Low energy shock wave therapy induces angiogenesis in acute hind-limb ischemia via VEGF receptor 2 phosphorylation
Low energy shock waves have been shown to induce angiogenesis, improve left ventricular ejection fraction and decrease angina symptoms in patients suffering from chronic ischemic heart disease. Whether there is as well an effect in acute ischemia was not yet investigated. Hind-limb ischemia was indu...
Gespeichert in:
Veröffentlicht in: | PloS one 2014-08, Vol.9 (8), p.e103982-e103982 |
---|---|
Hauptverfasser: | , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | e103982 |
---|---|
container_issue | 8 |
container_start_page | e103982 |
container_title | PloS one |
container_volume | 9 |
creator | Holfeld, Johannes Tepeköylü, Can Blunder, Stefan Lobenwein, Daniela Kirchmair, Elke Dietl, Marion Kozaryn, Radoslaw Lener, Daniela Theurl, Markus Paulus, Patrick Kirchmair, Rudolf Grimm, Michael |
description | Low energy shock waves have been shown to induce angiogenesis, improve left ventricular ejection fraction and decrease angina symptoms in patients suffering from chronic ischemic heart disease. Whether there is as well an effect in acute ischemia was not yet investigated.
Hind-limb ischemia was induced in 10-12 weeks old male C57/Bl6 wild-type mice by excision of the left femoral artery. Animals were randomly divided in a treatment group (SWT, 300 shock waves at 0.1 mJ/mm2, 5 Hz) and untreated controls (CTR), n = 10 per group. The treatment group received shock wave therapy immediately after surgery.
Higher gene expression and protein levels of angiogenic factors VEGF-A and PlGF, as well as their receptors Flt-1 and KDR have been found. This resulted in significantly more vessels per high-power field in SWT compared to controls. Improvement of blood perfusion in treatment animals was confirmed by laser Doppler perfusion imaging. Receptor tyrosine kinase profiler revealed significant phosphorylation of VEGF receptor 2 as an underlying mechanism of action. The effect of VEGF signaling was abolished upon incubation with a VEGFR2 inhibitor indicating that the effect is indeed VEGFR 2 dependent.
Low energy shock wave treatment induces angiogenesis in acute ischemia via VEGF receptor 2 stimulation and shows the same promising effects as known from chronic myocardial ischemia. It may therefore develop as an adjunct to the treatment armentarium of acute muscle ischemia in limbs and myocardium. |
doi_str_mv | 10.1371/journal.pone.0103982 |
format | Article |
fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_2014034009</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_532048a2c68c421a9149dd7e39701682</doaj_id><sourcerecordid>2014034009</sourcerecordid><originalsourceid>FETCH-LOGICAL-c592t-9e7ae78b5c6f549c076cabfeba70526228d010251f940c229d14f199460791d33</originalsourceid><addsrcrecordid>eNptUk1v1DAQjRCIloV_gMASFy5Z_J34goSqfkkrcQGuluNMEi_ZONjJVvvv8bJp1VYcRrZm3rzxG78se0_wmrCCfNn6OQymX49-gDUmmKmSvsjOiWI0lxSzl4_uZ9mbGLcYC1ZK-To7owIrVhJ5noWNv0MwQGgPKHbe_kZ3Zg9o6iCY8YDcUM8WIjJD63ybcNHFlETGzhOgLpXz3u0q5KLtYOcM2qf4dXl9hQJYGCcfEEVj52OKcOjN5PzwNnvVmD7Cu-VcZT-vLn9c3OSb79e3F982uRWKTrmCwkBRVsLKRnBlcSGtqRqoTIEFlZSWdVJNBWkUx5ZSVRPeEKW4xIUiNWOr7OOJd-x91Mu6oqaYcMw4ThtYZbcnRO3NVo_B7Uw4aG-c_pfwodUmTM72oAWjmJeGWllaTolRhKu6LoCpAhNZ0sT1dZk2VzuoLQxTMP0T0qeVwXW69XvNCaXp7xLB54Ug-D8zxEnv0lah780Afo6aCEFKWjByVPbpGfT_6vgJZYOPMUDz8BiC9dFC9136aCG9WCi1fXgs5KHp3jPsL2nExBc</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2014034009</pqid></control><display><type>article</type><title>Low energy shock wave therapy induces angiogenesis in acute hind-limb ischemia via VEGF receptor 2 phosphorylation</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Holfeld, Johannes ; Tepeköylü, Can ; Blunder, Stefan ; Lobenwein, Daniela ; Kirchmair, Elke ; Dietl, Marion ; Kozaryn, Radoslaw ; Lener, Daniela ; Theurl, Markus ; Paulus, Patrick ; Kirchmair, Rudolf ; Grimm, Michael</creator><contributor>Vinci, Maria Cristina</contributor><creatorcontrib>Holfeld, Johannes ; Tepeköylü, Can ; Blunder, Stefan ; Lobenwein, Daniela ; Kirchmair, Elke ; Dietl, Marion ; Kozaryn, Radoslaw ; Lener, Daniela ; Theurl, Markus ; Paulus, Patrick ; Kirchmair, Rudolf ; Grimm, Michael ; Vinci, Maria Cristina</creatorcontrib><description>Low energy shock waves have been shown to induce angiogenesis, improve left ventricular ejection fraction and decrease angina symptoms in patients suffering from chronic ischemic heart disease. Whether there is as well an effect in acute ischemia was not yet investigated.
