ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2010
The role of bradykinin B(1) and B(2) receptors for secondary brain damage after traumatic brain injury in mice.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 81 citations in OpenAlex.
- Therapeutic Targeting of the Bradykinin B2 Receptor in Immunological and Vascular Diseases: Insights from Kinin Biology to Clinical Outcomes.Clinical reviews in allergy & immunology · 2026Review
- Brain Hydration Correlates with Cerebral Oxygen Saturation in Perilesional Foci in Moderate Traumatic Brain Injury.Advances in experimental medicine and biology · 2026Article
- Net Water Uptake and Cerebral Microcirculation in Perilesional Penumbra in TBI: CT Perfusion Study.Advances in experimental medicine and biology · 2026Article
- Escin's Action on Bradykinin Pathway: Advantageous Clinical Properties for an Unknown Mechanism?Antioxidants (Basel, Switzerland) · 2024Review
- Article
- Cdk5 mediates rotational force-induced brain injury.Scientific reports · 2023Article
- Tackling Neuroinflammation After Traumatic Brain Injury: Complement Inhibition as a Therapy for Secondary Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- CaeLife · 2022Article
- Amelioration of Cognitive and Behavioral Deficits after Traumatic Brain Injury in Coagulation Factor XII Deficient Mice.International journal of molecular sciences · 2021Article
- Between two storms, vasoactive peptides or bradykinin underlie severity of COVID-19?Physiological reports · 2021Review
- Neurolysin substrates bradykinin, neurotensin and substance P enhance brain microvascular permeability in a human in vitro model.Journal of neuroendocrinology · 2021Article
- The Bradykinin B2 Receptor Agonist (NG291) Causes Rapid Onset of Transient Blood-Brain Barrier Disruption Without Evidence of Early Brain Injury.Frontiers in neuroscience · 2021Article
- Microenvironmental Variations After Blood-Brain Barrier Breakdown in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Review
- The Complexity of Secondary Cascade Consequent to Traumatic Brain Injury: Pathobiology and Potential Treatments.Current neuropharmacology · 2021Article
- Pharmacological Modulation of Blood-Brain Barrier Permeability by Kinin Analogs in Normal and Pathologic Conditions.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Toward a Long-Term Artificial Lung.ASAIO journal (American Society for Artificial Internal Organs : 1992) · 2020Review
- Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice.Journal of neurochemistry · 2020Article
- Recovery From Repeat Mild Traumatic Brain Injury in Adolescent Rats Is Dependent on Pre-injury Activity State.Frontiers in neurology · 2020Article
- Enduring Neuroprotective Effect of Subacute Neural Stem Cell Transplantation After Penetrating TBI.Frontiers in neurology · 2018Review
- Neuroprotective effect of kinin B1 receptor activation in acute cerebral ischemia in diabetic mice.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory mechanisms are known to contribute to the pathophysiology of traumatic brain injury (TBI). Since bradykinin is one of the first mediators activated during inflammation, we investigated the role of bradykinin and its receptors in posttraumatic secondary brain damage. We subjected wild-type (WT), B(1)-, and B(2)-receptor-knockout mice to controlled cortical impact (CCI) and analyzed tissue bradykinin as well as kinin receptor mRNA and protein expression up to 48 h thereafter. Brain edema, contusion volume, and functional outcome were assessed 24 h and 7 days after CCI. Tissue bradykinin was maximally increased 2 h after trauma (P<0.01 versus sham). Kinin B(1) receptor mRNA was upregulated up to four-fold 24 h after CCI. Immunohistochemistry showed that B(1) and B(2) receptors were expressed in the brain and were significantly upregulated in the traumatic penumbra 1 to 24 h after CCI. B(2)R(-/-) mice had significantly less brain edema (-51% versus WT, 24 h; P<0.001), smaller contusion volumes ( approximately 50% versus WT 24 h and 7 d after CCI; P<0.05), and better functional outcome 7 days after TBI as compared with WT mice (P<0.05). The present results show that bradykinin and its B(2) receptors play a causal role for brain edema formation and cell death after TBI.
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