmune Pharmacology : Volume 1

IL-17A Induces MIP-1α Expression in Primary Astrocytes via Src/MAPK/PI3K/NF-kB Pathways: Implications for Multiple Sclerosis

Content Provider	Springer Nature Link
Author	Yi, Hongwei Bai, Ying Zhu, Xinjian lin, Lin Zhao, Lei Wu, Xiaodong Buch, Shilpa Wang, Longxin Chao, Jie Yao, Honghong
Copyright Year	2014
Abstract	Neuroinflammation plays critical roles in multiple sclerosis (MS). In addition to the part played by the lymphocytes, the underlying mechanisms could, in part, be also attributed to activation mediated by astrocytes. Macrophage inflammatory protein-1α (MIP-1α) has been implicated in a number of pathological conditions, specifically attributable to its potent chemottractant effects. Its modulation by IL-17, however, has received very little attention. In the present study, we demonstrated IL-17-mediated induction of MIP-1α in rat primary astroctyes through its binding to the cognate IL-17RA. Furthermore, this effect was mediated via the activation of Src, mitogen-activated protein kinases (MAPKs), PI3K/Akt and NF-kB pathways, culminating ultimately into increased expression of MIP-1α. Exposure of primary mouse astrocytes to IL-17 resulted in increased expression of glial fibrillary acidic protein and, this effect was abrogated in cells cultured in presence of the MIP-1α neutralizing antibody, thus underscoring its role in the activation of astrocytes. In vivo relevance of these findings was further corroborated in experimental autoimmune encephalomyelitis mice that demonstrated significantly increased activation of astrocytes with concomitant increased expression of MIP-1α in the corpus callosum compared with control group. Understanding the regulation of MIP-1α expression may provide insights into the development of potential therapeutic targets for neuroinflammation associated with multiple sclerosis.
Starting Page	629
Ending Page	641
Page Count	13
File Format	PDF
ISSN	15571890
Journal	Journal of Neuroimmune Pharmacology
Volume Number	9
Issue Number	5
e-ISSN	15571904
Language	English
Publisher	Springer US
Publisher Date	2014-07-03
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	IL-17 Astrocytes MIP-1α Src Neurosciences Immunology Pharmacology/Toxicology Virology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Allergy Pharmacology Immunology

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

IL-17 induces MIP-1α expression in primary mouse astrocytes via TRPC channel

Human immunodeficiency virus type 1 viral protein R (Vpr) induces CCL5 expression in astrocytes via PI3K and MAPK signaling pathways

Mechanism of Neuroinflammation: Enhanced Cytotoxicity and IL-17 Production via CD46 Binding

TLR2 ligation induces the production of IL-23/IL-17 via IL-6, STAT3 and NF-kB pathway in patients with primary Sjogren's syndrome

Modulation of Inflammatory Cytokines and Mitogen-activated Protein Kinases by Acetate in Primary Astrocytes

Fingolimod Modulates Peripheral Effector and Regulatory T Cells in MS Patients

IL-17 Induces Autophagy Dysfunction to Promote Inflammatory Cell Death and Fibrosis in Keloid Fibroblasts via the STAT3 and HIF-1α Dependent Signaling Pathways

Oxidative Stress Kills Human Primary Oligodendrocytes Via Neutral Sphingomyelinase: Implications for Multiple Sclerosis

Regulation of Complement Component C3 in Astrocytes by IL-1β and Morphine

IL-17A Induces MIP-1α Expression in Primary Astrocytes via Src/MAPK/PI3K/NF-kB Pathways: Implications for Multiple Sclerosis

Similar Documents

IL-17 induces MIP-1α expression in primary mouse astrocytes via TRPC channel

Human immunodeficiency virus type 1 viral protein R (Vpr) induces CCL5 expression in astrocytes via PI3K and MAPK signaling pathways

Mechanism of Neuroinflammation: Enhanced Cytotoxicity and IL-17 Production via CD46 Binding

TLR2 ligation induces the production of IL-23/IL-17 via IL-6, STAT3 and NF-kB pathway in patients with primary Sjogren's syndrome

Modulation of Inflammatory Cytokines and Mitogen-activated Protein Kinases by Acetate in Primary Astrocytes

Fingolimod Modulates Peripheral Effector and Regulatory T Cells in MS Patients

IL-17 Induces Autophagy Dysfunction to Promote Inflammatory Cell Death and Fibrosis in Keloid Fibroblasts via the STAT3 and HIF-1α Dependent Signaling Pathways

Oxidative Stress Kills Human Primary Oligodendrocytes Via Neutral Sphingomyelinase: Implications for Multiple Sclerosis

Regulation of Complement Component C3 in Astrocytes by IL-1β and Morphine

IL-17A Induces MIP-1α Expression in Primary Astrocytes via Src/MAPK/PI3K/NF-kB Pathways: Implications for Multiple Sclerosis