Hind-limb ischemia was induced in 10-12 weeks old male C57/Bl6 wild-type mice by excision of the left femoral artery. Animals were randomly divided in a treatment group (SWT, 300 shock waves at 0.1 mJ/mm2, 5 Hz) and untreated controls (CTR), n = 10 per group. The treatment group received shock wave therapy immediately after surgery.
Higher gene expression and protein levels of angiogenic factors VEGF-A and PlGF, as well as their receptors Flt-1 and KDR have been found. This resulted in significantly more vessels per high-power field in SWT compared to controls. Improvement of blood perfusion in treatment animals was confirmed by laser Doppler perfusion imaging. Receptor tyrosine kinase profiler revealed significant phosphorylation of VEGF receptor 2 as an underlying mechanism of action. The effect of VEGF signaling was abolished upon incubation with a VEGFR2 inhibitor indicating that the effect is indeed VEGFR 2 dependent.
Low energy shock wave treatment induces angiogenesis in acute ischemia via VEGF receptor 2 stimulation and shows the same promising effects as known from chronic myocardial ischemia. It may therefore develop as an adjunct to the treatment armentarium of acute muscle ischemia in limbs and myocardium.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0103982</identifier><identifier>PMID: 25093816</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acute Disease ; Angina ; Angiogenesis ; Animals ; Biology and life sciences ; Blood vessels ; Cardiology ; Cardiovascular disease ; Cardiovascular diseases ; Coronary artery disease ; Coronary vessels ; Doppler effect ; Energy ; Femoral artery ; Femur ; Gene expression ; Gene therapy ; Heart ; Heart attacks ; Heart diseases ; Heart surgery ; High-Energy Shock Waves - therapeutic use ; Hindlimb - blood supply ; Hindlimb - radiation effects ; Hospitals ; Internal medicine ; Ischemia ; Ischemia - metabolism ; Ischemia - therapy ; Kinases ; Laboratory animals ; Lithotripsy ; Male ; Medicine ; Medicine and Health Sciences ; Mice ; Mice, Inbred C57BL ; Muscles ; Myocardial ischemia ; Myocardium ; Neovascularization, Physiologic - radiation effects ; Perfusion ; Peripheral Vascular Diseases - metabolism ; Peripheral Vascular Diseases - therapy ; Phosphorylation ; Protein Kinases - metabolism ; Protein-tyrosine kinase receptors ; Quality of life ; Receptors ; Rodents ; Shock ; Shock waves ; Signaling ; Surgery ; Therapy ; Tyrosine ; Ultrasonic Therapy - methods ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor Receptor-2 - metabolism ; Vascular endothelial growth factor receptors ; Ventricle</subject><ispartof>PloS one, 2014-08, Vol.9 (8), p.e103982-e103982</ispartof><rights>2014 Holfeld et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Holfeld et al 2014 Holfeld et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c592t-9e7ae78b5c6f549c076cabfeba70526228d010251f940c229d14f199460791d33</citedby><cites>FETCH-LOGICAL-c592t-9e7ae78b5c6f549c076cabfeba70526228d010251f940c229d14f199460791d33</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/PMC4122398/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4122398/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25093816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Vinci, Maria Cristina</contributor><creatorcontrib>Holfeld, Johannes</creatorcontrib><creatorcontrib>Tepeköylü, Can</creatorcontrib><creatorcontrib>Blunder, Stefan</creatorcontrib><creatorcontrib>Lobenwein, Daniela</creatorcontrib><creatorcontrib>Kirchmair, Elke</creatorcontrib><creatorcontrib>Dietl, Marion</creatorcontrib><creatorcontrib>Kozaryn, Radoslaw</creatorcontrib><creatorcontrib>Lener, Daniela</creatorcontrib><creatorcontrib>Theurl, Markus</creatorcontrib><creatorcontrib>Paulus, Patrick</creatorcontrib><creatorcontrib>Kirchmair, Rudolf</creatorcontrib><creatorcontrib>Grimm, Michael</creatorcontrib><title>Low energy shock wave therapy induces angiogenesis in acute hind-limb ischemia via VEGF receptor 2 phosphorylation</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Low energy shock waves have been shown to induce angiogenesis, improve left ventricular ejection fraction and decrease angina symptoms in patients suffering from chronic ischemic heart disease. Whether there is as well an effect in acute ischemia was not yet investigated.
