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@ARTICLE{Merz:306684,
author = {J. Merz and E. Müller and W. Darwisch and R. Fairless$^*$
and Y. Wang and S. Vorwald and S. Darwisch and E. R.
Curticean and F. Shao and I. Wacker and R. R. Schröder and
C. Pitzer and C. Schultz and J.-B. van Klinken and F. M. Vaz
and F. Kratzer and K. Schwarz and J. G. Okun and Y. Feng and
C. Hopf and M. Islinger},
title = {{L}ocal accumulation of very long-chain {PUFA} in plexiform
layers associates with retinal dysfunction in a mouse model
of peroxisomal {ACBD}5-deficiency.},
journal = {Cellular and molecular life sciences},
volume = {83},
number = {1},
issn = {1420-682X},
address = {Cham (ZG)},
publisher = {Springer International Publishing AG},
reportid = {DKFZ-2025-02676},
pages = {26},
year = {2025},
note = {2025 Dec 1;83(1):26},
abstract = {Patients deficient in the peroxisomal membrane protein
ACBD5 regularly exhibit a dystrophy of the retina along with
decline in visual acuity. Despite the prevalent retinal
phenotype, information on the pathogenesis of the
retinodystrophy is limited. To gain insight into the
cellular, subcellular and molecular alterations occurring in
the retina, we analyzed an ACBD5-deficient mouse model by
immunofluorescence microscopy, electron microscopy,
full-field electroretinography (ffERG) and as well as
analytical and spatial mass spectrometry (MS)-based
lipidomics techniques. Histological results implied that
ACBD5-deficient mice exhibit a moderate degeneration of
photoreceptor, bipolar, ganglion and retinal pigment
epithelial cells accompanied, however, by a prominent
activation of astroglia and microglia. Reduced a- and b-wave
amplitudes from ffERG point to a severe functional
dysregulation of retinal signal transduction with a focus at
the level of the information-processing cell of the inner
retina. At the lipidome level, very long-chain
polyunsaturated fatty acids (VLC-PUFA) accumulated in
phosphatidylcholines from retina homogenates, most likely
disrupted by a decline in peroxisome functions. Remarkably,
as revealed by MALDI MS imaging, these lipidome changes
affected neither the whole retina nor the photoreceptor
outer segments (POS), where VLC-PUFAs display the highest
concentration in phospholipids of POS membrane discs. In
contrast, VLC-PUFAs in ACBD5-deficient mice consistently
accumulated in the inner retinal region from the outer (OPL)
to inner plexiform layer (IPL). In line with
VLC-PUFA-accumulations, photoreceptor ribbon synapses in the
OPL showed morphological signs of degeneration on the
ultrastructural level. Hence, peroxisomal dysfunction
appears to affect cell type-specific lipid homeostasis,
thereby disrupting local retinal membrane physiology leading
to a severe neuroinflammation of the ACBD5-deficient mouse
retina.},
keywords = {Metabolic disorders (Other) / Peroxisomes (Other) / RDLKD
(ACBD5-deficiency) (Other) / Retinodystrophy (Other) / Very
long-chain fatty acids (VLCFA) (Other)},
cin = {B320 / HD01},
ddc = {610},
cid = {I:(DE-He78)B320-20160331 / I:(DE-He78)HD01-20160331},
pnm = {312 - Funktionelle und strukturelle Genomforschung
(POF4-312)},
pid = {G:(DE-HGF)POF4-312},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41324649},
doi = {10.1007/s00018-025-05971-8},
url = {https://inrepo02.dkfz.de/record/306684},
}