PARP1 Gene Knock-Out Increases Resistance to Retinal Degeneration without Affecting Retinal Function

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Fältnamn	Indikatorer	Metadata
000		03913naa a2200457 4500
001		oai:lup.lub.lu.se:02ea0d74-281f-4024-a37e-23a64c3cde5c
003		SwePub
008		160401s2010 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://lup.lub.lu.se/record/17516202 URI
024	7	a https://doi.org/10.1371/journal.pone.00154952 DOI
040		a (SwePub)lu
041		a engb eng
042		9 SwePub
072	7	a art2 swepub-publicationtype
072	7	a ref2 swepub-contenttype
100	1	a Sahaboglu, Ayse4 aut
245	1 0	a PARP1 Gene Knock-Out Increases Resistance to Retinal Degeneration without Affecting Retinal Function
264		c 2010-11-23
264	1	b Public Library of Science (PLoS),c 2010
338		a electronic2 rdacarrier
520		a Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases affecting photoreceptors and causing blindness in humans. Previously, excessive activation of enzymes belonging to the poly-ADP-ribose polymerase (PARP) group was shown to be involved in photoreceptor degeneration in the human homologous rd1 mouse model for RP. Since there are at least 16 different PARP isoforms, we investigated the exact relevance of the predominant isoform - PARP1 - for photoreceptor cell death using PARP1 knock-out (KO) mice. In vivo and ex vivo morphological analysis using optic coherence tomography (OCT) and conventional histology revealed no major alterations of retinal phenotype when compared to wild-type (wt). Likewise, retinal function as assessed by electroretinography (ERG) was normal in PARP1 KO animals. We then used retinal explant cultures derived from wt, rd1, and PARP1 KO animals to test their susceptibility to chemically induced photoreceptor degeneration. Since photoreceptor degeneration in the rd1 retina is triggered by a loss-of-function in phosphodiesterase-6 (PDE6), we used selective PDE6 inhibition to emulate the rd1 situation on non-rd1 genotypes. While wt retina subjected to PDE6 inhibition showed massive photoreceptor degeneration comparable to rd1 retina, in the PARP1 KO situation, cell death was robustly reduced. Together, these findings demonstrate that PARP1 activity is in principle dispensable for normal retinal function, but is of major importance for photoreceptor degeneration under pathological conditions. Moreover, our results suggest that PARP dependent cell death or PARthanatos may play a major role in retinal degeneration and highlight the possibility to use specific PARP inhibitors for the treatment of RP.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Oftalmologi0 (SwePub)302172 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Ophthalmology0 (SwePub)302172 hsv//eng
700	1	a Tanimoto, Naoyuki4 aut
700	1	a Kaur, Jasvir4 aut
700	1	a Sancho-Pelluz, Javier4 aut
700	1	a Huber, Gesine4 aut
700	1	a Fahl, Edda4 aut
700	1	a Arango-Gonzalez, Blanca4 aut
700	1	a Zrenner, Eberhart4 aut
700	1	a Ekström, Peru Lund University,Lunds universitet,Oftalmologi, Lund,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Ophthalmology, Lund,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)zoof-pek
700	1	a Loewenheim, Hubert4 aut
700	1	a Seeliger, Mathias4 aut
700	1	a Paquet-Durand, Francois4 aut
710	2	a Oftalmologi, Lundb Sektion IV4 org
773	0	t PLoS ONEd : Public Library of Science (PLoS)g 5:11q 5:11x 1932-6203
856	4	u https://portal.research.lu.se/files/3153984/1762451.pdfx primaryx freey FULLTEXT
856	4	u http://dx.doi.org/10.1371/journal.pone.0015495x freey FULLTEXT
856	4	u https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0015495&type=printable
856	4 8	u https://lup.lub.lu.se/record/1751620
856	4 8	u https://doi.org/10.1371/journal.pone.0015495

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Av författaren/redakt...: Sahaboglu, Ayse; Tanimoto, Naoyuk ...; Kaur, Jasvir; Sancho-Pelluz, J ...; Huber, Gesine; Fahl, Edda; visa fler...; Arango-Gonzalez, ...; Zrenner, Eberhar ...; Ekström, Per; Loewenheim, Hube ...; Seeliger, Mathia ...; Paquet-Durand, F ...; visa färre...

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Av lärosätet: Lunds universitet

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