Dataset Information

CCAAT/Enhancer-Binding Protein ? Mediates Oxygen-Induced Retinal Neovascularization via Retinal Vascular Damage and Vascular Endothelial Growth Factor.

ABSTRACT:

Objective

To evaluate the role of CCAAT/enhancer-binding protein ? (C/EBP ? (C/EBP.

Methods

Rats with OIR were exposed to alternating hypoxic and hyperopic conditions for 14 days. Then, the rats with OIR were assigned randomly to groups that received intravitreal injections of either shRNA lentiviral particles targeting C/EBP ? (C/EBP ? (C/EBP ? (C/EBP ? (C/EBP ? (C/EBP ? (C/EBP.

Results

In OIR rats, the expression levels of C/EBP ? (C/EBP P < 0.01). The p-C/EBP ? (C/EBP ? (C/EBP ? (C/EBP ? (C/EBP ? (C/EBP P < 0.01). The p-C/EBP ? (C/EBP ? (C/EBP ? (C/EBP P < 0.01). The p-C/EBP.

Conclusions

C/EBP ? shRNA inhibits RNV in OIR. A potential mechanism may be that the activity of C/EBP ? increases with its overexpression, which in turn aggravates the amount of the retinal vascular damage and promotes transcription of VEGF. C/EBP ? might be a new therapeutic target for preventing RNV.? (C/EBP ? (C/EBP ? (C/EBP.

SUBMITTER: Li T

PROVIDER: S-EPMC7085405 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Publications

CCAAT/Enhancer-Binding Protein <i>β</i> Mediates Oxygen-Induced Retinal Neovascularization via Retinal Vascular Damage and Vascular Endothelial Growth Factor.

Li Tingting T Cai Xuan X Wang Xiangning X Zhang Xueyan X Zhang Hui H Xu Biwei B Li Shiwei S Hu Jianyan J Wu Qiang Q

Journal of diabetes research 20200309

<h4>Objective</h4>To evaluate the role of CCAAT/enhancer-binding protein <i>β</i> (C/EBP <i>β</i> (C/EBP.<h4>Methods</h4>Rats with OIR were exposed to alternating hypoxic and hyperopic conditions for 14 days. Then, the rats with OIR were assigned randomly to groups that received intravitreal injections of either shRNA lentiviral particles targeting C/EBP <i>β</i> (C/EBP <i>β</i> (C/EBP <i>β</i> (C/EBP <i>β</i> (C/EBP <i>β</i> (C/EBP <i>β</i> (C/EBP.<h4>Results</h4>In OIR rats, the expression lev ...[more]

PMID: 32215270

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Project description:The sensitization of hepatocytes to cell death from tumor necrosis factor ? (TNF?) underlies many forms of hepatic injury, including that from toxins. Critical for hepatocyte resistance to TNF? toxicity is activation of nuclear factor ?B (NF-?B) signaling, which prevents TNF?-induced death by the up-regulation of protective proteins. To further define the mechanisms of hepatocyte sensitization to TNF? killing, immunoblot analysis comparing livers from mice treated with lipopolysaccharide (LPS) alone or LPS together with the hepatotoxin galactosamine (GalN) was performed to identify TNF?-induced protective proteins blocked by GalN. Levels of CCAAT/enhancer-binding protein ? (C/EBP?) were increased after LPS treatment but not GalN/LPS treatment. In a nontransformed rat hepatocyte cell line, TNF?-induced increases in C/EBP? protein levels were dependent on NF-?B-mediated inhibition of proteasomal degradation. Pharmacological inhibition of c-Jun N-terminal kinase (JNK) did not affect C/EBP? degradation, indicating that the process was JNK-independent. C/EBP? functioned to prevent cell death as adenoviral C/EBP? overexpression blocked TNF?-induced apoptosis in cells sensitized to TNF? toxicity by NF-?B inhibition. C/EBP? inhibited TNF?-induced caspase 8 activation and downstream mitochondrial cytochrome c release and caspase 3 and caspase 7 activation. Studies in primary hepatocytes from c/ebp?(-/-) mice confirmed that loss of C/EBP? increased death from TNF?. c/ebp?(-/-) mice were also sensitized to liver injury from a nontoxic dose of LPS or TNF?. The absence of jnk2 failed to reverse the GalN-induced block in C/EBP? induction by LPS, again demonstrating that C/EBP? degradation was JNK-independent.C/EBP? is up-regulated by TNF? and mediates hepatocyte resistance to TNF? toxicity by inhibiting caspase-dependent apoptosis. In the absence of NF-?B signaling, proteasomal degradation of C/EBP? is increased by a JNK-independent mechanism and promotes death from TNF?.