Mice Deficient in Neuropeptide PACAP Demonstrate Increased Sensitivity to In Vitro Kidney Hypoxia
Abstract One of the well-known effects of pituitary adenylate cyclase activating polypeptide (PACAP) is its neuroprotective and cytoprotective actions including renoprotective effects. Mice deficient in endogenous PACAP exhibit several behavioral, metabolic, and developmental alterations. Furthermor...
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| Veröffentlicht in: | Transplantation proceedings 2010-07, Vol.42 (6), p.2293-2295 |
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| creator | Horvath, G Racz, B Szakaly, P Kiss, P Laszlo, E Hau, L Tamas, A Helyes, Z Lubics, A Hashimoto, H Baba, A Reglodi, D |
| description | Abstract One of the well-known effects of pituitary adenylate cyclase activating polypeptide (PACAP) is its neuroprotective and cytoprotective actions including renoprotective effects. Mice deficient in endogenous PACAP exhibit several behavioral, metabolic, and developmental alterations. Furthermore, PACAP-deficient mice have larger infarct volume in a model of cerebral ischemia, delayed axonal regeneration, and increased cell death in cerebellar oxidative stress. We have previously demonstrated that PACAP-deficient mice have increased susceptibility to in vitro oxidative stress, which can be counteracted by exogenous PACAP treatment. These results demonstrate that endogenous PACAP has a protective role against various stressors. The objective of the present study was to investigate whether endogenous PACAP has a protective effect in the kidney against in vitro hypoxia. Kidney cell cultures were isolated from wild-type and PACAP-deficient mice, and cell viability was assessed after in vitro hypoxia induced using CoCl2 . The sensitivity of cells from PACAP-deficient mice was increased to hypoxia: both after 24 and 48 hours of exposure, cell viability was significantly reduced compared with that in control wild-type mice. These results show that endogenous PACAP protects against noxious stimuli in the kidney and that PACAP may act as a stress sensor in renal cells. |
| doi_str_mv | 10.1016/j.transproceed.2010.05.015 |
| format | Article |
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Mice deficient in endogenous PACAP exhibit several behavioral, metabolic, and developmental alterations. Furthermore, PACAP-deficient mice have larger infarct volume in a model of cerebral ischemia, delayed axonal regeneration, and increased cell death in cerebellar oxidative stress. We have previously demonstrated that PACAP-deficient mice have increased susceptibility to in vitro oxidative stress, which can be counteracted by exogenous PACAP treatment. These results demonstrate that endogenous PACAP has a protective role against various stressors. The objective of the present study was to investigate whether endogenous PACAP has a protective effect in the kidney against in vitro hypoxia. Kidney cell cultures were isolated from wild-type and PACAP-deficient mice, and cell viability was assessed after in vitro hypoxia induced using CoCl2 . The sensitivity of cells from PACAP-deficient mice was increased to hypoxia: both after 24 and 48 hours of exposure, cell viability was significantly reduced compared with that in control wild-type mice. These results show that endogenous PACAP protects against noxious stimuli in the kidney and that PACAP may act as a stress sensor in renal cells.</description><identifier>ISSN: 0041-1345</identifier><identifier>EISSN: 1873-2623</identifier><identifier>DOI: 10.1016/j.transproceed.2010.05.015</identifier><identifier>PMID: 20692466</identifier><identifier>CODEN: TRPPA8</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Brain Ischemia - genetics ; Cell Death ; Cell Survival ; Cerebellum - pathology ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Hypoxia - genetics ; Hypoxia - pathology ; Infarction - genetics ; Kidney - metabolism ; Kidney - pathology ; Kidney Diseases - genetics ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Medical sciences ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Oxidative Stress ; Pituitary Adenylate Cyclase-Activating Polypeptide - deficiency ; Surgery ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Tissue, organ and graft immunology</subject><ispartof>Transplantation proceedings, 2010-07, Vol.42 (6), p.2293-2295</ispartof><rights>Elsevier Inc.