Preconditioning Triggered by Carbon Monoxide (CO) Provides Neuronal Protection Following Perinatal Hypoxia-Ischemia
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{"title"=>"Preconditioning Triggered by Carbon Monoxide (CO) Provides Neuronal Protection Following Perinatal Hypoxia-Ischemia", "type"=>"journal", "authors"=>[{"first_name"=>"Cláudia S.F.", "last_name"=>"Queiroga", "scopus_author_id"=>"25123132100"}, {"first_name"=>"Simone", "last_name"=>"Tomasi", "scopus_author_id"=>"14049426700"}, {"first_name"=>"Marius", "last_name"=>"Widerøe", "scopus_author_id"=>"6507167354"}, {"first_name"=>"Paula M.", "last_name"=>"Alves", "scopus_author_id"=>"57200143732"}, {"first_name"=>"Alessandro", "last_name"=>"Vercelli", "scopus_author_id"=>"7003369233"}, {"first_name"=>"Helena L.A.", "last_name"=>"Vieira", "scopus_author_id"=>"7003272572"}], "year"=>2012, "source"=>"PLoS ONE", "identifiers"=>{"sgr"=>"84865516196", "doi"=>"10.1371/journal.pone.0042632", "pui"=>"365529055", "pmid"=>"22952602", "scopus"=>"2-s2.0-84865516196", "issn"=>"19326203", "isbn"=>"1932-6203 (Electronic)\\r1932-6203 (Linking)"}, "id"=>"1b8eb395-b141-3c39-b8c1-d6ddf8e6d602", "abstract"=>"Perinatal hypoxia-ischemia is a major cause of acute mortality in newborns and cognitive and motor impairments in children. Cerebral hypoxia-ischemia leads to excitotoxicity and necrotic and apoptotic cell death, in which mitochondria play a major role. Increased resistance against major damage can be achieved by preconditioning triggered by subtle insults. CO, a toxic molecule that is also generated endogenously, may have a role in preconditioning as low doses can protect against inflammation and apoptosis. In this study, the role of CO-induced preconditioning on neurons was addressed in vitro and in vivo. The effect of 1 h of CO treatment on neuronal death (plasmatic membrane permeabilization and chromatin condensation) and bcl-2 expression was studied in cerebellar granule cells undergoing to glutamate-induced apoptosis. CO's role was studied in vivo in the Rice-Vannucci model of neonatal hypoxia-ischemia (common carotid artery ligature +75 min at 8% oxygen). Apoptotic cells, assessed by Nissl staining were counted with a stereological approach and cleaved caspase 3-positive profiles in the hippocampus were assessed. Apoptotic hallmarks were analyzed in hippocampal extracts by Western Blot. CO inhibited excitotoxicity-induced cell death and increased Bcl-2 mRNA in primary cultures of neurons. In vivo, CO prevented hypoxia-ischemia induced apoptosis in the hippocampus, limited cytochrome c released from mitochondria and reduced activation of caspase-3. Still, Bcl-2 protein levels were higher in hippocampus of CO pre-treated rat pups. Our results show that CO preconditioning elicits a molecular cascade that limits neuronal apoptosis. This could represent an innovative therapeutic strategy for high-risk cerebral hypoxia-ischemia patients, in particular neonates.", "link"=>"http://www.mendeley.com/research/preconditioning-triggered-carbon-monoxide-co-provides-neuronal-protection-following-perinatal-hypoxi", "reader_count"=>34, "reader_count_by_academic_status"=>{"Unspecified"=>2, "Professor > Associate Professor"=>2, "Librarian"=>2, "Student > Doctoral Student"=>3, "Researcher"=>7, "Student > Ph. D. Student"=>5, "Student > Postgraduate"=>1, "Student > Master"=>6, "Other"=>3, "Student > Bachelor"=>3}, "reader_count_by_user_role"=>{"Unspecified"=>2, "Professor > Associate Professor"=>2, "Librarian"=>2, "Student > Doctoral Student"=>3, "Researcher"=>7, "Student > Ph. D. Student"=>5, "Student > Postgraduate"=>1, "Student > Master"=>6, "Other"=>3, "Student > Bachelor"=>3}, "reader_count_by_subject_area"=>{"Unspecified"=>2, "Biochemistry, Genetics and Molecular Biology"=>3, "Agricultural and Biological Sciences"=>14, "Medicine and Dentistry"=>10, "Design"=>2, "Neuroscience"=>3}, "reader_count_by_subdiscipline"=>{"Design"=>{"Design"=>2}, "Medicine and Dentistry"=>{"Medicine and Dentistry"=>10}, "Neuroscience"=>{"Neuroscience"=>3}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>14}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>3}, "Unspecified"=>{"Unspecified"=>2}}, "reader_count_by_country"=>{"United States"=>1, "Poland"=>1, "Portugal"=>1, "Germany"=>1}, "group_count"=>2}

