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DC Field | Value | Language |
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dc.contributor.author | Becker, F | - |
dc.contributor.author | Kebschull, L | - |
dc.contributor.author | Rieger, C | - |
dc.contributor.author | Mohr, A | - |
dc.contributor.author | Heitplatz, B | - |
dc.contributor.author | Van Marck, V | - |
dc.contributor.author | Hansen, U | - |
dc.contributor.author | Ansari, J | - |
dc.contributor.author | Reuter, S | - |
dc.contributor.author | Strücker, B | - |
dc.contributor.author | Pascher, A | - |
dc.contributor.author | Brockmann, JG | - |
dc.contributor.author | Castor, T | - |
dc.contributor.author | Alexander, JS | - |
dc.contributor.author | Gavins, FNE | - |
dc.date.accessioned | 2022-03-18T19:25:23Z | - |
dc.date.available | 2022-03-18T19:25:23Z | - |
dc.date.issued | 2022-03-10 | - |
dc.identifier.citation | Becker, F., Kebschull, L., Rieger, C., Mohr, A., Heitplatz, B., Van Marck, V.,Hansen, U., Ansari, A., Reuter, S., Strücker, B., Pascher, A., Brockmann, J.G., Castor, T., Alexander, J.S. and Gavins, F.N.E. (2022) ‘Bryostatin-1 Attenuates Ischemia-Elicited Neutrophil Transmigration and Ameliorates Graft Injury after Kidney Transplantation’, Cells, 11 (6), 948, pp. 1 - 19. doi: 10.3390/cells11060948. | en_US |
dc.identifier.uri | https://bura.brunel.ac.uk/handle/2438/24289 | - |
dc.description | Data Availability Statement: Not applicable. | en_US |
dc.description.abstract | Copyright: © 2022 by the authors. Ischemia reperfusion injury (IRI) is a form of sterile inflammation whose severity determines short- and long-term graft fates in kidney transplantation. Neutrophils are now recognized as a key cell type mediating early graft injury, which activates further innate immune responses and intensifies acquired immunity and alloimmunity. Since the macrolide Bryostatin-1 has been shown to block neutrophil transmigration, we aimed to determine whether these findings could be translated to the field of kidney transplantation. To study the effects of Bryostatin-1 on ischemia-elicited neutrophil transmigration, an in vitro model of hypoxia and normoxia was equipped with human endothelial cells and neutrophils. To translate these findings, a porcine renal autotransplantation model with eight hours of reperfusion was used to study neutrophil infiltration in vivo. Graft-specific treatment using Bryostatin-1 (100 nM) was applied during static cold storage. Bryostatin-1 dose-dependently blocked neutrophil activation and transmigration over ischemically challenged endothelial cell monolayers. When applied to porcine renal autografts, Bryostatin-1 reduced neutrophil graft infiltration, attenuated histological and ultrastructural damage, and improved renal function. Our novel findings demonstrate that Bryostatin-1 is a promising pharmacological candidate for graft-specific treatment in kidney transplantation, as it provides protection by blocking neutrophil infiltration and attenuating functional graft injury. | en_US |
dc.description.sponsorship | Royal Society Wolfson Foundation (RSWF\R3\18300 to F.N.E.G); Eastern Star New Idea Award, LSUHSC-S (to F.N.E.G. and J.S.A.). | en_US |
dc.format.extent | 1 - 19 | - |
dc.format.medium | Electronic | - |
dc.language | Engish | - |
dc.language.iso | en_US | en_US |
dc.publisher | MDPI AG | en_US |
dc.rights | Copyright: © 2022 by the authors. Licensee MDPI, Basel, Switzerland. This is an open access article distributed under the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited | - |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | - |
dc.subject | kidney transplant | en_US |
dc.subject | ischemia reperfusion injury | en_US |
dc.subject | Bryostatin-1 | en_US |
dc.subject | translational research | en_US |
dc.title | Bryostatin-1 Attenuates Ischemia-Elicited Neutrophil Transmigration and Ameliorates Graft Injury after Kidney Transplantation | en_US |
dc.type | Article | en_US |
dc.identifier.doi | https://doi.org/10.3390/cells11060948 | - |
dc.relation.isPartOf | Cells | - |
pubs.issue | 6 | - |
pubs.publication-status | Published online | - |
pubs.volume | 11 | - |
dc.identifier.eissn | 2073-4409 | - |
Appears in Collections: | Dept of Life Sciences Research Papers |
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