Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia

Activated microglia may exacerbate damage in neural disorders; however, it is unknown how they affect stem cells transplanted after stroke. Focal ischemia was induced by microinjections of 40 pmol of endothelin-1 into the motor cortex of adult rats. Ischemic animals were treated with sterile salin...

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Principais autores: Edna C.S. Franco, Marcelo M. Cardoso, Amauri Gouvêia, Antonio Pereira, Walace Gomes-Leal
Formato: article
Idioma:eng
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Assuntos:
Acute stroke
Stem cells
Microglia
Inflammation
Minocycline
Neuroprotection
Endereço do item:https://repositorio.ufrn.br/jspui/handle/123456789/23259
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spelling ri-123456789-232592017-11-04T22:58:32Z Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia Edna C.S. Franco Marcelo M. Cardoso Amauri Gouvêia Antonio Pereira Walace Gomes-Leal Acute stroke Stem cells Microglia Inflammation Minocycline Neuroprotection Activated microglia may exacerbate damage in neural disorders; however, it is unknown how they affect stem cells transplanted after stroke. Focal ischemia was induced by microinjections of 40 pmol of endothelin-1 into the motor cortex of adult rats. Ischemic animals were treated with sterile saline (n = 5), bone marrow mononuclear cells (BMMCs, n = 8), minocycline (n = 5) or concomitantly with minocycline and BMMCs (n = 5). BMMC-treated animals received 5 × 106 BMMCs through the caudal vein 24 h post-ischemia. Behavioral tests were performed to evaluate functional recovery. Morphometric and histological analyses were performed to assess infarct area, neuronal loss and microglia/macrophage activation up to 21 days post-ischemia. Treatments with minocycline, BMMCs or minocycline-BMMCs reduced infarct area, increased neuronal survival and decreased the number of caspase-3+ and ED-1+ cells, but these effects were more prominent in the minocycline-BMMC group. Behavioral analyses using the modified sticky-tape and open-field tests showed that ischemic rats concomitantly treated with BMMCs and minocycline showed better motor performance than rats treated with BMMCs or minocycline only. The results suggest that proper modulation of the inflammatory response through the blockage of microglia activation enhances neuroprotection and functional recovery induced by intravenous transplantation of BMMCs after motor cortex ischemia. 2017-05-31T12:11:29Z 2017-05-31T12:11:29Z 2012-03-23 article 0168-0102 https://repositorio.ufrn.br/jspui/handle/123456789/23259 eng Acesso Aberto application/pdf
institution Repositório Institucional
collection RI - UFRN
language eng
topic Acute stroke
Stem cells
Microglia
Inflammation
Minocycline
Neuroprotection
spellingShingle Acute stroke
Stem cells
Microglia
Inflammation
Minocycline
Neuroprotection
Edna C.S. Franco
Marcelo M. Cardoso
Amauri Gouvêia
Antonio Pereira
Walace Gomes-Leal
Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia
description Activated microglia may exacerbate damage in neural disorders; however, it is unknown how they affect stem cells transplanted after stroke. Focal ischemia was induced by microinjections of 40 pmol of endothelin-1 into the motor cortex of adult rats. Ischemic animals were treated with sterile saline (n = 5), bone marrow mononuclear cells (BMMCs, n = 8), minocycline (n = 5) or concomitantly with minocycline and BMMCs (n = 5). BMMC-treated animals received 5 × 106 BMMCs through the caudal vein 24 h post-ischemia. Behavioral tests were performed to evaluate functional recovery. Morphometric and histological analyses were performed to assess infarct area, neuronal loss and microglia/macrophage activation up to 21 days post-ischemia. Treatments with minocycline, BMMCs or minocycline-BMMCs reduced infarct area, increased neuronal survival and decreased the number of caspase-3+ and ED-1+ cells, but these effects were more prominent in the minocycline-BMMC group. Behavioral analyses using the modified sticky-tape and open-field tests showed that ischemic rats concomitantly treated with BMMCs and minocycline showed better motor performance than rats treated with BMMCs or minocycline only. The results suggest that proper modulation of the inflammatory response through the blockage of microglia activation enhances neuroprotection and functional recovery induced by intravenous transplantation of BMMCs after motor cortex ischemia.
format article
author Edna C.S. Franco
Marcelo M. Cardoso
Amauri Gouvêia
Antonio Pereira
Walace Gomes-Leal
author_facet Edna C.S. Franco
Marcelo M. Cardoso
Amauri Gouvêia
Antonio Pereira
Walace Gomes-Leal
author_sort Edna C.S. Franco
title Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia
title_short Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia
title_full Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia
title_fullStr Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia
title_full_unstemmed Modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia
title_sort modulation of microglial activation enhances neuroprotection and functional recovery derived from bone marrow mononuclear cell transplantation after cortical ischemia
publishDate 2017
url https://repositorio.ufrn.br/jspui/handle/123456789/23259
work_keys_str_mv AT ednacsfranco modulationofmicroglialactivationenhancesneuroprotectionandfunctionalrecoveryderivedfrombonemarrowmononuclearcelltransplantationaftercorticalischemia
AT marcelomcardoso modulationofmicroglialactivationenhancesneuroprotectionandfunctionalrecoveryderivedfrombonemarrowmononuclearcelltransplantationaftercorticalischemia
AT amaurigouveia modulationofmicroglialactivationenhancesneuroprotectionandfunctionalrecoveryderivedfrombonemarrowmononuclearcelltransplantationaftercorticalischemia
AT antoniopereira modulationofmicroglialactivationenhancesneuroprotectionandfunctionalrecoveryderivedfrombonemarrowmononuclearcelltransplantationaftercorticalischemia
AT walacegomesleal modulationofmicroglialactivationenhancesneuroprotectionandfunctionalrecoveryderivedfrombonemarrowmononuclearcelltransplantationaftercorticalischemia
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