Senescence Associated Secretory Phenotype
Location
Medical Education Building, LSUHSC-NO
Presentation Date
10-10-2019 10:00 AM
End Date
10-10-2019 12:00 PM
Description
As mammals age, they accumulate senescent cells, which are cells that become irreversible growth arrested. Senescent can occur in all cell types, and senescent cells can also no longer undergo apoptosis. In addition, heavy alcohol consumption has been linked to an increase in the number of senescent cells. Certain stresses can induce senescence such as telomeric dysfunction from repeated cell division, mitochondrial deterioration, oxidative stress, severe DNA damage, and expression of certain oncogenes. Senescent cells can also become pro-inflammatory through acquisition of senescence-associated secretory phenotype (SASP). This process turns senescent tells into cells that can promote inflammation and aging through secretions such as inflammatory cytokines and growth factors. These pro-inflammatory secretions can then lead to tissue breakdown and further spread of senescence of nonsenescent cells. In this project, I tested the hypothesis that senescent CD8+ T-cells display an enhanced senescence-associated secretory phenotype (SASP), which is exacerbated by in vitro alcohol treatment.
I used flow cytometry to determine CD8+ T-cells with senescent markers between a positive alcohol group and a negative alcohol group. Human PBMCs were stimulated in vitro to activate the T-cells. Then they were stained to assess whether they underwent cellular division and stimulated to undergo clonal expansion. The cells were stained intracellularly and extracellularly. Flow cytometry was used to detect the SASP profile of the CD8+ T-cells.
Recommended Citation
Do, Steven T., "Senescence Associated Secretory Phenotype" (2019). Medical Student Research Poster Symposium. 11.
https://digitalscholar.lsuhsc.edu/sommrd/2019/posters/11
Senescence Associated Secretory Phenotype
Medical Education Building, LSUHSC-NO
As mammals age, they accumulate senescent cells, which are cells that become irreversible growth arrested. Senescent can occur in all cell types, and senescent cells can also no longer undergo apoptosis. In addition, heavy alcohol consumption has been linked to an increase in the number of senescent cells. Certain stresses can induce senescence such as telomeric dysfunction from repeated cell division, mitochondrial deterioration, oxidative stress, severe DNA damage, and expression of certain oncogenes. Senescent cells can also become pro-inflammatory through acquisition of senescence-associated secretory phenotype (SASP). This process turns senescent tells into cells that can promote inflammation and aging through secretions such as inflammatory cytokines and growth factors. These pro-inflammatory secretions can then lead to tissue breakdown and further spread of senescence of nonsenescent cells. In this project, I tested the hypothesis that senescent CD8+ T-cells display an enhanced senescence-associated secretory phenotype (SASP), which is exacerbated by in vitro alcohol treatment.
I used flow cytometry to determine CD8+ T-cells with senescent markers between a positive alcohol group and a negative alcohol group. Human PBMCs were stimulated in vitro to activate the T-cells. Then they were stained to assess whether they underwent cellular division and stimulated to undergo clonal expansion. The cells were stained intracellularly and extracellularly. Flow cytometry was used to detect the SASP profile of the CD8+ T-cells.
Comments
Mentor: Dr. Robert Siggins (Department of Physiology)