Scopus | Further Information

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Figshare

  • {"files"=>["https://ndownloader.figshare.com/files/584996"], "description"=>"<p>(<b>A</b>) Representative micrographs of neurons treated or not with 20 µM of glutamate and 10 µM of CO. Apoptotic hallmarks were analyzed by fluorescent microscopy. <i>Upper panel</i>, for the photos taken with the filter for phase contrast, <i>middle panel</i>, for Hoechst (white arrows for nuclei with condensed chromatin) and <i>lower panel</i>, for propidium iodide (white arrows for cells which membrane integrity was lost). (<b>B</b>) Primary cultures of neuronal cells were pre-treated with 10 µM CO, followed by 24 h of glutamate (10–30 µM) treatment. Cell viability was assessed by counting cells containing normal nuclei and plasmatic membrane integrity. For each coverslip, at least 1500 cells were counted. All values are mean ± SD (error bars), n = 5; *<i>p</i><0.05 compared to control. (<b>C</b>) The effect of 10 µM CO treatment on Bcl-2 expression was assessed by its mRNA quantification.</p>", "links"=>[], "tags"=>["carbon", "monoxide", "neuronal"], "article_id"=>255488, "categories"=>["Neuroscience", "Cell Biology", "Medicine"], "users"=>["Cláudia S. F. Queiroga", "Simone Tomasi", "Marius Widerøe", "Paula M. Alves", "Alessandro Vercelli", "Helena L. A. Vieira"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0042632.g002", "stats"=>{"downloads"=>2, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Effect_of_carbon_monoxide_treatment_on_neuronal_apoptosis_/255488", "title"=>"Effect of carbon monoxide treatment on neuronal apoptosis.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-08-28 01:31:28"}
  • {"files"=>["https://ndownloader.figshare.com/files/585356"], "description"=>"<p>Low (scale bar = 100 µm) magnification CLSM photographs of the hippocampus of HI (A, B), CO-HI (C, D) and CO sham operated (E, F) rat pups. In blue, DAPI-stained nuclei; in red, cleaved caspase 3-positive cells. Caspase 3-positive profiles following HI were particularly frequent in CA1–2 and in the dentate gyrus, and were decreased in number following CO preconditioning. CO preconditioning alone did not induce caspase 3 activation in sham operated animals.</p>", "links"=>[], "tags"=>["monoxide", "hippocampus", "perinatal", "hypoxia-ischemia", "cleaved", "caspase"], "article_id"=>255842, "categories"=>["Neuroscience", "Cell Biology", "Medicine"], "users"=>["Cláudia S. F. Queiroga", "Simone Tomasi", "Marius Widerøe", "Paula M. Alves", "Alessandro Vercelli", "Helena L. A. Vieira"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0042632.g004", "stats"=>{"downloads"=>4, "page_views"=>66, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Carbon_monoxide_effect_in_hippocampus_after_perinatal_hypoxia_ischemia_8211_cleaved_caspase_3_expression_/255842", "title"=>"Carbon monoxide effect in hippocampus after perinatal hypoxia-ischemia – cleaved caspase 3 expression.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-08-28 01:37:22"}
