Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
Mechanism of age-dependent senescence development in Tnfrsf10 knock out mice.
Author Affiliations & Notes
  • Iori Wada
    Doheny Eye Institute, Los Angeles, Japan
    Kyushu Daigaku, Fukuoka, Fukuoka, Japan
  • Kenichiro Mori
    Kyushu Daigaku, Fukuoka, Fukuoka, Japan
  • Parameswaran G Sreekumar
    Doheny Eye Institute, Los Angeles, Japan
  • Christine Spee
    Doheny Eye Institute, Los Angeles, Japan
  • Elise Hong
    Doheny Eye Institute, Los Angeles, Japan
  • Keijiro Ishikawa
    Kyushu Daigaku, Fukuoka, Fukuoka, Japan
  • Koh-Hei Sonoda
    Kyushu Daigaku, Fukuoka, Fukuoka, Japan
  • Ram Kannan
    Doheny Eye Institute, Los Angeles, Japan
  • Footnotes
    Commercial Relationships   Iori Wada None; Kenichiro Mori None; Parameswaran Sreekumar None; Christine Spee None; Elise Hong None; Keijiro Ishikawa None; Koh-Hei Sonoda None; Ram Kannan None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 6044. doi:
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      Iori Wada, Kenichiro Mori, Parameswaran G Sreekumar, Christine Spee, Elise Hong, Keijiro Ishikawa, Koh-Hei Sonoda, Ram Kannan; Mechanism of age-dependent senescence development in Tnfrsf10 knock out mice.. Invest. Ophthalmol. Vis. Sci. 2024;65(7):6044.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Our lab reported that tumor necrosis factor receptor superfamily 10A dysregulation leads to AMD progression and RPE dysfunction (PMID:35103281). Recently, we further showed a marked upregulation of senescence in TNFRS10A knockdown in RPE and in RPE/choroid of Tnfrsf10 KO mice (ARVO 2023). This study intends to investigate the age-related changes in senescence development in Tnfrs10 KO retina and attempts to identify potential senolytic agent(s) using TNFRS10A-silenced hRPE.

Methods : Subconfluent primary hRPE cells and TNFRSF10A silenced hRPE were exposed to H2O2 (500 μM) alone or co-treated with a PKC activator, phorbol 12-myristate 13-acetate (PMA) for 48h. The effect of PMA treatment on senescence was quantified using immunostaining, RT-PCR, and WB analysis of senescence-associated markers (beta-gal, p16, p21, cGAS, and STING). Mitochondrial metabolic parameters in the control and treated groups were determined using a seahorse XF96e analyzer. In in vivo studies, 3, 6, and 12-month-old male Tnfrsf10 KO (Tnfrsf10-/-) mice were used to examine the effect of aging on senescence. Expression p16 and p21 in KO mice was determined by RT-PCR, WB, and immunostaining analysis.

Results : The senescence biomarkers p16 and p21 showed a significant downregulation with PMA treatment at the gene (p < 0.05) and protein (p < 0.01) levels in hRPE cells. Mitochondrial oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) (pmol/min/total protein) increased with senescence induction and/or knockdown of TNFRSF10, and PMA treatment decreased both OCR and ECAR. Similarly, mitochondria-associated markers (Fis1, DRP1, PGC1-α, and mtTFA) showed a similar trend. Age-dependent upregulation of p16 and p21 was observed in the RPE/choroid of Tnfrsf10 KO mice.

Conclusions : Our studies reveal an important age-dependent role of TNFRSF10A in senescence. Our results further suggest the potential that PKC activator could serve as a senolytic agent.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

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