Publications by authors named "Lisa Selzner"
Article Synopsis
- HO-1 mRNA levels increased significantly in cerebrospinal fluid (CSF) of patients with subarachnoid hemorrhage (SAH) over a 14-day period, indicating a response to cerebral inflammation.
- While higher levels of HO-1 in CSF correlated with the burden of intracranial blood, it did not serve as an effective predictor of clinical outcomes measured by the Modified Rankin Scale.
- Interestingly, patients with vasospasm had lower HO-1 levels by day 7, while those experiencing delayed cerebral ischemia (DCI) exhibited higher levels by day 14, suggesting a complex relationship between inflammation and injury patterns post-SAH.
Circadian rhythm gene expression in cerebral pacemaker regions is regulated by a transcriptional-translational feedback loop across the 24-h day-night cycle. In preclinical models of subarachnoid hemorrhage (SAH), cyclic gene expression is disrupted. Stabilization of circadian rhythm gene expression attenuates susceptibility to ischemic damage in both neuronal and myocardial tissues.
View Article and Find Full Text PDFMicroglial erythrophagocytosis is crucial in injury response to hemorrhagic stroke. We hypothesized that regulation of microglial erythrophagocytosis via HO-1/CO depends on a pathway involving reactive oxygen species (ROS) and CD36 surface-expression. The microglial BV-2 cell line and primary microglia (PMG) were incubated +/-blood and +/-CO-exposure.
View Article and Find Full Text PDFNeuroprotection after Hemorrhagic Stroke Depends on Cerebral Heme Oxygenase-1.
Antioxidants (Basel)
October 2019
Article Synopsis
- Hemorrhagic stroke's pathophysiology remains poorly understood, but the study suggests that heme oxygenase-1 (HO-1) in microglia may protect against cell death after blood exposure.
- The research involved exposing neuronal cells to blood components and evaluating HO-1 expression and cytokine release in microglial cells, alongside assessing HO-1 mRNA levels in the cerebrospinal fluid of patients with subarachnoid hemorrhage (SAH).
- Findings indicated that HO-1 induction in microglia enhanced the protective response against neuronal death, correlating higher HO-1 levels with larger hematomas but better functional recovery in SAH patients, shedding light on inflammation's role in neuronal damage.