Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling
BACKGROUND—We investigated the putative proangiogenic activity and molecular pathway(s) of the tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) in a model of surgically induced hindlimb ischemia. METHODS AND RESULTS—Hindlimb ischemia was induced by femoral artery ligature and an osmotic minipump was i...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2006-04, Vol.26 (4), p.773-779 |
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| creator | Waeckel, Ludovic Bignon, Jérôme Liu, Jian-Miao Markovits, Delphine Ebrahimian, Téni G Vilar, José Mees, Barend Blanc-Brude, Olivier Barateau, Véronique Le ricousse-Roussanne, Sophie Duriez, Micheline Tobelem, Gérard Wdzieczak-Bakala, Joanna Lévy, Bernard I Silvestre, Jean-Sébastien |
| description | BACKGROUND—We investigated the putative proangiogenic activity and molecular pathway(s) of the tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) in a model of surgically induced hindlimb ischemia.
METHODS AND RESULTS—Hindlimb ischemia was induced by femoral artery ligature and an osmotic minipump was implanted subcutaneously to deliver low (0.12 mg/kg per day) or high (1.2 mg/kg per day) doses of AcSDKP, for 7 or 21 days. Angiography scores, arteriole density, capillary number, and foot perfusion were increased at day 21 in the high-dose AcSDKP-treated mice (by 1.9-, 1.8-, 1.3-, and 1.6-fold, respectively) compared with control animals (P |
| doi_str_mv | 10.1161/01.ATV.0000203510.96492.14 |
| format | Article |
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METHODS AND RESULTS—Hindlimb ischemia was induced by femoral artery ligature and an osmotic minipump was implanted subcutaneously to deliver low (0.12 mg/kg per day) or high (1.2 mg/kg per day) doses of AcSDKP, for 7 or 21 days. Angiography scores, arteriole density, capillary number, and foot perfusion were increased at day 21 in the high-dose AcSDKP-treated mice (by 1.9-, 1.8-, 1.3-, and 1.6-fold, respectively) compared with control animals (P<0.05, P<0.01, P<0.01, respectively). AcSDKP treatment for 24 hours upregulated the monocyte chemoattractant protein-1 (MCP-1) mRNA and protein levels by 1.5-fold in cultured endothelial cells (P<0.01). In the ischemic hindlimb model, administration of AcSDKP also enhanced MCP-1 mRNA levels by 90-fold in ischemic leg (P<0.001) and MCP-1 plasma levels by 3-fold (P<0.001 versus untreated ischemic control mice). MCP-1 levels upregulation were associated with a 2.3-fold increase in the number of Mac3-positive cells in ischemic area of AcSDKP-treated mice (P<0.001 versus untreated animals). Interestingly, AcSDKP-induced monocyte/macrophage infiltration and postischemic neovascularization was fully blunted in MCP-1-deficient animals.
