Cardiolipin-mediated procoagulant activity of mitochondria contributes to traumatic brain injury–associated coagulopathy in mice
Open accessAbstract
Key Points: Mitochondria were released from traumatically injured brain into systemic circulation and exposed CL on their surface. CL-exposed mitochondria are highly procoagulant and induced traumatic brain injury–associated coagulopathy.
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Extracellular mitochondria have been identified in damaged tissues, diverse inflammatory conditions, and in the blood of critical care patients.
“Extracellular mitochondria have been identified in damaged tissues (8, 18–20); diverse inflammatory conditions (11, 12, 14, 21–24); and in the blood of critical care patients (22).”
From Autoantibodies in Systemic Lupus Erythematosus Target Mitochondrial RNA (2019) · cites this paper as [21]
The Results section on injured mice reports mitochondrial microparticles in mouse plasma, and the cell-culture section reports minimal detection after an inflammatory stimulus. Those findings do not establish their presence across diverse inflammatory conditions or in the blood of critical care patients; the paper reports no patient blood measurements (page unavailable in our copy). (LLM, conf=0.86)
Experimental — accuracy not yet measuredIt is not known whether mtRNA can contribute to the autoantigenic load in SLE.
“Whereas, the mitochondrion has already been described as a source of mtDNA during inflammation (17, 21, 32), it is not known whether its important RNA content (mtRNA) can contribute to the autoantigenic load in SLE.”
From Autoantibodies in Systemic Lupus Erythematosus Target Mitochondrial RNA (2019) · cites this paper as [21]
The citation is attached to the statement that mitochondria are a source of mtDNA, not to the citing authors’ statement that mtRNA’s contribution to SLE autoantigens is unknown. The paper reports mtDNA in plasma after traumatic brain injury (Results, ‘FPI-induced anti-brain antibodies cross-reacted with CL’), but its ‘Neuronal and glial cells released mtMPs after injury’ section found mtDNA release after apoptotic stimulation and only minimal release after the inflammatory stimulus LPS. It therefore supports mtDNA release after injury, but not the broader ‘during inflammation’ characterization without qualification. (LLM, conf=0.83)
Experimental — accuracy not yet measuredExtracellular mtDNA is associated with various pathologies, including trauma, burn injury, cancer, and rheumatoid arthritis.
“As extracellular mtDNA is reportedly associated with various pathologies, including trauma25,26, burn injury27, cancer28 and rheumatoid arthritis17,29”
From Anti-mitochondrial autoantibodies in systemic lupus erythematosus and their association with disease manifestations (2019) · cites this paper as [25]
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References 48 · Cited by 110
Research works printed but not linked: 1
- Alberts B, Bray D, Lewis J, et al. Intracellular Compartments and Protein Sorting. Molecular Biology of the Cell. New York: Garland Publishing Inc.; 1994:551-598.
- Authors
- Zhao, Z., Wang, M., Tian, Y., Hilton, T., Salsbery, B., Zhou, E. Z., Wu, X., Thiagarajan, P., Boilard, E., Li, M., Zhang, J., & Dong, J.-F.
- Affiliations
- Bloodworks Northwest (US)
- Lanzhou University (CN)
- Tianjin Medical University General Hospital (CN)
- Baylor College of Medicine (US)
- Centre de Recherche du Centre Hospitalier Universitaire de Québec, Department of Infectious Diseases and Immunity, Université Laval and Faculté de Médecine de l’Université Laval, Quebec City, QC, Canada; and
- University of Washington (US)
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2016-06-02
- Volume
- 127
- Issue
- 22
- Pages
- 2763-2772
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- PMC
- PMC4891956
- OpenAlex
- W2329970613
- Cited by
- 110
- References
- 48
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 11 · 2023: 15 · 2022: 10 · 2021: 14 · 2020: 15 · 2019: 15 · 2018: 4 · 2017: 6 · 2016: 2
- FWCI
- 8.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Lanzhou University Institutional Repository (submittedVersion)
- Funders
- National Natural Science Foundation of China (81271361, 81372575, 81271359, 81330029)
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL 71895, R01HL071895)
- National Institute of Neurological Disorders and Stroke (R21NS087296)
- Topics
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Trauma, Hemostasis, Coagulopathy, Resuscitation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- cardiolipin, traumatic brain injury, coagulopathy, procoagulant activity, fluid percussion injury, platelet activation, vascular leakage, endothelial barrier disruption, fibrin deposition, thrombosis, lactadherin, mitochondrial membrane permeability, apoptosis
- MeSH terms
- Brain Injuries, Traumatic, Animals, Antigens, Surface, Blood Coagulation Disorders, Cardiolipins, Milk Proteins, Mitochondria, Annexin A5, Mitochondrial Membranes, Mice, Cell-Derived Microparticles
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