Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema
Department of Anesthesia, University of California Medical School, San Francisco, California 94143-0542 The mechanism by which hypoxia causes high-altitude cerebral edema (HACE) is unknown. Tissue hypoxia triggers angiogenesis, initially by expressing vascular endothelial growth factor (VEGF), which...
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| Veröffentlicht in: | Journal of applied physiology (1985) 1998-07, Vol.85 (1), p.53-57 |
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| creator | Xu, Fengping Severinghaus, John W |
| description | Department of Anesthesia, University of California Medical
School, San Francisco, California 94143-0542
The mechanism by which hypoxia causes high-altitude
cerebral edema (HACE) is unknown. Tissue hypoxia triggers angiogenesis, initially by expressing vascular endothelial growth factor (VEGF), which has been shown to increase extracerebral capillary permeability. This study investigated brain VEGF expression in 32 rats exposed to
progressively severe normobaric hypoxia (9-6%
O 2 ) for 0 (control), 3, 6, or 12 h or 1, 2, 3, or 6 days. O 2
concentration was adjusted intermittently to the limit of tolerance by
activity and intake, but no attempt was made to detect HACE. Northern
blot analysis demonstrated that two molecular bands of transcribed VEGF
mRNA (~3.9 and 4.7 kb) were upregulated in cortex and cerebellum
after as little as 3 h of hypoxia, with a threefold increase peaking at
12-24 h. Western blot revealed that VEGF protein was increased after 12 h of hypoxia, reaching a maximum in ~2 days. The expression of flt-1 mRNA was enhanced after 3 days of hypoxia. We conclude that VEGF production in hypoxia is
consistent with the hypothesis that angiogenesis may be involved in
HACE.
angiogenesis; cytokines; brain capillary leak; acute mountain
sickness |
| doi_str_mv | 10.1152/jappl.1998.85.1.53 |
| format | Article |
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School, San Francisco, California 94143-0542
The mechanism by which hypoxia causes high-altitude
cerebral edema (HACE) is unknown. Tissue hypoxia triggers angiogenesis, initially by expressing vascular endothelial growth factor (VEGF), which has been shown to increase extracerebral capillary permeability. This study investigated brain VEGF expression in 32 rats exposed to
progressively severe normobaric hypoxia (9-6%
O 2 ) for 0 (control), 3, 6, or 12 h or 1, 2, 3, or 6 days. O 2
concentration was adjusted intermittently to the limit of tolerance by
activity and intake, but no attempt was made to detect HACE. Northern
blot analysis demonstrated that two molecular bands of transcribed VEGF
mRNA (~3.9 and 4.7 kb) were upregulated in cortex and cerebellum
after as little as 3 h of hypoxia, with a threefold increase peaking at
12-24 h. Western blot revealed that VEGF protein was increased after 12 h of hypoxia, reaching a maximum in ~2 days. The expression of flt-1 mRNA was enhanced after 3 days of hypoxia. We conclude that VEGF production in hypoxia is
consistent with the hypothesis that angiogenesis may be involved in
HACE.
