Abstract TP099: Diabetes mediates phenotypic changes in brain pericytes after ischemic stroke: Relevance to post-stroke cognitive impairment (PSCI)

Precapillary arteriolar and capillary pericytes contribute to the regulation of cerebral blood flow (CBF) and blood-brain barrier (BBB) integrity, both of which are critical for brain health. Diabetes causes a decrease in microvascular pericytes. Since diabetes increases the risk of PSCI, our first goal was to investigate the impact of diabetes on pericyte phenotype after stroke. Given that endothelin-1 (ET-1) mediates pericyte constriction and senescence via the ETA receptors (ETAR), the second goal was to assess ETAR expression after stroke and the impact of ETAR inhibition on pericyte phenotype. Methods and Results: We used tissue sections from our rodent brain bank. Pericyte numbers and surface area (SA) were assessed by immunohistochemistry using CD13 and Atp13a5 pericyte markers. CD13+/high aSMA and Atp13a5-expressing cells were classified as contractile precapillary arteriolar and capillary pericytes, respectively. The first set of specimens was from diabetic male rats that were subjected to sham or 60-min transient middle cerebral artery occlusion (tMCAO) surgery and followed for 2 weeks. Stroke caused an increase in the number of CD13+ cells (3.3 ± 0.5 vs 7.5 ± 1.6, p