http://www.cnr.it/ontology/cnr/individuo/prodotto/ID313414
Autophagy impairment in the preproliferative diabetic retinophaty: A new target for estradiol prevention (Abstract/Poster in rivista)
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- Autophagy impairment in the preproliferative diabetic retinophaty: A new target for estradiol prevention (Abstract/Poster in rivista) (literal)
- Anno
- 2014-01-01T00:00:00+01:00 (literal)
- Alternative label
C. CASCIO, D. RUSSO, I. DEIDDA, G. GALIZZI1, A. MAENZA, G. CASSATA, P.
GUARNERI (2014)
Autophagy impairment in the preproliferative diabetic retinophaty: A new target for estradiol prevention
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- C. CASCIO, D. RUSSO, I. DEIDDA, G. GALIZZI1, A. MAENZA, G. CASSATA, P.
GUARNERI (literal)
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- Abstract (literal)
- Scopus (literal)
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- Istituto di Biomedicina e Immunologia Molecolare, IBIM - CNR, Palermo,
Istituto Zooprofilattico Sperimentale della Sicilia (literal)
- Titolo
- Autophagy impairment in the preproliferative diabetic retinophaty: A new target for estradiol prevention (literal)
- Abstract
- Diabetic retinopathy (DR) is a common microvascular complication in patients with diabetes
leading to a sudden and debilitating impact on visual acuity and eventually blindness. Advanced
stages of DR are characterized by the growth of abnormal retinal blood vessels secondary to
ischemia, whilst precocious stages are linked to altered glutamate excitation, reduced trophic factor
signaling, oxidative stress, and neuro-inflammation. Although these alterations are among the many
potential causes of retinal neuronal cell death, understanding of neurodegenerative mechanisms in
the preproliferative stage of diabetic retinopathy is still unclear and no treatment is currently
directed towards this stage. We and others have previously showed that estradiol is neuroprotective
against ischemic insult and glutamate- or oxidative-mediated retinal cell death. We also found that
the intraocular injection of 17?-estradiol regulates small heat shock proteins involved in preventing
aggregation of denatured or unfolded proteins (D'Anna C et al., Proteomics 2011, 11, 986-90).
Using a STZ rat model of diabetes, we here investigated the autophagic pathway along with
mitochondrial dysfunction and apoptotic cell death in retinas at different times from the onset of
diabetes and following or not the intraocular injection of 17?-estradiol. After 7 days of diabetes,
there were changes in autophagic markers, such as LC3II/LC3I ratio and p62, as well as in receptor
adapters involved in mitophagy, including parkin and BINP3, that suggested a blockade of
autophagosomal-lysosomal flux. Consistently, accumulation of polyubiquitinated substrates and
mitochondrial oxidative stress were early detected. Neuronal ganglion cells of diabetic retinas
primarily showed co-localization of LC3 and TUNEL staining, indicating an initial cross-talk
between autophagy and apoptosis. At the early stage of diabetic retinopathy, one week of 17?-
estradiol intraocularly injected reverted autophagic dysfunction and apoptosis. These results support
the hypothesis that advanced neurodegenerative events, likely related to autophagy/mitophagy,
occur in the preproliferative diabetic retinopathy and the local treatment with estradiol may be a
potential neuroprotective strategy (literal)
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