Investigation on ncRNA in senescence in senescence cellular models (ICPSR doi:10.13130/RD_UNIMI/OXXJ1N)

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Document Description

Citation

Title:

Investigation on ncRNA in senescence in senescence cellular models

Identification Number:

doi:10.13130/RD_UNIMI/OXXJ1N

Distributor:

UNIMI Dataverse

Date of Distribution:

2022-01-05

Version:

1

Bibliographic Citation:

Battaglia, Cristina, 2022, "Investigation on ncRNA in senescence in senescence cellular models", https://doi.org/10.13130/RD_UNIMI/OXXJ1N, UNIMI Dataverse, V1

Study Description

Citation

Title:

Investigation on ncRNA in senescence in senescence cellular models

Identification Number:

doi:10.13130/RD_UNIMI/OXXJ1N

Authoring Entity:

Battaglia, Cristina (University of Milan)

Other identifications and acknowledgements:

Marco Venturin

Other identifications and acknowledgements:

Cristina Battaglia

Date of Production:

2021-09-12

Grant Number:

PSD-2020

Distributor:

UNIMI Dataverse

Access Authority:

Battaglia, Cristina

Depositor:

Battaglia, Cristina

Date of Deposit:

2021-12-29

Study Scope

Keywords:

Medicine, Health and Life Sciences, cellular senescence, Noncoding RNA, Long, lncRNA, Untranslated RNA, Real-Time PCR

Abstract:

Cellular senescence is a hallmark of aging and is the result of a variety of stresses, such as telomere attrition, DNA damage and mitochondrial dysfunction. Moreover, senescent cells display a typical secretory phenotype, which involves the secretion of several inflammatory factors, as well as increased levels of beta-galactosidase activity in the lysosomes. Senescent cells accumulate during aging and have been implicated in promoting a variety of age-related diseases, including neurodegenerative diseases. Autophagy, the degradation system whereby the cells recycle dysfunctional proteins and damaged organelles, is one of the processes affected by senescence, but it is also able to induce senescence. Among the different mechanisms controlling the senescence status and the autophagic process, a key role of non-coding RNAs (ncRNAs), both miRNAs and long non-coding RNAs (lncRNAs), is now clearly emerging. AIM OF THE PROJECT With the aim to explore a possible dysregulation of ncRNAs in senescence, we will measured by qPCR the levels of a set of miRNAs and lncRNAs associated to autophagy, senescence and aging in different cellular models of replicative and chemical induced senescence. SUPPORTED BY The investigation was supported by PSD2020, University of Milan to Cristina Battaglia and Marco Venturin.

Time Period:

2020-11-01-2021-09-28

Date of Collection:

2020-11-01-

Country:

Italy

Geographic Coverage:

Milan

Kind of Data:

aggregate data

Kind of Data:

exprimental data

Kind of Data:

textual data

Methodology and Processing

Sources Statement

Data Access

Notes:

CC0 Waiver

Other Study Description Materials

Other Study-Related Materials

Label:

BIOMETRA_poster_2021_final.pdf

Text:

POSTER was presented on 2021-09-27 during BIOMETRA Workshop2021(Mlilan). The poster described the results obtained in a model of replicative senescence of Normal Human Dermal Fibroblasts (NHDFs) in replicative senescence, following prolonged culturing: young (passage 14,n=3) vs. old (passage 32-33, n=3). Cells characterization by multi-biomarker analyses; QPCR evaluation of ncRNAs expression of 15 lncRNAs and 9 miRNAs previuosly selected by literature mining.

Notes:

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Other Study-Related Materials

Label:

Briguglio_MasterThesis_Poster_2021.pdf

Text:

POSTER presented by Sabrina Briguglio titled "Investigation of non-coding-RNAs targeting senescence and autophagy in “zombie” cells" on 2021-23-09. The poster described the results obtained in two models of senescence. Normal Human Dermal Fibroblasts (NHDF) in replicative senescence, following prolonged culturing and neuroblastoma cell line (SH-SY5Y) in oxidative stress-induced senescence, following treatment with H2O2. Cells characterization was performed by biochemical and molecular methods; the expression level of selected protein-coding RNAs and non-coding RNAs was evaluated by QPCR.

Notes:

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