Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
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Target Concepts:
Gene/Protein
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Query: UMLS:C0086543 (
cataract
)
29,165
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Oxidative stress plays an important role in the pathogenesis of cataracts. Small ubiquitin-like modifier (SUMO) proteins have great effects on cell stress response. Previous studies have shown that
TP53INP1
can arrest cell growth and induce apoptosis by modulating p53 transcriptional activity and that both
TP53INP1
and p53 are substrates of SUMOylation. However, no previous research has studied the effect of SUMOylation on the oxidative stress response in cataracts. This is the first study to investigate the effect of SUMOylation of
TP53INP1
in oxidative stress-induced lens epithelial cell injury and age-related
cataract
formation. We found that the oxidative stress-induced endogenous SUMOylation of
TP53INP1
promoted human lens epithelial cell (holed) apoptosis and regulated hLEC antioxidant effects by increasing the stability and transcription of
TP53INP1
in age-related cataracts. SUMO-1, SUMOylation, and
TP53INP1
were upregulated in lens tissues affected by age-related cataracts. A SUMO-1-specific protease, SENP1, acted as an oxidative stress-sensitive target gene in hLECs. This study identified for the first time that
TP53INP1
can be SUMOylated in vivo, that the SUMOylation of
TP53INP1
is induced by oxidative stress, and that SUMOylation/deSUMOylation can affect the stability and transcription of
TP53INP1
in hLECs.
...
PMID:SUMOylation Evoked by Oxidative Stress Reduced Lens Epithelial Cell Antioxidant Functions by Increasing the Stability and Transcription of TP53INP1 in Age-Related Cataracts. 3128 92
Age-related
cataract
(ARC) is the leading cause of visual impairment or even blindness among the aged population globally. Long non-coding RNA (LncRNA) has been proven to be the potential regulator of ARC. The latest study reveals that maternally expressed gene 3 (MEG3) promotes the apoptosis and inhibits the proliferation of multiple cancer cells. However, the expression and role of MEG3 in ARC are unclear. In this study, we investigated the effects of MEG3 in ARC and explored the regulatory mechanisms underlying these effects. We observed that MEG3 expression was up-regulated in the age-related cortical
cataract
(ARCC) lens capsules and positively correlated with the histological degree of ARCC. The pro-apoptosis protein, active caspase-3 and Bax increased in the anterior lens capsules of ARCC tissue, while the anti-apoptotic protein Bcl-2 decreased compared to normal lens. Knockdown of MEG3 increased the viability and inhibited the apoptosis of LECs upon the oxidative stress induced by H
2
O
2
. MEG3 was localized in both nucleus and cytoplasm in LECs. MEG3 facilitated
TP53INP1
expression via acting as miR-223 sponge and promoting P53 expression. Additionally,
TP53INP1
knockdown alleviated H
2
O
2
-induced lens turbidity. In summary, MEG3 promoted ARC progression by up-regulating
TP53INP1
expression through suppressing miR-223 and promoting P53 expression, which would provide a novel insight into the pathogenesis of ARC.
...
PMID:Long non-coding RNA MEG3 promotes cataractogenesis by upregulating TP53INP1 expression in age-related cataract. 3284 49
