Cerebral Ischemia Increases Small Ubiquitin-Like Modifier Conjugation within Human Penumbral Tissue: Radiological-Pathological Correlation

Joshua D Bernstock; Daniel G Ye; Allison Griffin; Yang-Ja Lee; John Lynch; Lawrence L Latour; Gregory K Friedman; Dragan Maric; John M Hallenbeck

doi:10.3389/fneur.2017.00738

Cerebral Ischemia Increases Small Ubiquitin-Like Modifier Conjugation within Human Penumbral Tissue: Radiological-Pathological Correlation

Front Neurol. 2018 Jan 12:8:738. doi: 10.3389/fneur.2017.00738. eCollection 2017.

Authors

Joshua D Bernstock^{1

2}, Daniel G Ye¹, Allison Griffin^{3

4}, Yang-Ja Lee¹, John Lynch³, Lawrence L Latour³, Gregory K Friedman⁵, Dragan Maric⁶, John M Hallenbeck¹

Affiliations

¹ Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States.
² Department of Clinical Neurosciences, Wellcome Trust-Medical Research Council Stem Cell Institute, University of Cambridge, Cambridge, United Kingdom.
³ Section on Stroke Diagnostics and Therapeutics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States.
⁴ Center for Neuroscience and Regenerative Medicine at the Uniformed Services University of the Health Sciences, Bethesda, MD, United States.
⁵ Division of Pediatric Hematology and Oncology, Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, United States.
⁶ Flow and Imaging Cytometry Core Facility, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, United States.

Abstract

Posttranslational modification by small ubiquitin-like modifier (SUMO) regulates myriad physiological processes within cells and has been demonstrated to be highly activated in murine brains after cerebral ischemia. Numerous in vitro and murine in vivo studies have demonstrated that this increased SUMO conjugation is an endogenous neuroprotective stress response that has potential in being leveraged to develop novel therapies for ischemic stroke. However, SUMO activation has not yet been studied in poststroke human brains, presenting a clear limitation in translating experimental successes in murine models to human patients. Accordingly, here, we present a case wherein the brain tissue of a stroke patient (procured shortly after death) was processed by multiplex immunohistochemistry to investigate SUMO activation.

Keywords: SUMOylation; ischemic stroke; magnetic resonance imaging; neuroprotection; penumbra.

Publication types

Case Reports