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Autophagy facilitates age-related cell apoptosis - a new insight from senile cataract

ABSTRACT: Autophagy facilitates age-related cell apoptosis - a new insight from senile cataract

PROVIDER: PRJNA679210 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13079949_1.fastq.gz	Fastqsanger.gz
	SRR13079949_2.fastq.gz	Fastqsanger.gz
	SRR13079950_1.fastq.gz	Fastqsanger.gz
	SRR13079950_2.fastq.gz	Fastqsanger.gz
	SRR13079951_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Autophagy facilitates age-related cell apoptosis - a new insight from senile cataract

Project description:Age-related cell loss underpins many senescence-associated diseases. Senile cataract is a primary blindness-causing age-related ocular disease. Apoptosis of lens epithelial cells (LECs) is the common cellular basis of senile cataract resulted from prolonged exposure to oxidative stress, the mechanism of which remains elusive. Here we reported the concomitance of increased autophagy and apoptosis in the same LEC from senile cataract patients. Oxidative stress triggered autophagy preceded apoptosis, while blocking autophagy by ablation of Atg7 or Atg3 gene remarkably suppressed apoptosis in HLE-B3 cell line. We identified autophagy adaptor SQSTM1/p62 as the critical scaffold protein to sustain a pro-survival signaling PKCι-NF-κB cascades, which antagonized the pro-apoptotic signaling in LECs. Importantly, prolonged autophagy in human senescent LECs responding to oxidative stress induced extensive degradation of p62 protein and therefore facilitated apoptosis. Moreover, pharmacological inhibitor of autophagy, 3-MA, significantly rescued apoptosis of human senescent LECs challenged by oxidative stress. Collectively, our data demonstrated that hyperactivation of autophagy aggravates age-related apoptotic cell death via inhibiting the p62-PKCι-NF-κB pro-survival axis in human senescent LECs. This work expands the understanding of the etiology of senile cataract and provides insight for mechanisms of age-related cell death in senescence-associated diseases.

2022-01-19 | GSE161701 | GEO

Gene regulation in autophagy and apoptosis juncture

Project description:Autophagy to apoptosis switching event is an unexplored area. We were interested to explore the gene expression profile at this juncture. Our Microarray data emphasized that among all eNOS and p62 genes were markedly induced. In fuctional level eNOS expression activates mTORC1 followed by inhibition of autophagy. This ultimately allowed accumulation of p62 . Intraccellular accumulation of p62 sequestered unfolded toxic protein aggregates in mitochondria and ER resulting in to impaired redox regulation. Intraccelular ROS generation further sensitized cells for apoptosis and tilted autophagic response to apoptosis. Cells were treated with Tunicamycin as an inducer of both autophagy and apoptosis. At early stage of Tunicamycin treatment 24h , prostate cancer cell PC3 showed activation of autophagic process where apoptosis was not evident. Sustained ER stress with Tunicamycin induced late apoptoisis at 72h of treatment. Hence we isolated total RNA from Untreated cells, cells with Tunicamycin treatment after 24h and 72h. Further the RNA were used to perform whole genome microarray to analyze the gene expression profile at autophagy and apoptosis juncture. The selected genes were also validated by qPCR and western bot. Morover RNAi study were implemented to evaluate the signaling crosstalk at the juncture of autophagy and apoptosis.

2014-05-22 | E-GEOD-38643 | biostudies-arrayexpress

Autophagy facilitates age-related cell apoptosis-a new insight from senile cataract.

Project description:Age-related cell loss underpins many senescence-associated diseases. Apoptosis of lens epithelial cells (LECs) is the important cellular basis of senile cataract resulted from prolonged exposure to oxidative stress, although the specific mechanisms remain elusive. Our data indicated the concomitance of high autophagy activity, low SQSTM1/p62 protein level and apoptosis in the same LEC from senile cataract patients. Meanwhile, in primary cultured LECs model, more durable autophagy activation and more obvious p62 degradation under oxidative stress were observed in LECs from elder healthy donors, compared with that from young healthy donors. Using autophagy-deficiency HLE-B3 cell line, autophagy adaptor p62 was identified as the critical scaffold protein sustaining the pro-survival signaling PKCι-IKK-NF-κB cascades, which antagonized the pro-apoptotic signaling. Moreover, the pharmacological inhibitor of autophagy, 3-MA, significantly inhibited p62 degradation and rescued oxidative stress-induced apoptosis in elder LECs. Collectively, this study demonstrated that durable activation of autophagy promoted age-related cell death in LECs. Our work contributes to better understanding the pathogenesis of senescence-associated diseases.

