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Published on: June 22, 2013
Spatio-Temporal Characterization of Cellular Senescence Hallmarks in Experimental Ischemic Stroke
Júlia Baixauli-Martín1,2, Maria Consuelo Burguete1,2, Mikahela A López-Morales1,3
1Unidad Mixta de Investigación Cerebrovascular, Instituto de Investigación Sanitaria La Fe, Hospital Universitario y Politécnico La Fe, 46026 Valencia, Spain.
Abstract:
In recent years, evidence of the existence of cellular senescence in the central nervous system has accumulated. In ischemic stroke, cellular senescence has been suggested as an unidentified pathophysiological mechanism, prompting research into the neuroprotective potential of senolytic drugs. This study aims to provide spatio-temporal evidence of the existence of brain senescence following ischemic stroke and to elucidate the involved pathways and cell types. We focused on the most established markers of senescence: cell cycle arrest (p16, p21); lysosomal activity (senescence-associated β-galactosidase [SA-β-gal]); the senescence-associated secretory phenotype ([SASP]; Interleukin-6 [IL-6], Interleukin-1β [IL-1β], Tumor necrosis factor [TNF]); and DNA/nuclear damage (Checkpoint kinase 1 [Chk1], Checkpoint kinase 2 [Chk2], Lamin B1 [LB1]). Male Wistar rats underwent 60 min of transient middle cerebral artery occlusion, followed by 24 h and 3, 7, and 14 days of recovery. Our results show significant increases in p16 expression, particularly in neurons and microglia/macrophages; SA-β-gal accumulation in the infarcted tissue; significant increases in SASP markers as early as 24 h after reperfusion; and significant changes in Chk1, Chk2, and LB1 at 14 days. Overall, our findings lend support to the existence of senescence after ischemic stroke in neurons and microglia/macrophages. However, there is still room to gain further insight into the role of senescence in the pathophysiology of ischemic stroke and in the implementation of successful senolytic therapy.
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