Wang, Maoren ORCID: 0000-0002-5470-8771, Milic, Marija, Gericke, Adrian, Mercieca, Karl, Liu, Hanhan, Ruan, Yue, Jiang, Subao, van Beers, Tim, von Pein, Harald D., Mueller, Marianne B. and Prokosch, Verena (2021). Chronic social defeat stress causes retinal vascular dysfunction. Exp. Eye Res., 213. LONDON: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD. ISSN 1096-0007

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Abstract

Purpose: The roles of vascular dysfunction and chronic stress have been extensively discussed in the pathophysiology of glaucoma. Our aim was to test whether chronic stress causes retinal vascular dysfunction and therewith induces retinal ganglion cells (RGCs) loss. Methods: Twelve mice underwent chronic social defeat (CSD) stress, while 12 mice received control treatment only. Intraocular pressure (IOP) was measured with a rebound tonometer. Blood plasma corticosterone concentration and adrenal gland weight were used to assess stress levels. Brn-3a staining in retinas and PPD staining in optic nerve cross sections were conducted to assess the survival of RGCs and axons respectively. The ET-1 and alpha-SMA levels were determined in retina. Retinal vascular autoregulation, functional response to various vasoactive agents and vascular mechanics were measured using video microscopy. Results: No significant difference in IOP levels was observed during and after CSD between CSD mice and controls. CSD stress caused hypercortisolemia 2 days post-CSD. However, increased corticosterone levels went back to normal 8 months after CSD. CSD-exposed mice developed adrenal hyperplasia 3 days post-CSD, which was normalized by 8 months. RGC and axon survival were similar between CSD mice and controls. However, CSD stress caused irreversible, impaired autoregulation and vascular dysfunction of retinal arterioles in CSD mice. In addition, impaired maximal dilator capacity of retinal arterioles was observed 8 months post-CSD rather than 3 days post-CSD. Remarkably, ET-1 levels were increased 3 days post-CSD while alpha-SMA levels were decreased 8 months post-CSD. Conclusions: We found that CSD stress does not cause IOP elevation, nor loss of RGCs and their axons. However, it strikingly causes irreversible impaired autoregulation and endothelial function in murine retinal arterioles. In addition, CSD changed vascular mechanics on a long-term basis. Increased ET-1 levels and loss of pericytes in retina vessels may involve in this process.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Wang, MaorenUNSPECIFIEDorcid.org/0000-0002-5470-8771UNSPECIFIED
Milic, MarijaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Gericke, AdrianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Mercieca, KarlUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Liu, HanhanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ruan, YueUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Jiang, SubaoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
van Beers, TimUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
von Pein, Harald D.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Mueller, Marianne B.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Prokosch, VerenaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-587083
DOI: 10.1016/j.exer.2021.108853
Journal or Publication Title: Exp. Eye Res.
Volume: 213
Date: 2021
Publisher: ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Place of Publication: LONDON
ISSN: 1096-0007
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
OCULAR PERFUSION-PRESSURE; PRIMARY ANGLE-CLOSURE; BLOOD-FLOW; INTRAOCULAR-PRESSURE; NITRIC-OXIDE; ENDOTHELIAL DYSFUNCTION; MENTAL STRESS; VISUAL-FIELD; GLAUCOMA; AUTOREGULATIONMultiple languages
OphthalmologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/58708

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