CONCLUSION—AcSDKP stimulates postischemic neovascularization through activation of a proinflammatory MCP-1-related pathway.]]></description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000203510.96492.14</identifier><identifier>PMID: 16410461</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Associated diseases and complications ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Bone Marrow Cells - pathology ; Cardiology. Vascular system ; Cell Differentiation ; Cell Line, Transformed ; Chemical Sciences ; Chemokine CCL2 - deficiency ; Chemokine CCL2 - physiology ; Diabetes. Impaired glucose tolerance ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - pathology ; Femoral Artery - pathology ; Hindlimb - blood supply ; Ischemia - drug therapy ; Ischemia - physiopathology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Monocytes - pathology ; Neovascularization, Physiologic - drug effects ; Oligopeptides - administration & dosage ; Organic chemistry ; Signal Transduction - drug effects</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2006-04, Vol.26 (4), p.773-779</ispartof><rights>2006 American Heart Association, Inc.</rights><rights>2006 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5775-89af0f204de3f7af3e448de02047df77d6bf924d3b0992a81b8fc27320b5e9cc3</citedby><cites>FETCH-LOGICAL-c5775-89af0f204de3f7af3e448de02047df77d6bf924d3b0992a81b8fc27320b5e9cc3</cites><orcidid>0000-0002-6294-9671</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17665272$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16410461$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00023244$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Waeckel, Ludovic</creatorcontrib><creatorcontrib>Bignon, Jérôme</creatorcontrib><creatorcontrib>Liu, Jian-Miao</creatorcontrib><creatorcontrib>Markovits, Delphine</creatorcontrib><creatorcontrib>Ebrahimian, Téni G</creatorcontrib><creatorcontrib>Vilar, José</creatorcontrib><creatorcontrib>Mees, Barend</creatorcontrib><creatorcontrib>Blanc-Brude, Olivier</creatorcontrib><creatorcontrib>Barateau, Véronique</creatorcontrib><creatorcontrib>Le ricousse-Roussanne, Sophie</creatorcontrib><creatorcontrib>Duriez, Micheline</creatorcontrib><creatorcontrib>Tobelem, Gérard</creatorcontrib><creatorcontrib>Wdzieczak-Bakala, Joanna</creatorcontrib><creatorcontrib>Lévy, Bernard I</creatorcontrib><creatorcontrib>Silvestre, Jean-Sébastien</creatorcontrib><title>Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description><![CDATA[BACKGROUND—We investigated the putative proangiogenic activity and molecular pathway(s) of the tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) in a model of surgically induced hindlimb ischemia.
METHODS AND RESULTS—Hindlimb ischemia was induced by femoral artery ligature and an osmotic minipump was implanted subcutaneously to deliver low (0.12 mg/kg per day) or high (1.2 mg/kg per day) doses of AcSDKP, for 7 or 21 days. Angiography scores, arteriole density, capillary number, and foot perfusion were increased at day 21 in the high-dose AcSDKP-treated mice (by 1.9-, 1.8-, 1.3-, and 1.6-fold, respectively) compared with control animals (P<0.05, P<0.01, P<0.01, respectively). AcSDKP treatment for 24 hours upregulated the monocyte chemoattractant protein-1 (MCP-1) mRNA and protein levels by 1.5-fold in cultured endothelial cells (P<0.01). In the ischemic hindlimb model, administration of AcSDKP also enhanced MCP-1 mRNA levels by 90-fold in ischemic leg (P<0.001) and MCP-1 plasma levels by 3-fold (P<0.001 versus untreated ischemic control mice). MCP-1 levels upregulation were associated with a 2.3-fold increase in the number of Mac3-positive cells in ischemic area of AcSDKP-treated mice (P<0.001 versus untreated animals). Interestingly, AcSDKP-induced monocyte/macrophage infiltration and postischemic neovascularization was fully blunted in MCP-1-deficient animals.