Hind-limb ischemia was induced in 10-12 weeks old male C57/Bl6 wild-type mice by excision of the left femoral artery. Animals were randomly divided in a treatment group (SWT, 300 shock waves at 0.1 mJ/mm2, 5 Hz) and untreated controls (CTR), n = 10 per group. The treatment group received shock wave therapy immediately after surgery.
Higher gene expression and protein levels of angiogenic factors VEGF-A and PlGF, as well as their receptors Flt-1 and KDR have been found. This resulted in significantly more vessels per high-power field in SWT compared to controls. Improvement of blood perfusion in treatment animals was confirmed by laser Doppler perfusion imaging. Receptor tyrosine kinase profiler revealed significant phosphorylation of VEGF receptor 2 as an underlying mechanism of action. The effect of VEGF signaling was abolished upon incubation with a VEGFR2 inhibitor indicating that the effect is indeed VEGFR 2 dependent.
Low energy shock wave treatment induces angiogenesis in acute ischemia via VEGF receptor 2 stimulation and shows the same promising effects as known from chronic myocardial ischemia. It may therefore develop as an adjunct to the treatment armentarium of acute muscle ischemia in limbs and myocardium.</description><subject>Acute Disease</subject><subject>Angina</subject><subject>Angiogenesis</subject><subject>Animals</subject><subject>Biology and life sciences</subject><subject>Blood vessels</subject><subject>Cardiology</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Coronary artery disease</subject><subject>Coronary vessels</subject><subject>Doppler effect</subject><subject>Energy</subject><subject>Femoral artery</subject><subject>Femur</subject><subject>Gene expression</subject><subject>Gene therapy</subject><subject>Heart</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Heart surgery</subject><subject>High-Energy Shock Waves - therapeutic use</subject><subject>Hindlimb - blood supply</subject><subject>Hindlimb - radiation effects</subject><subject>Hospitals</subject><subject>Internal medicine</subject><subject>Ischemia</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - therapy</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lithotripsy</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscles</subject><subject>Myocardial ischemia</subject><subject>Myocardium</subject><subject>Neovascularization, Physiologic - radiation effects</subject><subject>Perfusion</subject><subject>Peripheral Vascular Diseases - metabolism</subject><subject>Peripheral Vascular Diseases - therapy</subject><subject>Phosphorylation</subject><subject>Protein Kinases - metabolism</subject><subject>Protein-tyrosine kinase receptors</subject><subject>Quality of life</subject><subject>Receptors</subject><subject>Rodents</subject><subject>Shock</subject><subject>Shock waves</subject><subject>Signaling</subject><subject>Surgery</subject><subject>Therapy</subject><subject>Tyrosine</subject><subject>Ultrasonic Therapy - methods</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor Receptor-2 - metabolism</subject><subject>Vascular endothelial growth factor receptors</subject><subject>Ventricle</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUk1v1DAQjRCIloV_gMASFy5Z_J34goSqfkkrcQGuluNMEi_ZONjJVvvv8bJp1VYcRrZm3rzxG78se0_wmrCCfNn6OQymX49-gDUmmKmSvsjOiWI0lxSzl4_uZ9mbGLcYC1ZK-To7owIrVhJ5noWNv0MwQGgPKHbe_kZ3Zg9o6iCY8YDcUM8WIjJD63ybcNHFlETGzhOgLpXz3u0q5KLtYOcM2qf4dXl9hQJYGCcfEEVj52OKcOjN5PzwNnvVmD7Cu-VcZT-vLn9c3OSb79e3F982uRWKTrmCwkBRVsLKRnBlcSGtqRqoTIEFlZSWdVJNBWkUx5ZSVRPeEKW4xIUiNWOr7OOJd-x91Mu6oqaYcMw4ThtYZbcnRO3NVo_B7Uw4aG-c_pfwodUmTM72oAWjmJeGWllaTolRhKu6LoCpAhNZ0sT1dZk2VzuoLQxTMP0T0qeVwXW69XvNCaXp7xLB54Ug-D8zxEnv0lah780Afo6aCEFKWjByVPbpGfT_6vgJZYOPMUDz8BiC9dFC9136aCG9WCi1fXgs5KHp3jPsL2nExBc</recordid><startdate>20140805</startdate><enddate>20140805</enddate><creator>Holfeld, Johannes</creator><creator>Tepeköylü, Can</creator><creator>Blunder, Stefan</creator><creator>Lobenwein, Daniela</creator><creator>Kirchmair, Elke</creator><creator>Dietl, Marion</creator><creator>Kozaryn, Radoslaw</creator><creator>Lener, Daniela</creator><creator>Theurl, Markus</creator><creator>Paulus, Patrick</creator><creator>Kirchmair, Rudolf</creator><creator>Grimm, Michael</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140805</creationdate><title>Low