| S-EPMC8748728 | biostudies-literature

Comparative evaluation of the aqueous humor proteome of primary angle closure and primary open angle glaucomas and senile cataract eyes

Project description:Comparative evaluation of the aqueous humor proteome of primary angle closure and primary open angle glaucomas and senile cataract eyes

2020-05-29 | PXD004928 | Pride

Gene regulation in autophagy and apoptosis juncture

2014-05-22 | GSE38643 | GEO

Down-regulation of SRD5A1 induces autophagy and apoptosis in multiple myeloma

Project description:Steroid 5α-reductase type I (SRD5A1) is a validated oncogene in many sex hormone-related cancers, but its role in multiple myeloma (MM) remains unknown. Based on gene expression profiling of sequential MM samples during disease course, we found that high SRD5A1 expression was correlated with progression and poor prognosis in MM patients. In this study, we assessed the SRD5A1 function in promoting MM cell growth, cell cycle and tumorigenesis by using different human MM cell lines, the xenograft mouse and 5TMM mouse models. Applying lentivirus-mediated short-hairpin RNA (shRNA) method, inducible knockdown of SRD5A1 inhibited myeloma cell growth and induced cell apoptosis as well as autophagy. Meanwhile, the SRD5A1 knockdown-induced apoptosis was aggravated by the autophagy inhibitor 3-methyladenine. Mechanistically, SRD5A1 downregulation simultaneously regulated both the Bcl-2 family proteins mediated apoptosis and the autophagic process via PI3K/Akt/mTOR signaling pathway in MM cells. We also evaluated the therapeutic effect of SRD5A1 inhibitor, Dutasteride, on improving the survival rate of MM mouse model. To summarize, our findings demonstrate that SRD5A1 may serve as a biomarker for MM progression and prognosis, indicating that the dual autophagy-apoptosis regulatory SRD5A1 is a potential target for future therapies in MM patients.

2021-03-03 | GSE155858 | GEO

Real-time quantitative PCR analysis of autophagy and apoptosis in Myelodysplastic syndromes (MDS)

Project description:A large series of genes involved in autophagy and apoptosis process was screened in samples with different types of MDS (low/high grade of malignancy) versus samples from healthy individuals qPCR gene expression profiling

2022-05-26 | GSE204797 | GEO

Down-regulation of SRD5A1 induces autophagy and apoptosis in multiple myeloma

Project description:Down-regulation of SRD5A1 induces autophagy and apoptosis in multiple myeloma

| PRJNA655885 | ENA

RNA-Seq Quantitative Analysis of the regulation of SARS-CoV-2 infection on autophagy and apoptosis related gene transcriptome in infected cells

Project description:In our study, we found that SARS-CoV-2-S pseudovirions infection induced high levels of autophagy and apoptosis in infected cells. To further investigate the underlying regualtion of SARS-CoV-2-S pseudovirions infection in infected cells, ACE2-expressing HEK293T-hACE2 and Vero E6 cells were treated with Mock or SARS-CoV-2-S pseudovirions for RNA-Seq analysis to exame the expression of autophagy- and apoptosis-related genes. Our results indicate that the majority of autophagy- and apoptosis-promoting genes were significantly increased in SARS-CoV-2-S pseudovirions treated HEK293T-hACE2 and Vero E6 cells. In contrast, the subset of autophagy- and apoptosis-suppressing genes was significantly decreased in SARS-CoV-2-S pseudovirions-treated HEK293T-hACE2 and Vero E6 cells than Mock-treated HEK293T-hACE2 and Vero E6 cells. Meanwhile, SARS-CoV-2-S pseudovirions infection enhanced the expression of pro-inflammatory cytokines in infected cells.

2021-03-23 | GSE169370 | GEO

High-throughput transcriptomics of Celf1 conditional knockout lens identifies downstream networks linked to cataract pathology

Project description:Celf1 germline or conditional deletion mouse mutants exhibit fully penetrant lens defects including cataract. To gain insight into gene expression changes underlying these lens defects Differential Gene Expression analysis was performed for lenses obtained from control and Celf1 conditional deletion mutant mice.

2023-03-18 | GSE227293 | GEO

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