Work

LDHB-deficient brain exhibits resistance to ischemic neuronal cell death due to increased vasodilation

Year: 2024

Type: article

Abstract: Ischemic stroke triggers a cascade of metabolic and inflammatory events leading to neuronal death, particularly in the hippocampus. Here, we investigate the role of lactate metabolism in ischemic resistance using LDHB-deficient mice, which exhibit impaired lactate utilization. Contrary to expectations of severe neuronal damage due to metabolic defects, LDHB-deficient mice displayed significantly increased neuronal survival following ischemic insult. Magnetic resonance spectroscopy revealed elevated lactate levels in LDHB-deficient brains, which correlated with enhanced vasodilation of the posterior communicating artery (PComA) and increased extracellular PGE 2 levels. These findings suggest that elevated lactate inhibits PGE 2 reabsorption, promoting vasodilation and neuronal protection. Our results highlight lactate's potential role in neuroprotection and its therapeutic promise for ischemic stroke. • LDHB-deficient mice show resistance to ischemic neuronal cell death. • Vasodilation of the posterior communicating artery correlates with neuroprotection. • Elevated lactate inhibits PGE 2 reabsorption, promoting vasodilation.

Source: Biochemical and Biophysical Research Communications

DOI: 10.1016/j.bbrc.2024.150766

Authors: Jin Soo Lee, Bok Seon Yoon, Yihyang Kim, Chan Bae Park

Institutions: Ajou University Hospital, Ajou University Medical Center, Ajou University

Language: English

Topic: Neurological Disorders and Treatments

Subfield: Neurology

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $2,880