  • {"files"=>["https://ndownloader.figshare.com/files/307386"], "description"=>"<div><p>Perinatal hypoxia-ischemia is a major cause of acute mortality in newborns and cognitive and motor impairments in children. Cerebral hypoxia-ischemia leads to excitotoxicity and necrotic and apoptotic cell death, in which mitochondria play a major role. Increased resistance against major damage can be achieved by preconditioning triggered by subtle insults. CO, a toxic molecule that is also generated endogenously, may have a role in preconditioning as low doses can protect against inflammation and apoptosis. In this study, the role of CO-induced preconditioning on neurons was addressed <em>in vitro</em> and <em>in vivo</em>. The effect of 1 h of CO treatment on neuronal death (plasmatic membrane permeabilization and chromatin condensation) and bcl-2 expression was studied in cerebellar granule cells undergoing to glutamate-induced apoptosis. CO's role was studied <em>in vivo</em> in the Rice-Vannucci model of neonatal hypoxia-ischemia (common carotid artery ligature +75 min at 8% oxygen). Apoptotic cells, assessed by Nissl staining were counted with a stereological approach and cleaved caspase 3-positive profiles in the hippocampus were assessed. Apoptotic hallmarks were analyzed in hippocampal extracts by Western Blot. CO inhibited excitotoxicity-induced cell death and increased Bcl-2 mRNA in primary cultures of neurons. <em>In vivo</em>, CO prevented hypoxia-ischemia induced apoptosis in the hippocampus, limited cytochrome c released from mitochondria and reduced activation of caspase-3. Still, Bcl-2 protein levels were higher in hippocampus of CO pre-treated rat pups. Our results show that CO preconditioning elicits a molecular cascade that limits neuronal apoptosis. This could represent an innovative therapeutic strategy for high-risk cerebral hypoxia-ischemia patients, in particular neonates.</p> </div>", "links"=>[], "tags"=>["preconditioning", "triggered", "carbon", "monoxide", "provides", "neuronal", "perinatal", "hypoxia-ischemia"], "article_id"=>120644, "categories"=>["Neuroscience", "Cell Biology", "Medicine"], "users"=>["Cláudia S. F. Queiroga", "Simone Tomasi", "Marius Widerøe", "Paula M. Alves", "Alessandro Vercelli", "Helena L. A. Vieira"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0042632", "stats"=>{"downloads"=>2, "page_views"=>9, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/Preconditioning_Triggered_by_Carbon_Monoxide_CO_Provides_Neuronal_Protection_Following_Perinatal_Hypoxia_Ischemia/120644", "title"=>"Preconditioning Triggered by Carbon Monoxide (CO) Provides Neuronal Protection Following Perinatal Hypoxia-Ischemia", "pos_in_sequence"=>0, "defined_type"=>3, "published_date"=>"2012-08-28 00:10:44"}
  • {"files"=>["https://ndownloader.figshare.com/files/584869"], "description"=>"<p><b>Control group</b>, <i>n = 22</i>, untreated animals that did not suffer any treatment; <b>Carbon Monoxide (CO) group</b>, <i>n = 16</i>, subjected to 3 exposures of 250 ppm, for 1 h at P4, P5 and P6; <b>Hypoxia-Ischemia (HI) group</b>, <i>n = 17</i>, animals that underwent surgery and hypoxia (8% of O<sub>2</sub> in nitrogen) exposure for 75 minutes; <b>CO+HI group</b>, <i>n = 19</i>, CO treatment plus hypoxia-ischemia. Animals were euthanized at 6 and 24 h <i>post</i>-HI. Brains were collected and analyzed for lesion volume and cell death markers, as described in the methods section. <i>Histo</i>, for brains analyzed by histological methods; <i>WB</i>, for brains collected and processed for western blot analysis.</p>", "links"=>[], "tags"=>["groups", "time-points", "schematic"], "article_id"=>255369, "categories"=>["Neuroscience", "Cell Biology", "Medicine"], "users"=>["Cláudia S. F. Queiroga", "Simone Tomasi", "Marius Widerøe", "Paula M. Alves", "Alessandro Vercelli", "Helena L. A. Vieira"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0042632.g001", "stats"=>{"downloads"=>0, "page_views"=>4, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Experimental_groups_and_time_points_schematic_representation_/255369", "title"=>"Experimental groups and time-points schematic representation.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-08-28 01:29:29"}
