Intracerebral hemorrhage outcomes following selective blockade or stimulation of the PGE2 EP1 receptor
Inflammation following intracerebral hemorrhage (ICH) significantly contributes to secondary brain damage and poor outcomes. Prostaglandin E2 (PGE2) is known to modulate neuroinflammatory responses and is upregulated in response to brain injury as a result of changes in inducible cyclooxygenase 2 (C...
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| description | Inflammation following intracerebral hemorrhage (ICH) significantly contributes to secondary brain damage and poor outcomes. Prostaglandin E2 (PGE2) is known to modulate neuroinflammatory responses and is upregulated in response to brain injury as a result of changes in inducible cyclooxygenase 2 (COX-2) and the membrane-bound type of PGE synthase. Inhibition of COX-2 activity has been reported to attenuate ICH-induced brain injury; however, the clinical utility of such drugs is limited due to the potential for severe side effects. Therefore, it is now important to search for downstream targets capable of preferentially modulating PGE2 signaling, and the four E prostanoid receptors, EP1-4, which are the main targets of PGE2, remain a viable therapeutic option. We have previously shown that EP1 receptor deletion aggravates ICH-induced brain injury and impairs functional recovery, thus the current study aimed to elaborate on these results by including a pharmacologic approach targeting the EP1 receptor.
Chronic post-treatment with the selective EP1 receptor antagonist, SC-51089, increased lesion volume by 30.1 ± 14.5% (p |
| doi_str_mv | 10.1186/s12868-015-0182-2 |
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Chronic post-treatment with the selective EP1 receptor antagonist, SC-51089, increased lesion volume by 30.1 ± 14.5% (p < 0.05) and treatment with the EP1 agonist, 17-pt-PGE2, improved neuromuscular functional recovery on grip strength (p < 0.01) and hanging wire (p < 0.05) behavioral testing. To begin identifying the mechanisms involved in EP1-mediated neuroprotection after ICH, histology was performed to assess ferric iron content, neuroinflammation, leukocyte transendothelial migratory potential, and peripheral neutrophil and immunoglobulin infiltration. Following ICH, mice treated with the antagonist displayed increased ferric iron (p < 0.05) and cortical microgliosis (p < 0.05), whereas treatment with the agonist decreased cortical (p < 0.01) and striatal (p < 0.001) astrogliosis, leukocyte transendothelial migratory potential (p < 0.01), neutrophil infiltration (p < 0.05), and blood brain barrier breakdown (p < 0.05).
In agreement with our previous results, selective antagonism of the EP1 receptor aggravated ICH-induced brain injury. Furthermore, EP1 receptor agonism improved anatomical outcomes and functional recovery. Thus, the present data continues to reinforce a putative role for EP1 as a new and more selective therapeutic target for the treatment of ICH that could reduce the side effects associated with COX-2 inhibition while still exploiting the beneficial effects.]]></description><identifier>ISSN: 1471-2202</identifier><identifier>EISSN: 1471-2202</identifier><identifier>DOI: 10.1186/s12868-015-0182-2</identifier><identifier>PMID: 26232001</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Astrocytes - drug effects ; Astrocytes - immunology ; Astrocytes - pathology ; Blood-Brain Barrier - drug effects ; Blood-Brain Barrier - immunology ; Blood-Brain Barrier - pathology ; Brain - drug effects ; Brain - immunology ; Brain - pathology ; Cerebral Hemorrhage - drug therapy ; Cerebral Hemorrhage - immunology ; Cerebral Hemorrhage - pathology ; Collagenases ; Complications and side effects ; COX-2 inhibitors ; Disease Models, Animal ; Gliosis - drug therapy ; Gliosis - immunology ; Gliosis - pathology ; Hydrazines - pharmacology ; Iron - metabolism ; Leukocytes - drug effects ; Leukocytes - immunology ; Leukocytes - pathology ; Male ; Mice, Inbred C57BL ; Microglia - drug effects ; Microglia - immunology ; Microglia - pathology ; Neuroimmunomodulation - drug effects ; Neuroimmunomodulation - physiology ; Neuroprotective Agents - pharmacology ; Oxazepines - pharmacology ; Prostaglandins E ; Receptors, Prostaglandin E, EP1 Subtype - agonists ; Receptors, Prostaglandin E, EP1 Subtype - antagonists & inhibitors ; Receptors, Prostaglandin E, EP1 Subtype - metabolism ; Recovery of Function - drug effects</subject><ispartof>BMC neuroscience, 2015-08, Vol.16 (1), p.48-48, Article 48</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Leclerc et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3812-ab2f9a47a7da48ce8ed85362a7b9e85a38e8fc5fa4dc015ca2aecb2cc6cbba053</citedby><cites>FETCH-LOGICAL-c3812-ab2f9a47a7da48ce8ed85362a7b9e85a38e8fc5fa4dc015ca2aecb2cc6cbba053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521449/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4521449/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26232001$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Leclerc, Jenna L</creatorcontrib><creatorcontrib>Ahmad, Abdullah S</creatorcontrib><creatorcontrib>Singh, Nilendra</creatorcontrib><creatorcontrib>Soshnik-Schierling, Luke</creatorcontrib><creatorcontrib>Greene, Ellis</creatorcontrib><creatorcontrib>Dang, Alex</creatorcontrib><creatorcontrib>Doré, Sylvain</creatorcontrib><title>Intracerebral hemorrhage outcomes following selective blockade or stimulation of the PGE2 EP1 receptor</title><title>BMC neuroscience</title><addtitle>BMC Neurosci</addtitle><description><![CDATA[Inflammation following intracerebral hemorrhage (ICH) significantly contributes to secondary brain damage and poor outcomes. Prostaglandin E2 (PGE2) is known to modulate neuroinflammatory responses and is upregulated in response to brain injury as a result of changes in inducible cyclooxygenase 2 (COX-2) and the membrane-bound type of PGE synthase. Inhibition of COX-2 activity has been reported to attenuate ICH-induced brain injury; however, the clinical utility of such drugs is limited due to the potential for severe side effects. Therefore, it is now important to search for downstream targets capable of preferentially modulating PGE2 signaling, and the four E prostanoid receptors, EP1-4, which are the main targets of PGE2, remain a viable therapeutic option. We have previously shown that EP1 receptor deletion aggravates ICH-induced brain injury and impairs functional recovery, thus the current study aimed to elaborate on these results by including a pharmacologic approach targeting the EP1 receptor.
Chronic post-treatment with the selective EP1 receptor antagonist, SC-51089, increased lesion volume by 30.1 ± 14.5% (p < 0.05) and treatment with the EP1 agonist, 17-pt-PGE2, improved neuromuscular functional recovery on grip strength (p < 0.01) and hanging wire (p < 0.05) behavioral testing. To begin identifying the mechanisms involved in EP1-mediated neuroprotection after ICH, histology was performed to assess ferric iron content, neuroinflammation, leukocyte transendothelial migratory potential, and peripheral neutrophil and immunoglobulin infiltration. Following ICH, mice treated with the antagonist displayed increased ferric iron (p < 0.05) and cortical microgliosis (p < 0.05), whereas treatment with the agonist decreased cortical (p < 0.01) and striatal (p < 0.001) astrogliosis, leukocyte transendothelial migratory potential (p < 0.01), neutrophil infiltration (p < 0.05), and blood brain barrier breakdown (p < 0.05).
In agreement with our previous results, selective antagonism of the EP1 receptor aggravated ICH-induced brain injury. Furthermore, EP1 receptor agonism improved anatomical outcomes and functional recovery. Thus, the present data continues to reinforce a putative role for EP1 as a new and more selective therapeutic target for the treatment of ICH that could reduce the side effects associated with COX-2 inhibition while still exploiting the beneficial effects.]]></description><subject>Animals</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - immunology</subject><subject>Astrocytes - pathology</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Blood-Brain Barrier - immunology</subject><subject>Blood-Brain Barrier - pathology</subject><subject>Brain - drug effects</subject><subject>Brain - immunology</subject><subject>Brain - pathology</subject><subject>Cerebral Hemorrhage - drug therapy</subject><subject>Cerebral Hemorrhage - immunology</subject><subject>Cerebral Hemorrhage - pathology</subject><subject>Collagenases</subject><subject>Complications and side effects</subject><subject>COX-2 inhibitors</subject><subject>Disease