energy shock wave therapy induces angiogenesis in acute hind-limb ischemia via VEGF receptor 2 phosphorylation</title><author>Holfeld, Johannes ; Tepeköylü, Can ; Blunder, Stefan ; Lobenwein, Daniela ; Kirchmair, Elke ; Dietl, Marion ; Kozaryn, Radoslaw ; Lener, Daniela ; Theurl, Markus ; Paulus, Patrick ; Kirchmair, Rudolf ; Grimm, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-9e7ae78b5c6f549c076cabfeba70526228d010251f940c229d14f199460791d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acute Disease</topic><topic>Angina</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Biology and life sciences</topic><topic>Blood vessels</topic><topic>Cardiology</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Coronary artery disease</topic><topic>Coronary vessels</topic><topic>Doppler effect</topic><topic>Energy</topic><topic>Femoral artery</topic><topic>Femur</topic><topic>Gene expression</topic><topic>Gene therapy</topic><topic>Heart</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>Heart surgery</topic><topic>High-Energy Shock Waves - therapeutic use</topic><topic>Hindlimb - blood supply</topic><topic>Hindlimb - radiation effects</topic><topic>Hospitals</topic><topic>Internal medicine</topic><topic>Ischemia</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - therapy</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lithotripsy</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Muscles</topic><topic>Myocardial ischemia</topic><topic>Myocardium</topic><topic>Neovascularization, Physiologic - radiation effects</topic><topic>Perfusion</topic><topic>Peripheral Vascular Diseases - metabolism</topic><topic>Peripheral Vascular Diseases - therapy</topic><topic>Phosphorylation</topic><topic>Protein Kinases - metabolism</topic><topic>Protein-tyrosine kinase receptors</topic><topic>Quality of life</topic><topic>Receptors</topic><topic>Rodents</topic><topic>Shock</topic><topic>Shock waves</topic><topic>Signaling</topic><topic>Surgery</topic><topic>Therapy</topic><topic>Tyrosine</topic><topic>Ultrasonic Therapy - methods</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor Receptor-2 - metabolism</topic><topic>Vascular endothelial growth factor receptors</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Holfeld, Johannes</creatorcontrib><creatorcontrib>Tepeköylü, Can</creatorcontrib><creatorcontrib>Blunder, Stefan</creatorcontrib><creatorcontrib>Lobenwein, Daniela</creatorcontrib><creatorcontrib>Kirchmair, Elke</creatorcontrib><creatorcontrib>Dietl, Marion</creatorcontrib><creatorcontrib>Kozaryn, Radoslaw</creatorcontrib><creatorcontrib>Lener, Daniela</creatorcontrib><creatorcontrib>Theurl, Markus</creatorcontrib><creatorcontrib>Paulus, Patrick</creatorcontrib><creatorcontrib>Kirchmair, Rudolf</creatorcontrib><creatorcontrib>Grimm, Michael</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Holfeld, Johannes</au><au>Tepeköylü, Can</au><au>Blunder, Stefan</au><au>Lobenwein, Daniela</au><au>Kirchmair, Elke</au><au>Dietl, Marion</au><au>Kozaryn, Radoslaw</au><au>Lener, Daniela</au><au>Theurl, Markus</au><au>Paulus, Patrick</au><au>Kirchmair, Rudolf</au><au>Grimm, Michael</au><au>Vinci, Maria Cristina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Low energy shock wave therapy induces angiogenesis in acute hind-limb ischemia via VEGF receptor 2 phosphorylation</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-08-05</date><risdate>2014</risdate><volume>9</volume><issue>8</issue><spage>e103982</spage><epage>e103982</epage><pages>e103982-e103982</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Low energy shock waves have been shown to induce angiogenesis, improve left ventricular ejection fraction and decrease angina symptoms in patients suffering from chronic ischemic heart disease. Whether there is as well an effect in acute ischemia was not yet investigated.