  • {"files"=>["https://ndownloader.figshare.com/files/585479"], "description"=>"<p>Representative immunoblots (<b>upper panels</b>) and the corresponding quantifications, as relative percentages to the hippocampus from control rat pups (<b>lower panels</b>). (<b>A</b>) Bcl-2 expression in total hippocampal extracts. All values are mean ± SD (error bars), n = 3; *<i>p</i><0.05 compared to HI group for the corresponding side and **<i>p</i><0.05 compared to HI group ipsilateral hippocampus. (<b>B</b>) Cytochrome c levels in enriched mitochondrial fraction from hippocampus, which is an indirect way for measuring cytochrome c release. All values are mean ± SD (error bars), n = 3; *<i>p</i><0.05 compared to HI group hippocampus for the corresponding side. (<b>C</b>) Caspase-3 activation in total extracts. All values are mean ± SD (error bars), n = 3; *<i>p</i><0.05 compared to HI group for the ipsilateral hippocampus.</p>", "links"=>[], "tags"=>["carbon", "monoxide", "apoptotic", "markers", "hippocampal", "extracts", "24", "sub-cellular"], "article_id"=>255965, "categories"=>["Neuroscience", "Cell Biology", "Medicine"], "users"=>["Cláudia S. F. Queiroga", "Simone Tomasi", "Marius Widerøe", "Paula M. Alves", "Alessandro Vercelli", "Helena L. A. Vieira"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0042632.g005", "stats"=>{"downloads"=>1, "page_views"=>7, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Effect_of_carbon_monoxide_on_apoptotic_markers_in_hippocampal_extracts_after_6_and_24_h_of_HI_8211_protein_expression_and_sub_cellular_localization_/255965", "title"=>"Effect of carbon monoxide on apoptotic markers in hippocampal extracts after 6 and 24 h of HI – protein expression and sub-cellular localization.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-08-28 01:39:25"}
  • {"files"=>["https://ndownloader.figshare.com/files/585144"], "description"=>"<p>Whereas contralateral hippocampus displayed a preserved morphology (<b>A</b>) following HI, diffuse tissue disruption was detected in the hippocampus ipsilateral to the occlusion (<b>B</b>). C–E are representative pictures of ischemic hippocampus, where diffuse apoptosis was documented; with peculiar morphological features including pyknotic nuclei (<b>C</b>), indicating early stage of apoptosis, progressive nuclear fragmentation (<b>D</b>) and karyorrhexis as confirmed by detectable apoptotic bodies (<b>E</b>). Compared to HI group, the number of apoptotic profiles was significantly lower when animals were exposed to CO prior to HI (<b>F</b>). All values are mean ± SD (error bars); *<i>p</i><0.05 compared to Control group for the corresponding side and **<i>p</i><0.05 compared to HI group ischemic hippocampus. (<b>G</b>) For each group there is no significant difference in cytotoxic edema volume (mm<sup>3</sup>) between the ipsi- and the contralateral hippocampus.</p>", "links"=>[], "tags"=>["monoxide", "hippocampus", "perinatal", "hypoxia-ischemia", "apoptotic"], "article_id"=>255630, "categories"=>["Neuroscience", "Cell Biology", "Medicine"], "users"=>["Cláudia S. F. Queiroga", "Simone Tomasi", "Marius Widerøe", "Paula M. Alves", "Alessandro Vercelli", "Helena L. A. Vieira"], "doi"=>"https://dx.doi.org/10.1371/journal.pone.0042632.g003", "stats"=>{"downloads"=>4, "page_views"=>8, "likes"=>0}, "figshare_url"=>"https://figshare.com/articles/_Carbon_monoxide_effect_in_hippocampus_after_perinatal_hypoxia_ischemia_8211_apoptotic_profiles_/255630", "title"=>"Carbon monoxide effect in hippocampus after perinatal hypoxia-ischemia – apoptotic profiles.", "pos_in_sequence"=>0, "defined_type"=>1, "published_date"=>"2012-08-28 01:33:50"}

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Relative Metric

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