</rights><rights>2010 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright 2010 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c464t-195fa6a3a778ae6d14ad2971341d3b5044ebb2fdabfd2e9eb56add6aff22b59c3</citedby><cites>FETCH-LOGICAL-c464t-195fa6a3a778ae6d14ad2971341d3b5044ebb2fdabfd2e9eb56add6aff22b59c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0041134510006731$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>309,310,314,776,780,785,786,3537,23909,23910,25118,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23151870$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20692466$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Horvath, G</creatorcontrib><creatorcontrib>Racz, B</creatorcontrib><creatorcontrib>Szakaly, P</creatorcontrib><creatorcontrib>Kiss, P</creatorcontrib><creatorcontrib>Laszlo, E</creatorcontrib><creatorcontrib>Hau, L</creatorcontrib><creatorcontrib>Tamas, A</creatorcontrib><creatorcontrib>Helyes, Z</creatorcontrib><creatorcontrib>Lubics, A</creatorcontrib><creatorcontrib>Hashimoto, H</creatorcontrib><creatorcontrib>Baba, A</creatorcontrib><creatorcontrib>Reglodi, D</creatorcontrib><title>Mice Deficient in Neuropeptide PACAP Demonstrate Increased Sensitivity to In Vitro Kidney Hypoxia</title><title>Transplantation proceedings</title><addtitle>Transplant Proc</addtitle><description>Abstract One of the well-known effects of pituitary adenylate cyclase activating polypeptide (PACAP) is its neuroprotective and cytoprotective actions including renoprotective effects. Mice deficient in endogenous PACAP exhibit several behavioral, metabolic, and developmental alterations. Furthermore, PACAP-deficient mice have larger infarct volume in a model of cerebral ischemia, delayed axonal regeneration, and increased cell death in cerebellar oxidative stress. We have previously demonstrated that PACAP-deficient mice have increased susceptibility to in vitro oxidative stress, which can be counteracted by exogenous PACAP treatment. These results demonstrate that endogenous PACAP has a protective role against various stressors. The objective of the present study was to investigate whether endogenous PACAP has a protective effect in the kidney against in vitro hypoxia. Kidney cell cultures were isolated from wild-type and PACAP-deficient mice, and cell viability was assessed after in vitro hypoxia induced using CoCl2 . The sensitivity of cells from PACAP-deficient mice was increased to hypoxia: both after 24 and 48 hours of exposure, cell viability was significantly reduced compared with that in control wild-type mice. These results show that endogenous PACAP protects against noxious stimuli in the kidney and that PACAP may act as a stress sensor in renal cells.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain Ischemia - genetics</subject><subject>Cell Death</subject><subject>Cell Survival</subject><subject>Cerebellum - pathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Hypoxia - genetics</subject><subject>Hypoxia - pathology</subject><subject>Infarction - genetics</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - genetics</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Oxidative Stress</subject><subject>Pituitary Adenylate Cyclase-Activating Polypeptide - deficiency</subject><subject>Surgery</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Tissue, organ and graft immunology</subject><issn>0041-1345</issn><issn>1873-2623</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkl2L1DAUhoMo7rj6FyQI4lXHfHfqhTDMqru46sKqtyFNTiFjJ61Juth_b8rMonjlVQjvez54zovQC0rWlFD1er_O0YQ0xsECuDUjRSByTah8gFZ0U_OKKcYfohUhglaUC3mGnqS0J-XPBH-MzhhRDRNKrZD55C3gC-i89RAy9gF_hikOI4zZO8A32932puiHIaQyNQO-CjaCSeDwLYTks7_zecZ5KAL-7nMc8EfvAsz4ch6HX948RY860yd4dnrP0bf3777uLqvrLx-udtvrygolckUb2RlluKnrjQHlqDCONXXZnjreSiIEtC3rnGk7x6CBVirjnDJdx1grG8vP0atj38Ll5wQp64NPFvreBBimpGuxaaTacFacb45OG4eUInR6jP5g4qwp0Qthvdd_E9YLYU2kLoRL8fPTmKk9FO2-9B5pMbw8GUyypu9KI-vTHx-nstyIFN_F0QcFyp2HqNNyAgvOR7BZu8H_3z5v_2ljex98mfwDZkj7YYqhYNdUJ6aJvl0ysUSCljSomlP-G1pHtq8</recordid><startdate>20100701</startdate><enddate>20100701</enddate><creator>Horvath, G</creator><creator>Racz, B</creator><creator>Szakaly, P</creator><creator>Kiss, P</creator><creator>Laszlo, E</creator><creator>Hau, L</creator><creator>Tamas, A</creator><creator>Helyes, Z</creator><creator>Lubics, A</creator><creator>Hashimoto, H</creator><creator>Baba, A</creator><creator>Reglodi, D</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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></search><sort><creationdate>20100701</creationdate><title>Mice Deficient in Neuropeptide PACAP Demonstrate Increased Sensitivity to In Vitro Kidney Hypoxia</title><author>Horvath, G ; Racz, B ; Szakaly, P ; Kiss, P ; Laszlo, E ; Hau, L ; Tamas, A ; Helyes, Z ; Lubics, A ; Hashimoto, H ; Baba, A ; Reglodi, D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c464t-195fa6a3a778ae6d14ad2971341d3b5044ebb2fdabfd2e9eb56add6aff22b59c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain Ischemia - genetics</topic><topic>Cell Death</topic><topic>Cell Survival</topic><topic>Cerebellum - pathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fundamental immunology</topic><topic>Hypoxia - genetics</topic><topic>Hypoxia - pathology</topic><topic>Infarction - genetics</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - genetics</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Knockout</topic><topic>Oxidative Stress</topic><topic>Pituitary Adenylate Cyclase-Activating Polypeptide - deficiency</topic><topic>Surgery</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Tissue, organ and graft immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Horvath, G</creatorcontrib><creatorcontrib>Racz, B</creatorcontrib><creatorcontrib>Szakaly, P</creatorcontrib><creatorcontrib>Kiss, P</creatorcontrib><creatorcontrib>Laszlo, E</creatorcontrib><creatorcontrib>Hau, L</creatorcontrib><creatorcontrib>Tamas, A</creatorcontrib><creatorcontrib>Helyes, Z</creatorcontrib><creatorcontrib>Lubics, A</creatorcontrib><creatorcontrib>Hashimoto, H</creatorcontrib><creatorcontrib>Baba, A</creatorcontrib><creatorcontrib>Reglodi, D</creatorcontrib><collection>Pascal-Francis</collection><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><jtitle>Transplantation proceedings</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Horvath, G</au><au>Racz, B</au><au>Szakaly, P</au><au>Kiss, P</au><au>Laszlo, E</au><au>Hau, L</au><au>Tamas, A</au><au>Helyes, Z</au><au>Lubics, A</au><au>Hashimoto, H</au><au>Baba, A</au><au>Reglodi, D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mice Deficient in Neuropeptide PACAP Demonstrate Increased Sensitivity to In Vitro Kidney Hypoxia</atitle><jtitle>Transplantation proceedings</jtitle><addtitle>Transplant Proc</addtitle><date>2010-07-01</date><risdate>2010</risdate><volume>42</volume><issue>6</issue><spage>2293</spage><epage>2295</epage><pages>2293-2295</pages><issn>0041-1345</issn><eissn>1873-2623</eissn><coden>TRPPA8</coden><abstract>Abstract One of the well-known effects of pituitary adenylate cyclase activating polypeptide (PACAP) is its neuroprotective and cytoprotective actions including renoprotective effects. Mice deficient in endogenous PACAP exhibit several behavioral, metabolic, and developmental alterations. Furthermore, PACAP-deficient mice have larger infarct volume in a model of cerebral ischemia, delayed axonal regeneration, and increased cell death in cerebellar oxidative stress. We have previously demonstrated that PACAP-deficient mice have increased susceptibility to in vitro oxidative stress, which can be counteracted by exogenous PACAP treatment. These results demonstrate that endogenous PACAP has a protective role against various stressors. The objective of the present study was to investigate whether endogenous PACAP has a protective effect in the kidney against in vitro hypoxia. Kidney cell cultures were isolated from wild-type and PACAP-deficient mice, and cell viability was assessed after in vitro hypoxia induced using CoCl2 . The sensitivity of cells from PACAP-deficient mice was increased to hypoxia: both after 24 and 48 hours of exposure, cell viability was significantly reduced compared with that in control wild-type mice. These results show that endogenous PACAP protects against noxious stimuli in the kidney and that PACAP may act as a stress sensor in renal cells.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>20692466</pmid><doi>10.1016/j.transproceed.2010.05.015</doi><tpages>3</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Brain Ischemia - genetics Cell Death Cell Survival Cerebellum - pathology Fundamental and applied biological sciences. Psychology Fundamental immunology Hypoxia - genetics Hypoxia - pathology Infarction - genetics Kidney - metabolism Kidney - pathology Kidney Diseases - genetics Kidney Diseases - metabolism Kidney Diseases - pathology Medical sciences Mice Mice, Inbred Strains Mice, Knockout Oxidative Stress Pituitary Adenylate Cyclase-Activating Polypeptide - deficiency Surgery Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Tissue, organ and graft immunology |
| title | Mice Deficient in Neuropeptide PACAP Demonstrate Increased Sensitivity to In Vitro Kidney Hypoxia |
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