Adipose tissue senescence and inflammation in aging is reversed by young plasma.
dc.contributor.author | Ghosh, AK | |
dc.contributor.author | O'Brien, M | |
dc.contributor.author | Mau, T | |
dc.contributor.author | Qi, N | |
dc.contributor.author | Yung, R | |
dc.contributor.editor | Le Couteur, David | |
dc.coverage.spatial | United States | |
dc.date.accessioned | 2024-05-06T18:43:08Z | |
dc.date.available | 2024-05-06T18:43:08Z | |
dc.date.issued | 2019-10-04 | |
dc.identifier.issn | 1079-5006 | |
dc.identifier.issn | 1758-535X | |
dc.identifier.uri | https://www.ncbi.nlm.nih.gov/pubmed/30590424 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/193071 | en |
dc.description.abstract | Visceral adipose tissue (VAT) inflammation plays a central role in longevity and multiple age-related disorders. Cellular senescence (SEN) is a fundamental aging mechanism that contributes to age-related chronic inflammation and organ dysfunction, including VAT. Recent studies using heterochronic parabiosis models strongly suggested that circulating factors in young plasma alter the aging phenotypes of old animals. Our study investigated if young plasma rescued SEN phenotypes in the VAT of aging mice. With heterochronic parabiosis model using young (3 months) and old (18 months) mice, we found significant reduction in the levels of pro-inflammatory cytokines and altered adipokine profile that are protective of SEN in the VAT of old mice. These data are indicative of protection from SEN of aging VAT by young blood circulation. Old parabionts also exhibited diminished expression of cyclin-dependent kinase inhibitors (CDKi) genes p16 (Cdkn2a) and p21 (Cdkn1a/Cip1) in the VAT. In addition, when exposed to young serum condition in an ex vivo culture system, aging adipose tissue-derived stromovascular fraction cells produced significantly lower amounts of pro-inflammatory cytokines (MCP-1 and IL-6) compared to old condition. Expressions of p16 and p21 genes were also diminished in the old stromovascular fraction cells under young serum condition. Finally, in 3T3-preadipocytes culture system, we found reduced pro-inflammatory cytokines (Mcp-1 and Il-6) and diminished expression of cyclin-dependent kinase inhibitor genes in the presence of young serum compared to old serum. In summary, this study demonstrates that young milieu is capable of protecting aging adipose tissue from SEN and thereby inflammation. | |
dc.format.medium | ||
dc.language | eng | |
dc.publisher | Oxford University Press (OUP) | |
dc.subject | Adipose tissue | |
dc.subject | Aging | |
dc.subject | Inflammation | |
dc.subject | Plasma factors | |
dc.subject | Senescence | |
dc.subject | Age Factors | |
dc.subject | Aging | |
dc.subject | Analysis of Variance | |
dc.subject | Animals | |
dc.subject | Cells, Cultured | |
dc.subject | Cellular Senescence | |
dc.subject | Chemokine CCL2 | |
dc.subject | Cyclin-Dependent Kinase Inhibitor Proteins | |
dc.subject | Cytokines | |
dc.subject | Disease Models, Animal | |
dc.subject | Inflammation | |
dc.subject | Interleukin-6 | |
dc.subject | Intra-Abdominal Fat | |
dc.subject | Male | |
dc.subject | Mice, Inbred C57BL | |
dc.subject | Parabiosis | |
dc.subject | Random Allocation | |
dc.subject | Real-Time Polymerase Chain Reaction | |
dc.subject | Sensitivity and Specificity | |
dc.subject | Wound Healing | |
dc.subject | Wounds and Injuries | |
dc.title | Adipose tissue senescence and inflammation in aging is reversed by young plasma. | |
dc.type | Article | |
dc.identifier.pmid | 30590424 | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/193071/2/gly290.pdf | |
dc.identifier.doi | 10.1093/gerona/gly290 | |
dc.identifier.doi | https://dx.doi.org/10.7302/22716 | |
dc.identifier.source | Journal of Gerontology: Biological Sciences | |
dc.description.version | Published version | |
dc.date.updated | 2024-05-06T18:43:06Z | |
dc.identifier.orcid | 0000-0003-1919-9171 | |
dc.identifier.orcid | 0000-0002-8181-027X | |
dc.identifier.volume | 74 | |
dc.identifier.issue | 11 | |
dc.identifier.startpage | 1709 | |
dc.identifier.endpage | 1715 | |
dc.identifier.name-orcid | Ghosh, AK | |
dc.identifier.name-orcid | O'Brien, M | |
dc.identifier.name-orcid | Mau, T | |
dc.identifier.name-orcid | Qi, N; 0000-0003-1919-9171 | |
dc.identifier.name-orcid | Yung, R; 0000-0002-8181-027X | |
dc.working.doi | 10.7302/22716 | en |
dc.owningcollname | Internal Medicine, Department of |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.