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Publication
Diabetic Stroke Promotes a Sexually Dimorphic Expansion of T Cells.
Authors
Jackson L, Li W, Abdul Y, Dong G, Baban B, Ergul A
Submitted By
Weiguo Li on 10/14/2019
Status
Published
Journal
Neuromolecular medicine
Year
2019
Date Published
6/1/2019
Volume : Pages
Not Specified
:
Not Specified
PubMed Reference
31197651
Abstract
We recently reported that diabetes negates the cerebrovascular protection
typically seen in adult female rats resulting in cognitive impairment, which is
worsened by increased parenchymal bleeding and edema after ischemic stroke.
Although women experience more severe diabetes and suffer from a higher rate of
diabetic complications, including stroke and cognitive impairment, underlying
mechanisms contributing to sex differences are limited. Emerging evidence
suggests interleukin (IL)-17 contributes to cerebrovascular pathologies: (1)
high salt diet-mediated expansion of IL-17-producing T cells (Th17) in the gut
microbiome promotes cerebrovascular dysfunction and cognitive impairment in male
mice, (2) increased IL-17-producing ?dTCR cells exacerbates stroke injury in
male mice, and (3) IL-17 promotes rupture of cerebral aneurysms in female mice.
Based on these premises, we investigated the potential involvement of
IL-17-producing inflammatory cells in cerebrovascular dysfunction and
post-stroke vascular injury in diabetes by measuring intestinal, circulating, or
cerebral T cell profiles as well as in plasma IL-17 in both sexes. Cell
suspensions prepared from naive or stroked (3 days after stroke) diabetic and
control rats were analyzed by flow cytometry, and IL-17 levels were measured in
plasma using ELISA. Diabetes deferentially promoted the expansion of cerebral
Th17 cells in females. In response to stroke, diabetes had a sexually dimorphic
effect on the expansion of numerous T cell profiles. These results suggest that
a better understanding of the role of IL-17-producing cells in diabetes may
identify potential avenues in which the molecular mechanisms contributing to
these sex differences can be further elucidated.
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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