Models, Animal</subject><subject>Gliosis - drug therapy</subject><subject>Gliosis - immunology</subject><subject>Gliosis - pathology</subject><subject>Hydrazines - pharmacology</subject><subject>Iron - metabolism</subject><subject>Leukocytes - drug effects</subject><subject>Leukocytes - immunology</subject><subject>Leukocytes - pathology</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Microglia - drug effects</subject><subject>Microglia - immunology</subject><subject>Microglia - pathology</subject><subject>Neuroimmunomodulation - drug effects</subject><subject>Neuroimmunomodulation - physiology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Oxazepines - pharmacology</subject><subject>Prostaglandins E</subject><subject>Receptors, Prostaglandin E, EP1 Subtype - agonists</subject><subject>Receptors, Prostaglandin E, EP1 Subtype - antagonists & inhibitors</subject><subject>Receptors, Prostaglandin E, EP1 Subtype - metabolism</subject><subject>Recovery of Function - drug effects</subject><issn>1471-2202</issn><issn>1471-2202</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkUtr3DAUhUVoSdK0P6CbIuimG6d62ZY3hRCmaSDQLJK1uJavZtTK1lSyU_rvKzNpSKAIodd3Ljr3EPKes3POdfM5c6EbXTFel6lFJY7IKVctr4Rg4tWz_Ql5k_MPxnirlTgmJ6IRUpTjKXHX05zAYsI-QaA7HGNKO9gijcts44iZuhhC_O2nLc0Y0M7-AWkfov0JQ6ESzbMflwCzjxONjs47pLdXG0E3t5wmtLifY3pLXjsIGd89rmfk_uvm7vJbdfP96vry4qayUnNRQS9cB6qFdgClLWocdC0bAW3foa5BatTO1g7UYItrCwLQ9sLaxvY9sFqekS-HuvulH3GwuLoLZp_8COmPieDNy5fJ78w2PhhVC65UVwp8eiyQ4q8F82xGny2GABPGJRveMi5lIzUr6McDuoWAxk8urp1ccXNRKy7buutkoc7_Q5Ux4OhtnND5cv9CwA8Cm2LOCd3T7zkza-zmELspDTBr7EYUzYfntp8U_3KWfwGjwKpE</recordid><startdate>20150801</startdate><enddate>20150801</enddate><creator>Leclerc, Jenna L</creator><creator>Ahmad, Abdullah S</creator><creator>Singh, Nilendra</creator><creator>Soshnik-Schierling, Luke</creator><creator>Greene, Ellis</creator><creator>Dang, Alex</creator><creator>Doré, Sylvain</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150801</creationdate><title>Intracerebral hemorrhage outcomes following selective blockade or stimulation of the PGE2 EP1 receptor</title><author>Leclerc, Jenna L ; Ahmad, Abdullah S ; Singh, Nilendra ; Soshnik-Schierling, Luke ; Greene, Ellis ; Dang, Alex ; Doré, Sylvain</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3812-ab2f9a47a7da48ce8ed85362a7b9e85a38e8fc5fa4dc015ca2aecb2cc6cbba053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - immunology</topic><topic>Astrocytes - pathology</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Blood-Brain Barrier - immunology</topic><topic>Blood-Brain Barrier - pathology</topic><topic>Brain - drug effects</topic><topic>Brain - immunology</topic><topic>Brain - pathology</topic><topic>Cerebral Hemorrhage - drug therapy</topic><topic>Cerebral Hemorrhage - immunology</topic><topic>Cerebral Hemorrhage - pathology</topic><topic>Collagenases</topic><topic>Complications and side effects</topic><topic>COX-2 inhibitors</topic><topic>Disease Models, Animal</topic><topic>Gliosis - drug therapy</topic><topic>Gliosis - immunology</topic><topic>Gliosis - pathology</topic><topic>Hydrazines - pharmacology</topic><topic>Iron - metabolism</topic><topic>Leukocytes - drug effects</topic><topic>Leukocytes - immunology</topic><topic>Leukocytes - pathology</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Microglia - drug effects</topic><topic>Microglia - immunology</topic><topic>Microglia - pathology</topic><topic>Neuroimmunomodulation - drug effects</topic><topic>Neuroimmunomodulation - physiology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Oxazepines - pharmacology</topic><topic>Prostaglandins E</topic><topic>Receptors, Prostaglandin E, EP1 Subtype - agonists</topic><topic>Receptors, Prostaglandin E, EP1 Subtype - antagonists & inhibitors</topic><topic>Receptors, Prostaglandin E, EP1 Subtype - metabolism</topic><topic>Recovery of Function - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Leclerc, Jenna L</creatorcontrib><creatorcontrib>Ahmad, Abdullah S</creatorcontrib><creatorcontrib>Singh, Nilendra</creatorcontrib><creatorcontrib>Soshnik-Schierling, Luke</creatorcontrib><creatorcontrib>Greene, Ellis</creatorcontrib><creatorcontrib>Dang, Alex</creatorcontrib><creatorcontrib>Doré, Sylvain</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Leclerc, Jenna L</au><au>Ahmad, Abdullah