Deficiency in retinal TGF[beta] signaling aggravates neurodegeneration by modulating pro-apoptotic and MAP kinase pathways

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Abstract: Transforming growth factor β (TGFβ) signaling has manifold functions such as regulation of cell growth, differentiation, migration, and apoptosis. Moreover, there is increasing evidence that it also acts in a neuroprotective manner. We recently showed that TGFβ receptor type 2 (Tgfbr2) is upregulated in retinal neurons and Müller cells during retinal degeneration. In this study we investigated if this upregulation of TGFβ signaling would have functional consequences in protecting retinal neurons. To this end, we analyzed the impact of TGFβ signaling on photoreceptor viability using mice with cell type-specific deletion of Tgfbr2 in retinal neurons and Müller cells (Tgfbr2ΔOC) in combination with a genetic model of photoreceptor degeneration (VPP). We examined retinal morphology and the degree of photoreceptor degeneration, as well as alterations of the retinal transcriptome. In summary, retinal morphology was not altered due to TGFβ signaling deficiency. In contrast, VPP-induced photoreceptor degeneration was drastically exacerbated in double mutant mice (Tgfbr2ΔOC; VPP) by induction of pro-apoptotic genes and dysregulation of the MAP kinase pathway. Therefore, TGFβ signaling in retinal neurons and Müller cells exhibits a neuroprotective effect and might pose promising therapeutic options to attenuate photoreceptor degeneration in humans

Standort
Deutsche Nationalbibliothek Frankfurt am Main
Umfang
Online-Ressource
Sprache
Englisch
Anmerkungen
International journal of molecular sciences. - 23, 5 (2022) , 2626, ISSN: 1422-0067

Ereignis
Veröffentlichung
(wo)
Freiburg
(wer)
Universität
(wann)
2022
Urheber
Bielmeier, Christina B.
Schmitt, Sabrina I.
Kleefeldt, Nikolai
Boneva, Stefaniya
Schlecht, Anja
Vallon, Mario
Tamm, Ernst R.
Hillenkamp, Jost
Ergün, Süleyman
Neueder, Andreas
Braunger, Barbara M.

DOI
10.3390/ijms23052626
URN
urn:nbn:de:bsz:25-freidok-2254578
Rechteinformation
Kein Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Letzte Aktualisierung
15.08.2025, 07:21 MESZ

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