Erythropoietin in Combination of Tissue Plasminogen Activator Exacerbates Brain Hemorrhage When Treatment Is Initiated 6 Hours After Stroke
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Background and Purpose— Erythropoietin (EPO), a hematopoietic cytokine, exerts neuroprotective effects in experimental stroke. In the present study, we investigated the effect of recombinant human EPO (rhEPO) in combination with tissue plasminogen activator (tPA) on embolic stroke. Methods— Rats subjected to embolic middle cerebral artery occlusion (MCAO) were treated with rhEPO (5000 U/kg) in combination with tPA (10 mg/kg) at 2 or 6 hours after MCAO. Control groups consisted of ischemic rats treated with rhEPO (5000 U/kg) alone, tPA (10 mg/kg) alone, or saline at 2 or 6 hours after MCAO. Results— The combination therapy of rhEPO and tPA initiated 6 hours after MCAO did not reduce the ischemic lesion volume and significantly ( P <0.05) increased the incidence of brain hemorrhage measured by frequency of gross hemorrhage and a quantitative spectrophotometric hemoglobin assay compared with rats treated with rhEPO alone and tPA alone. However, when the combination therapy was initiated 2 hours after MCAO, the treatment significantly ( P <0.05) reduced the lesion volume and did not substantially increase the incidence of hemorrhagic transformation compared with saline-treated rats. Immunostaining analysis revealed that the combination therapy of rhEPO and tPA at 6 hours significantly ( P <0.05) increased matrix metalloproteinase-9, NF-κB, and interleukin-1 receptor-associated kinase-1 immunoreactive cerebral vessels compared with rats treated with rhEPO alone and saline. Conclusions— EPO exacerbates tPA-induced brain hemorrhage without reduction of ischemic brain damage when administered 6 hours after stroke in a rat model of embolic MCAO and that matrix metalloproteinase-9, NF-κB, and interleukin-1 receptor-associated kinase-1 upregulated by the delayed combination therapy may contribute to augmentation of brain hemorrhage.
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Subsequent experimental studies showed that erythropoietin activated MMP2 and 9 after focal cerebral ischaemia, an effect potentiated by alteplase, causing blood-brain barrier leakage, brain oedema, and haemorrhagic transformation.
“Subsequent experimental studies have shown that erythropoietin activated matrix metalloproteinases 2 and 9 after focal cerebral ischaemia, an effect that was potentiated by alteplase, thus provoking blood–brain barrier leakage, brain oedema, and haemorrhagic transformation of brain infarcts.91,92”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [92]
Such findings have been reported for severe associated systemic diseases (diabetic vasculopathy), after systemic thrombolysis, and when restorative treatments were initiated at inappropriate timepoints (before stroke).
“Such findings have been reported for severe associated systemic diseases (ie, diabetic vasculopathy),80 subsequent to systemic thrombolysis,91,92 and when restorative treat ments were initiated at inappropriate timepoints (ie, before stroke;93 table).”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [92]
Animal studies have identified medical conditions that specifically undermine neurorestorative therapies by making the brain prone to detrimental responses.
“Animal studies have identified medical conditions that specifically undermine neurorestorative therapies by making the brain prone to detrimental responses.”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [92]
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Sobolewski, P. K., Kozera, G., Szczuchniak, W., & Nyka, W. M. (2015) · Therapeutics and Clinical Risk Management · doi:10.2147/tcrm.s91119 · Cited by 3 · see citing works
O’Collins, V. E., Howells, D. W., & Markus, R. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_132 · Cited by 1 · see citing works
Levine, S. R., Kazim, S. F., Piran, P., & Barone, F. C. (2014) · Springer eBooks · doi:10.1007/978-3-319-07575-4_2 · Cited by 1 · see citing works
Combination Therapy with Thrombolysis
Yuluğ, B., & Schäbitz, W. (2017) · Springer series in translational stroke research · doi:10.1007/978-3-319-45345-3_25
Biologische Therapien in der Otologie
Roemer, A., Staecker, H., Sasse, S., Lenarz, T., & Warnecke, A. (2017) · HNO · doi:10.1007/s00106-016-0304-x
Oxygen Sensing, Homeostasis, and Disease
Bels, D. D., Corazza, F., & Balestra, C. (2011) · New England Journal of Medicine · doi:10.1056/nejmc1110602
- Authors
- Jia, L., Chopp, M., Zhang, L., Lu, M., & Zhang, Z.
- Affiliations
- Henry Ford Health (US)
- From the Departments of Neurology (L.J., M.C., L.Z., Z.Z.) and Biostatistics and Research Epidemiology (M.L.), Henry Ford Hospital, Detroit, Mich; and the Department of Physics (M.C.), Oakland University, Oakland, Mich.
- Venue
- Stroke
- Published
- 2010-09
- Volume
- 41
- Issue
- 9
- Pages
- 2071-2076
- ISSN
- 0039-2499 (ISSN-L)
- 1524-4628
- PMC
- PMC2950698
- OpenAlex
- W2123656924
- Cited by
- 62
- References
- 35
- Citations by year
- 2024: 1 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 5 · 2014: 5 · 2013: 10 · 2012: 6
- FWCI
- 6.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Stroke (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL064766, R01HL64766)
- National Institute of Neurological Disorders and Stroke (P01NS23393, R01NS062832, P01NS023393)
- Topics
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Keywords
- erythropoietin, tissue plasminogen activator, cerebral hemorrhage, hemorrhagic transformation, embolic stroke, middle cerebral artery occlusion, treatment delay, combination therapy, MMP-9, NF-κB, neuroprotection, ischemic lesion volume
- MeSH terms
- Analysis of Variance, Animals, Brain, Drug Therapy, Combination, Erythropoietin, Immunohistochemistry, Male, Tissue Plasminogen Activator, Time Factors, Blotting, Western, Chi-Square Distribution, NF-kappa B, Treatment Outcome, Rats, Wistar, Intracranial Hemorrhages, Stroke, Matrix Metalloproteinase 9, Rats, Interleukin-1 Receptor-Associated Kinases
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