S</au><au>Singh, Nilendra</au><au>Soshnik-Schierling, Luke</au><au>Greene, Ellis</au><au>Dang, Alex</au><au>Doré, Sylvain</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intracerebral hemorrhage outcomes following selective blockade or stimulation of the PGE2 EP1 receptor</atitle><jtitle>BMC neuroscience</jtitle><addtitle>BMC Neurosci</addtitle><date>2015-08-01</date><risdate>2015</risdate><volume>16</volume><issue>1</issue><spage>48</spage><epage>48</epage><pages>48-48</pages><artnum>48</artnum><issn>1471-2202</issn><eissn>1471-2202</eissn><abstract><![CDATA[Inflammation following intracerebral hemorrhage (ICH) significantly contributes to secondary brain damage and poor outcomes. Prostaglandin E2 (PGE2) is known to modulate neuroinflammatory responses and is upregulated in response to brain injury as a result of changes in inducible cyclooxygenase 2 (COX-2) and the membrane-bound type of PGE synthase. Inhibition of COX-2 activity has been reported to attenuate ICH-induced brain injury; however, the clinical utility of such drugs is limited due to the potential for severe side effects. Therefore, it is now important to search for downstream targets capable of preferentially modulating PGE2 signaling, and the four E prostanoid receptors, EP1-4, which are the main targets of PGE2, remain a viable therapeutic option. We have previously shown that EP1 receptor deletion aggravates ICH-induced brain injury and impairs functional recovery, thus the current study aimed to elaborate on these results by including a pharmacologic approach targeting the EP1 receptor.
Chronic post-treatment with the selective EP1 receptor antagonist, SC-51089, increased lesion volume by 30.1 ± 14.5% (p < 0.05) and treatment with the EP1 agonist, 17-pt-PGE2, improved neuromuscular functional recovery on grip strength (p < 0.01) and hanging wire (p < 0.05) behavioral testing. To begin identifying the mechanisms involved in EP1-mediated neuroprotection after ICH, histology was performed to assess ferric iron content, neuroinflammation, leukocyte transendothelial migratory potential, and peripheral neutrophil and immunoglobulin infiltration. Following ICH, mice treated with the antagonist displayed increased ferric iron (p < 0.05) and cortical microgliosis (p < 0.05), whereas treatment with the agonist decreased cortical (p < 0.01) and striatal (p < 0.001) astrogliosis, leukocyte transendothelial migratory potential (p < 0.01), neutrophil infiltration (p < 0.05), and blood brain barrier breakdown (p < 0.05).
In agreement with our previous results, selective antagonism of the EP1 receptor aggravated ICH-induced brain injury. Furthermore, EP1 receptor agonism improved anatomical outcomes and functional recovery. Thus, the present data continues to reinforce a putative role for EP1 as a new and more selective therapeutic target for the treatment of ICH that could reduce the side effects associated with COX-2 inhibition while still exploiting the beneficial effects.]]></abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26232001</pmid><doi>10.1186/s12868-015-0182-2</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Astrocytes - drug effects Astrocytes - immunology Astrocytes - pathology Blood-Brain Barrier - drug effects Blood-Brain Barrier - immunology Blood-Brain Barrier - pathology Brain - drug effects Brain - immunology Brain - pathology Cerebral Hemorrhage - drug therapy Cerebral Hemorrhage - immunology Cerebral Hemorrhage - pathology Collagenases Complications and side effects COX-2 inhibitors Disease Models, Animal Gliosis - drug therapy Gliosis - immunology Gliosis - pathology Hydrazines - pharmacology Iron - metabolism Leukocytes - drug effects Leukocytes - immunology Leukocytes - pathology Male Mice, Inbred C57BL Microglia - drug effects Microglia - immunology Microglia - pathology Neuroimmunomodulation - drug effects Neuroimmunomodulation - physiology Neuroprotective Agents - pharmacology Oxazepines - pharmacology Prostaglandins E Receptors, Prostaglandin E, EP1 Subtype - agonists Receptors, Prostaglandin E, EP1 Subtype - antagonists & inhibitors Receptors, Prostaglandin E, EP1 Subtype - metabolism Recovery of Function - drug effects |
| title | Intracerebral hemorrhage outcomes following selective blockade or stimulation of the PGE2 EP1 receptor |
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