Upregulation of antibody response to heat shock proteins and tissue antigens in an ocular ischemia model

The aim of this study was to characterize the serum antibody reactivities occurring after ocular ischemia reperfusion. The time course of serum antibody responses was examined. Wistar rats were exposed to transient ocular ischemia by elevating intraocular pressure to 130 mm Hg for 60 minutes. Axonal...

Full description

Saved in:

Bibliographic Details
Published in:	Investigative ophthalmology & visual science Vol. 52; no. 6; pp. 3468 - 3474
Main Authors:	Joachim, Stephanie C, Wax, Martin B, Boehm, Nils, Dirk, Desiree R, Pfeiffer, Norbert, Grus, Franz H
Format:	Journal Article
Language:	English
Published:	United States 01-06-2011
Subjects:	Animals Autoantibodies - blood Autoantigens - immunology Axons - pathology Eye Proteins - immunology Glial Fibrillary Acidic Protein - immunology HSP27 Heat-Shock Proteins - immunology Immunoglobulin G - blood Intraocular Pressure Male Myelin Basic Protein - immunology Myelin Proteins Myelin-Associated Glycoprotein - immunology Myelin-Oligodendrocyte Glycoprotein Optic Nerve - pathology Protein Array Analysis Rats Rats, Wistar Reperfusion Injury - immunology Retinal Diseases - immunology Retinal Vessels Spectrin - immunology Up-Regulation
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	The aim of this study was to characterize the serum antibody reactivities occurring after ocular ischemia reperfusion. The time course of serum antibody responses was examined. Wistar rats were exposed to transient ocular ischemia by elevating intraocular pressure to 130 mm Hg for 60 minutes. Axonal damage was evaluated on optic-nerve sections 2 and 4 weeks later. Blood samples collected before and several times after ischemia were used for antibody detection via customized protein microarrays. Different tissue antigens, including heat shock proteins (HSPs) and crystallins, were selected based on previous identification of antibody reactivities in studies on ischemic events or ophthalmic diseases associated with ischemia. Antibody reactivity was compared using multivariate statistical techniques. Significant axonal damage was observed 2 and 4 weeks after ocular ischemia (P < 0.05). Animals showed certain immunoreactivities against antigens even before ischemia, whereas many reactivities increased afterward. Significantly different responses were detected 2, 3, and 4 weeks after ischemia (P < 0.05). Antibody reactivity against actin, glial fibrillary acidic protein, HSP 27, vimentin, or spectrin continually increased. Ischemia induced by acute intraocular pressure elevation led to complex changes in antibody reactivities in sera of treated animals. Upregulation of serum autoantibodies, especially against heat shock and structural proteins, progressively increased throughout the 4-week follow-up period, whereas others such as ubiquitin decreased. The upregulation of anti-HSP 27 antibodies might be an attempt to protect the tissue from ischemic damage.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1552-5783 1552-5783
DOI:	10.1167/iovs.10-5763