Summary of Study ST002961

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001842. The data can be accessed directly via it's Project DOI: 10.21228/M8MH8P This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002961
Study TitleAnalysis of Metabolites Secreted from Fibroblast Young Cells
Study SummaryIn this experimental study, we aimed to uncover the factors in young cell secretions that trigger the reverse aging of mid-old cells, co-culturing them and observing a striking transformation, although we could not identify the specific factors responsible for this rejuvenation
Institute
Ajou University Medical Center
Last NameKim
First NameYoung Hwa
Address206, World cup-ro, Yeongtong-gu, Suwon-si, Gyeonggi-do, Republic of Korea
Emailskyblue32@nate.com
Phone+82-10-5153-3636
Submit Date2023-11-01
Raw Data AvailableYes
Raw Data File Type(s)mzML
Analysis Type DetailLC-MS
Release Date2023-11-22
Release Version1
Young Hwa Kim Young Hwa Kim
https://dx.doi.org/10.21228/M8MH8P
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR001842
Project DOI:doi: 10.21228/M8MH8P
Project Title:Mid-Old Cells are Potential Target for Anti-aging Interventions in the Elderly
Project Summary:The biological process of aging is thought to result in part from accumulation of senescent cells in organs. However, the present study identified a subset of fibroblasts and smooth muscle cells which are the major constituents of organ stroma neither proliferative nor senescent in tissues of the elderly, which we termed “mid-old status” cells. Upregulation of pro-inflammatory genes (IL1B and SAA1) and downregulation of anti-inflammatory genes (SLIT2 and CXCL12) were detected in mid-old cells. In the stroma, SAA1 promotes development of the inflammatory microenvironment via upregulation of MMP9, which decreases the stability of epithelial cells present on the basement membrane, decreasing epithelial cell function. Remarkably, the microenvironmental change and the functional decline of mid-old cells could be reversed by a young cell-originated protein, SLIT2. Our data identify functional reversion of mid-old cells as a potential method to prevent or ameliorate aspects of aging-related tissue dysfunction.
Institute:Ajou University Medical Center
Last Name:Kim
First Name:Young Hwa
Address:206, World cup-ro, Yeongtong-gu, Suwon-si, Gyeonggi-do, Republic of Korea
Email:skyblue32@nate.com
Phone:+82-10-5153-3636
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