angiogenesis; cytokines; brain capillary leak; acute mountain
sickness</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/jappl.1998.85.1.53</identifier><identifier>PMID: 9655755</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Altitude Sickness - metabolism ; Altitude Sickness - physiopathology ; Animals ; Biological and medical sciences ; Blotting, Western ; Brain ; Brain Chemistry - physiology ; Brain Edema - metabolism ; Brain Edema - physiopathology ; Endothelial Growth Factors - biosynthesis ; Female ; Humans ; Hypoxia - metabolism ; Hypoxia - physiopathology ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Lungs ; Lymphokines - biosynthesis ; Male ; Medical sciences ; Oxygen ; Proteins ; Pulmonary Alveoli - physiopathology ; Rats ; Rats, Sprague-Dawley ; RNA, Messenger - biosynthesis ; Rodents ; Space life sciences ; Traumas. Diseases due to physical agents ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>Journal of applied physiology (1985), 1998-07, Vol.85 (1), p.53-57</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Physiological Society Jul 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-1edf0015c4da44bbfcd9e2551131f07221e63af234e1ff82863041f1d9a51d9b3</citedby><cites>FETCH-LOGICAL-c492t-1edf0015c4da44bbfcd9e2551131f07221e63af234e1ff82863041f1d9a51d9b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3026,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2398045$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9655755$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Fengping</creatorcontrib><creatorcontrib>Severinghaus, John W</creatorcontrib><title>Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Department of Anesthesia, University of California Medical
School, San Francisco, California 94143-0542
The mechanism by which hypoxia causes high-altitude
cerebral edema (HACE) is unknown. Tissue hypoxia triggers angiogenesis, initially by expressing vascular endothelial growth factor (VEGF), which has been shown to increase extracerebral capillary permeability. This study investigated brain VEGF expression in 32 rats exposed to
progressively severe normobaric hypoxia (9-6%
O 2 ) for 0 (control), 3, 6, or 12 h or 1, 2, 3, or 6 days. O 2
concentration was adjusted intermittently to the limit of tolerance by
activity and intake, but no attempt was made to detect HACE. Northern
blot analysis demonstrated that two molecular bands of transcribed VEGF
mRNA (~3.9 and 4.7 kb) were upregulated in cortex and cerebellum
after as little as 3 h of hypoxia, with a threefold increase peaking at
12-24 h. Western blot revealed that VEGF protein was increased after 12 h of hypoxia, reaching a maximum in ~2 days. The expression of flt-1 mRNA was enhanced after 3 days of hypoxia. We conclude that VEGF production in hypoxia is
consistent with the hypothesis that angiogenesis may be involved in
HACE.
angiogenesis; cytokines; brain capillary leak; acute mountain
sickness</description><subject>Altitude Sickness - metabolism</subject><subject>Altitude Sickness - physiopathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Brain</subject><subject>Brain Chemistry - physiology</subject><subject>Brain Edema - metabolism</subject><subject>Brain Edema - physiopathology</subject><subject>Endothelial Growth Factors - biosynthesis</subject><subject>Female</subject><subject>Humans</subject><subject>Hypoxia - metabolism</subject><subject>Hypoxia - physiopathology</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Lungs</subject><subject>Lymphokines - biosynthesis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Oxygen</subject><subject>Proteins</subject><subject>Pulmonary Alveoli - physiopathology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Rodents</subject><subject>Space life sciences</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Vascular Endothelial Growth Factor A</subject><subject>Vascular Endothelial Growth Factors</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUV1r3DAQFKUhvab9A4WCKaVvdrT6sOW-hZBLC4FASPtUELK9yvnQ2a5kt3f_vnJjLlAKeVmBZnZmd4eQd0AzAMnOt2YYXAZlqTIlM8gkf0FWEWAp5BRekpUqJE0LqYpX5HUIW0pBCAmn5LTMpSykXJEfd2ZMKm_aLvl-db1OcD94DKHtuyR-GfcLe2d8sjkM_b41n5Ohj2DlMPF9LJGyaR82qXFjO04NJjV6jGouwQZ35g05scYFfLu8Z-Tb-ur-8kt6c3v99fLiJq1FycYUsLFxNFmLxghRVbZuSmRSAnCwtGAMMOfGMi4QrFVM5ZwKsNCURsZS8TPy6VF38P3PCcOod22o0TnTYT8FXcQLKcjVs0SWF0pKRZ8lQsE4L2AmfviHuO0n38VtNYuDi6g327JHUu3j-TxaPfh2Z_xBA9VzkvpvknpOUiupQUsem94vylO1w-bYskQX8Y8LbkJtnPWmq9twpDFeKirkk_cc1O_Wox42h5iv6x8Oej05d4_7cfZffPXQ2Kf1_9cUucch_wBn5MbT</recordid><startdate>19980701</startdate><enddate>19980701</enddate><creator>Xu, Fengping</creator><creator>Severinghaus, John