CONCLUSION—AcSDKP stimulates postischemic neovascularization through activation of a proinflammatory MCP-1-related pathway.]]></description><subject>Animals</subject><subject>Associated diseases and complications</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Bone Marrow Cells - pathology</subject><subject>Cardiology. Vascular system</subject><subject>Cell Differentiation</subject><subject>Cell Line, Transformed</subject><subject>Chemical Sciences</subject><subject>Chemokine CCL2 - deficiency</subject><subject>Chemokine CCL2 - physiology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - pathology</subject><subject>Femoral Artery - pathology</subject><subject>Hindlimb - blood supply</subject><subject>Ischemia - drug therapy</subject><subject>Ischemia - physiopathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monocytes - pathology</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Oligopeptides - administration & dosage</subject><subject>Organic chemistry</subject><subject>Signal Transduction - drug effects</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkduO0zAQhiMEYg_wCihCAomLFJ9iN9xVhWVXFKi0hVvLccaNwY2ztrOr5elxaUUtWR6PvvlHM39RvMZohjHH7xGeLTY_Zygfgmid0w1nDZlh9qQ4xzVhFeOUP80xEk1Vc0bOiosYf2WeEYKeF2eYM4wYx-fFuIEU1Ahjsh2UC3378cu6vBm6SUMs1z4mG3UPO6vLb-DvVdSTU8H-Ucn6odz0wU_bvvzqB68fE5TLjHqVsqJOakjlOvgEdqhweWu3g3J22L4onhnlIrw8vpfFj6tPm-V1tfr--Wa5WFW6FqKu5o0yyBDEOqBGKEOBsXkHeWAmOiNEx1vTENbRFjUNUXPczo0mghLU1tBoTS-LdwfdXjk5BrtT4VF6ZeX1YiX3uf32KGHsHmf27YEdg7-bICa5y2ODc2oAP0XJhZijvLIMfjiAOvgYA5j_yhjJvTcSYZm9kSdv5D9vJGa5-NWxy9TuoDuVHs3IwJsjkPesnAlq0DaeOMF5TQTJHDtwD94lCPG3mx4gyB6US_2-NaMc1RVBiCOWv1W-uKZ_AcTnp-0</recordid><startdate>200604</startdate><enddate>200604</enddate><creator>Waeckel, Ludovic</creator><creator>Bignon, Jérôme</creator><creator>Liu, Jian-Miao</creator><creator>Markovits, Delphine</creator><creator>Ebrahimian, Téni G</creator><creator>Vilar, José</creator><creator>Mees, Barend</creator><creator>Blanc-Brude, Olivier</creator><creator>Barateau, Véronique</creator><creator>Le ricousse-Roussanne, Sophie</creator><creator>Duriez, Micheline</creator><creator>Tobelem, Gérard</creator><creator>Wdzieczak-Bakala, Joanna</creator><creator>Lévy, Bernard I</creator><creator>Silvestre, Jean-Sébastien</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>American Heart Association</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><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-6294-9671</orcidid></search><sort><creationdate>200604</creationdate><title>Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling</title><author>Waeckel, Ludovic ; Bignon, Jérôme ; Liu, Jian-Miao ; Markovits, Delphine ; Ebrahimian, Téni G ; Vilar, José ; Mees, Barend ; Blanc-Brude, Olivier ; Barateau, Véronique ; Le ricousse-Roussanne, Sophie ; Duriez, Micheline ; Tobelem, Gérard ; Wdzieczak-Bakala, Joanna ; Lévy, Bernard I ; Silvestre, Jean-Sébastien</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5775-89af0f204de3f7af3e448de02047df77d6bf924d3b0992a81b8fc27320b5e9cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Associated diseases and complications</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Bone Marrow Cells - pathology</topic><topic>Cardiology. Vascular system</topic><topic>Cell Differentiation</topic><topic>Cell Line, Transformed</topic><topic>Chemical Sciences</topic><topic>Chemokine CCL2 - deficiency</topic><topic>Chemokine CCL2 - physiology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - pathology</topic><topic>Femoral Artery - pathology</topic><topic>Hindlimb - blood supply</topic><topic>Ischemia - drug therapy</topic><topic>Ischemia - physiopathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monocytes - pathology</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Oligopeptides - administration & dosage</topic><topic>Organic chemistry</topic><topic>Signal Transduction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Waeckel, Ludovic</creatorcontrib><creatorcontrib>Bignon, Jérôme</creatorcontrib><creatorcontrib>Liu, Jian-Miao</creatorcontrib><creatorcontrib>Markovits, Delphine</creatorcontrib><creatorcontrib>Ebrahimian, Téni