ArticleScientific reports2015
Traumatic brain injury results in rapid pericyte loss followed by reactive pericytosis in the cerebral cortex.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 98 citations in OpenAlex.
- Human brain pericytes protect the blood-brain barrier from triple-negative breast cancer cells while promoting tumor aggressiveness.Journal of cell communication and signaling · 2026Article
- Persistent dysmorphology and dysfunction of the brain microvasculature following repeated trauma.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Traumatic Brain Injury Induces Senescence in Brain Microvasculature.Biomolecules · 2026Article
- Diffuse traumatic brain injury in mice is associated with a transient mismatch of cerebral blood flow and energy metabolism.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Article
- Thyroxine Treatment after Traumatic Brain Injury Suppresses Astrogliosis and Enhances Neuronal Recovery in Mice.Thyroid : official journal of the American Thyroid Association · 2025Article
- Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025Review
- Contribution of brain pericytes to neuroinflammation following repetitive head trauma.Journal of inflammation (London, England) · 2025Article
- Traumatic Brain Injury and Alzheimer's Disease: A Shared Neurovascular Hypothesis.Neuroscience insights · 2025Review
- Assessment of cerebrovascular alterations induced by inflammatory response and oxidative-nitrative stress after traumatic intracranial hypertension and a potential mitigation strategy.Scientific reports · 2024Article
- Pericyte derivation and transplantation for blood-CNS barrier reconstitution in CNS disorders.IBRO neuroscience reports · 2024Article
- Neutralization of Interleukin 1-beta is associated with preservation of thalamic capillaries after experimental traumatic brain injury.Frontiers in neurology · 2024Article
- Mechanism of COVID-19-Induced Cardiac Damage from Patient, In Vitro and Animal Studies.Current heart failure reports · 2023Review
- Blood-Brain Barrier Breakdown in Neuroinflammation: Current In Vitro Models.International journal of molecular sciences · 2023Review
- Pericyte Loss in Diseases.Cells · 2023Review
- Vascular perfusion differs in two distinct PDGFRβ-positive zones within the ischemic core of male mice 2 weeks following photothrombotic stroke.Journal of neuroscience research · 2023Article
- Cellular and molecular mechanisms in vascular repair after traumatic brain injury: a narrative review.Burns & trauma · 2023Review
- Review
- Neurovascular unit dysfunction as a mechanism of seizures and epilepsy during aging.Epilepsia · 2022Review
- Chronic effects of blast injury on the microvasculature in a transgenic mouse model of Alzheimer's disease related Aβ amyloidosis.Fluids and barriers of the CNS · 2022Article
- Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence suggests a pivotal role of PDGFRß positive cells, a specific marker for central nervous system (CNS) pericytes, in tissue scarring. Identification of cells that contribute to tissue reorganization in the CNS upon injury is a crucial step to develop novel treatment strategies in regenerative medicine. It has been shown that pericytes contribute to scar formation in the spinal cord. It is further known that ischemia initially triggers pericyte loss in vivo, whilst brain trauma is capable of inducing pericyte detachment from cerebral vessels. These data point towards a significant role of pericytes in CNS injury. The temporal and spatial dynamics of PDGFRß cells and their responses in traumatic brain injury are poorly understood. Here we show that PDGFRß positive cells initially decline in the acute phase following experimental traumatic brain injury. However, PDGFRß positive cells increase significantly in the trauma zone days after brain injury. Using various pericyte markers we identify these cells to be pericytes that are demarcated by reactive gliosis. Our data indicate that brain trauma causes a biphasic response of pericytes in the early phase of brain trauma that may be of relevance for the understanding of pathological cellular responses in traumatic brain injury.
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