W</creator><general>Am Physiological Soc</general><general>American Physiological Society</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>H8D</scope><scope>L7M</scope><scope>7X8</scope></search><sort><creationdate>19980701</creationdate><title>Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema</title><author>Xu, Fengping ; Severinghaus, John W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c492t-1edf0015c4da44bbfcd9e2551131f07221e63af234e1ff82863041f1d9a51d9b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Altitude Sickness - metabolism</topic><topic>Altitude Sickness - physiopathology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Brain</topic><topic>Brain Chemistry - physiology</topic><topic>Brain Edema - metabolism</topic><topic>Brain Edema - physiopathology</topic><topic>Endothelial Growth Factors - biosynthesis</topic><topic>Female</topic><topic>Humans</topic><topic>Hypoxia - metabolism</topic><topic>Hypoxia - physiopathology</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Lungs</topic><topic>Lymphokines - biosynthesis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Oxygen</topic><topic>Proteins</topic><topic>Pulmonary Alveoli - physiopathology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Rodents</topic><topic>Space life sciences</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Vascular Endothelial Growth Factor A</topic><topic>Vascular Endothelial Growth Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Fengping</creatorcontrib><creatorcontrib>Severinghaus, John W</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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Aerospace Database</collection><collection>Advanced Technologies Database with Aerospace</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Fengping</au><au>Severinghaus, John W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>1998-07-01</date><risdate>1998</risdate><volume>85</volume><issue>1</issue><spage>53</spage><epage>57</epage><pages>53-57</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Department of Anesthesia, University of California Medical
School, San Francisco, California 94143-0542
The mechanism by which hypoxia causes high-altitude
cerebral edema (HACE) is unknown. Tissue hypoxia triggers angiogenesis, initially by expressing vascular endothelial growth factor (VEGF), which has been shown to increase extracerebral capillary permeability. This study investigated brain VEGF expression in 32 rats exposed to
progressively severe normobaric hypoxia (9-6%
O 2 ) for 0 (control), 3, 6, or 12 h or 1, 2, 3, or 6 days. O 2
concentration was adjusted intermittently to the limit of tolerance by
activity and intake, but no attempt was made to detect HACE. Northern
blot analysis demonstrated that two molecular bands of transcribed VEGF
mRNA (~3.9 and 4.7 kb) were upregulated in cortex and cerebellum
after as little as 3 h of hypoxia, with a threefold increase peaking at
12-24 h. Western blot revealed that VEGF protein was increased after 12 h of hypoxia, reaching a maximum in ~2 days. The expression of flt-1 mRNA was enhanced after 3 days of hypoxia. We conclude that VEGF production in hypoxia is
consistent with the hypothesis that angiogenesis may be involved in
HACE.
angiogenesis; cytokines; brain capillary leak; acute mountain
sickness</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>9655755</pmid><doi>10.1152/jappl.1998.85.1.53</doi><tpages>5</tpages></addata></record> |
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| source | MEDLINE; American Physiological Society Paid; Elektronische Zeitschriftenbibliothek - Freely accessible e-journals; Alma/SFX Local Collection |
| subjects | Altitude Sickness - metabolism Altitude Sickness - physiopathology Animals Biological and medical sciences Blotting, Western Brain Brain Chemistry - physiology Brain Edema - metabolism Brain Edema - physiopathology Endothelial Growth Factors - biosynthesis Female Humans Hypoxia - metabolism Hypoxia - physiopathology Injuries of the nervous system and the skull. Diseases due to physical agents Lungs Lymphokines - biosynthesis Male Medical sciences Oxygen Proteins Pulmonary Alveoli - physiopathology Rats Rats, Sprague-Dawley RNA, Messenger - biosynthesis Rodents Space life sciences Traumas. Diseases due to physical agents Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| title | Rat brain VEGF expression in alveolar hypoxia: possible role in high-altitude cerebral edema |
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