Hind-limb ischemia was induced in 10-12 weeks old male C57/Bl6 wild-type mice by excision of the left femoral artery. Animals were randomly divided in a treatment group (SWT, 300 shock waves at 0.1 mJ/mm2, 5 Hz) and untreated controls (CTR), n = 10 per group. The treatment group received shock wave therapy immediately after surgery.
Higher gene expression and protein levels of angiogenic factors VEGF-A and PlGF, as well as their receptors Flt-1 and KDR have been found. This resulted in significantly more vessels per high-power field in SWT compared to controls. Improvement of blood perfusion in treatment animals was confirmed by laser Doppler perfusion imaging. Receptor tyrosine kinase profiler revealed significant phosphorylation of VEGF receptor 2 as an underlying mechanism of action. The effect of VEGF signaling was abolished upon incubation with a VEGFR2 inhibitor indicating that the effect is indeed VEGFR 2 dependent.
Low energy shock wave treatment induces angiogenesis in acute ischemia via VEGF receptor 2 stimulation and shows the same promising effects as known from chronic myocardial ischemia. It may therefore develop as an adjunct to the treatment armentarium of acute muscle ischemia in limbs and myocardium.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25093816</pmid><doi>10.1371/journal.pone.0103982</doi><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2014-08, Vol.9 (8), p.e103982-e103982 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_2014034009 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Acute Disease Angina Angiogenesis Animals Biology and life sciences Blood vessels Cardiology Cardiovascular disease Cardiovascular diseases Coronary artery disease Coronary vessels Doppler effect Energy Femoral artery Femur Gene expression Gene therapy Heart Heart attacks Heart diseases Heart surgery High-Energy Shock Waves - therapeutic use Hindlimb - blood supply Hindlimb - radiation effects Hospitals Internal medicine Ischemia Ischemia - metabolism Ischemia - therapy Kinases Laboratory animals Lithotripsy Male Medicine Medicine and Health Sciences Mice Mice, Inbred C57BL Muscles Myocardial ischemia Myocardium Neovascularization, Physiologic - radiation effects Perfusion Peripheral Vascular Diseases - metabolism Peripheral Vascular Diseases - therapy Phosphorylation Protein Kinases - metabolism Protein-tyrosine kinase receptors Quality of life Receptors Rodents Shock Shock waves Signaling Surgery Therapy Tyrosine Ultrasonic Therapy - methods Vascular endothelial growth factor Vascular Endothelial Growth Factor Receptor-2 - metabolism Vascular endothelial growth factor receptors Ventricle |
title | Low energy shock wave therapy induces angiogenesis in acute hind-limb ischemia via VEGF receptor 2 phosphorylation |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T21%3A57%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Low%20energy%20shock%20wave%20therapy%20induces%20angiogenesis%20in%20acute%20hind-limb%20ischemia%20via%20VEGF%20receptor%202%20phosphorylation&rft.jtitle=PloS%20one&rft.au=Holfeld,%20Johannes&rft.date=2014-08-05&rft.volume=9&rft.issue=8&rft.spage=e103982&rft.epage=e103982&rft.pages=e103982-e103982&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0103982&rft_dat=%3Cproquest_plos_%3E2014034009%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2014034009&rft_id=info:pmid/25093816&rft_doaj_id=oai_doaj_org_article_532048a2c68c421a9149dd7e39701682&rfr_iscdi=true |