G</creatorcontrib><creatorcontrib>Vilar, José</creatorcontrib><creatorcontrib>Mees, Barend</creatorcontrib><creatorcontrib>Blanc-Brude, Olivier</creatorcontrib><creatorcontrib>Barateau, Véronique</creatorcontrib><creatorcontrib>Le ricousse-Roussanne, Sophie</creatorcontrib><creatorcontrib>Duriez, Micheline</creatorcontrib><creatorcontrib>Tobelem, Gérard</creatorcontrib><creatorcontrib>Wdzieczak-Bakala, Joanna</creatorcontrib><creatorcontrib>Lévy, Bernard I</creatorcontrib><creatorcontrib>Silvestre, Jean-Sébastien</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><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Waeckel, Ludovic</au><au>Bignon, Jérôme</au><au>Liu, Jian-Miao</au><au>Markovits, Delphine</au><au>Ebrahimian, Téni G</au><au>Vilar, José</au><au>Mees, Barend</au><au>Blanc-Brude, Olivier</au><au>Barateau, Véronique</au><au>Le ricousse-Roussanne, Sophie</au><au>Duriez, Micheline</au><au>Tobelem, Gérard</au><au>Wdzieczak-Bakala, Joanna</au><au>Lévy, Bernard I</au><au>Silvestre, Jean-Sébastien</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2006-04</date><risdate>2006</risdate><volume>26</volume><issue>4</issue><spage>773</spage><epage>779</epage><pages>773-779</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract><![CDATA[BACKGROUND—We investigated the putative proangiogenic activity and molecular pathway(s) of the tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) in a model of surgically induced hindlimb ischemia.
METHODS AND RESULTS—Hindlimb ischemia was induced by femoral artery ligature and an osmotic minipump was implanted subcutaneously to deliver low (0.12 mg/kg per day) or high (1.2 mg/kg per day) doses of AcSDKP, for 7 or 21 days. Angiography scores, arteriole density, capillary number, and foot perfusion were increased at day 21 in the high-dose AcSDKP-treated mice (by 1.9-, 1.8-, 1.3-, and 1.6-fold, respectively) compared with control animals (P<0.05, P<0.01, P<0.01, respectively). AcSDKP treatment for 24 hours upregulated the monocyte chemoattractant protein-1 (MCP-1) mRNA and protein levels by 1.5-fold in cultured endothelial cells (P<0.01). In the ischemic hindlimb model, administration of AcSDKP also enhanced MCP-1 mRNA levels by 90-fold in ischemic leg (P<0.001) and MCP-1 plasma levels by 3-fold (P<0.001 versus untreated ischemic control mice). MCP-1 levels upregulation were associated with a 2.3-fold increase in the number of Mac3-positive cells in ischemic area of AcSDKP-treated mice (P<0.001 versus untreated animals). Interestingly, AcSDKP-induced monocyte/macrophage infiltration and postischemic neovascularization was fully blunted in MCP-1-deficient animals.
CONCLUSION—AcSDKP stimulates postischemic neovascularization through activation of a proinflammatory MCP-1-related pathway.]]></abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>16410461</pmid><doi>10.1161/01.ATV.0000203510.96492.14</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-6294-9671</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1079-5642 |
| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2006-04, Vol.26 (4), p.773-779 |
| issn | 1079-5642 1524-4636 |
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| source | MEDLINE; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Animals Associated diseases and complications Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Bone Marrow Cells - pathology Cardiology. Vascular system Cell Differentiation Cell Line, Transformed Chemical Sciences Chemokine CCL2 - deficiency Chemokine CCL2 - physiology Diabetes. Impaired glucose tolerance Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endothelium, Vascular - drug effects Endothelium, Vascular - pathology Femoral Artery - pathology Hindlimb - blood supply Ischemia - drug therapy Ischemia - physiopathology Medical sciences Mice Mice, Inbred C57BL Monocytes - pathology Neovascularization, Physiologic - drug effects Oligopeptides - administration & dosage Organic chemistry Signal Transduction - drug effects |
| title | Tetrapeptide AcSDKP Induces Postischemic Neovascularization Through Monocyte Chemoattractant Protein-1 Signaling |
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