Strokes can cause permanent damage to the brain and rank among the leading causes of disability and mortality. The cellular responses that occur following a cerebral infarction are not fully understood, which hinders the development of effective methods to aid the recovery of injured nerve tissue. A recent study from MedUni Vienna, published in Nature Communications, addresses significant gaps in this area and sets the stage for new, focused therapeutic research.
To analyze the behavior of specific brain cells post-stroke, the research team, led by first author Daniel Bormann (Department of Thoracic Surgery) and study leaders Hendrik J. Ankersmit (Department of Thoracic Surgery) and Michael Mildner (Department of Dermatology), utilized single-cell RNA sequencing in animal models already recognized in stroke research. This innovative approach enabled the researchers to categorize various cell types and their responses during the initial stages following a cerebral infarction. Their attention was directed towards two particular cell types—astrocytes and oligodendrocytes—both of which are glial cells crucial to numerous essential brain functions.
Cell Interaction in the Damaged Area
Scientists are aware that astrocytes proliferate rapidly after a stroke, gathering around the damaged region.
“We found that oligodendrocyte precursor cells also undergo division during the acute phase of the infarction, collecting at the margin of the injured nerve tissue,” says Daniel Bormann. By conducting more detailed analyses, the team identified possible mechanisms involved in healing the affected brain region: “There was a significant overlap in the gene activity of both cell types, particularly in genes that are vital for forming the glial barrier around the infarct,” Bormann elaborates on a key finding from the study.
Additionally, they discovered that specific immune cells (microglia and macrophages) located near the infarct site secrete a signaling molecule named osteopontin. This molecule may play a crucial role in guiding glial cells to the perimeter of the infarct, which is essential for, among other things, creating a barrier between the healthy and damaged tissue. “Our findings on how immune and glial cells interact in the infarcted area significantly enhance our understanding of nerve tissue regeneration following a stroke,” Bormann emphasizes, highlighting the importance of these results.
In Austria, strokes rank as the third leading cause of death and are the primary reason for long-term disability and care requirements, following cardiovascular diseases and cancer. An ischemic stroke occurs due to a blockage in a brain blood vessel, leading to a lack of oxygen and essential nutrients, which results in irreversible nerve tissue damage. Current treatment strategies prioritize restoring blood flow within a 24-hour window, applicable only to a portion of patients. However, the cellular processes post-cerebral infarction remain poorly understood, and effective methods to foster nerve tissue recovery after a stroke are still lacking.
“The knowledge gained from our international and interdisciplinary study could serve as a valuable foundation for the development of new targeted therapies,” states Daniel Bormann, looking forward to further scientific exploration.
