Program/Event
KYINBRE Summer Undergraduate Research Program
Abstract
Cellular senescence is the phenomenon in which cells undergo permanent cell cycle arrest and is caused by natural aging or pathological mechanisms. Depending on the physiological context, pathological senescence can potentially be implicated in chronic inflammation but may also have a role in promoting tissue repair. Spinal cord injury (SCI) is a whole-body injury, in which patients with SCI often experience complications in organ systems outside of the CNS. Our recent data has shown that senescence can develop in the spinal cord after SCI but the extent that senescence contributes to dysfunctions of peripheral tissues remains unclear. This study sought to examine the presence of senescent cells after a moderate contusive SCI (50 kdyn, IH, T9) in peripheral tissues of C57Bl6 and P16-3MR transgenic mice. Transcript levels for two widely used cell senescence markers (p16/Cdkn2a and p21/Cdkn1a) were evaluated in the spinal cord, cortex, liver, and spleen. The data showed that the senescent markers p16 and mRFP were elevated transiently in the liver at 7 days post-injury. In the spleen, mRFP showed a trend (p=0.057) but no significance. In the cortex, there was no significance after SCI. Furthermore, across all groups, senescence markers were elevated over time. This data indicates that SCI may have a transient effect in peripheral tissues after 7 days but does not have a long-lasting senescence response up to 60 days after injury.
Recommended Citation
Valdez, Tanisha A.; Rood, Benjamin R.; Slomnicki, Lukasz P.; Gao, Yonglin; Miller, Mason; Andres, Kariena; Whittemore, Scott R.; and Hetman, Michal
(2024)
"Cellular Senescence in Peripheral Tissues after Spinal Cord Injury,"
The Cardinal Edge: Vol. 2:
Iss.
2, Article 2.
Available at:
https://ir.library.louisville.edu/tce/vol2/iss2/2
