Mechanisms of Amplified Arteriogenesis in Collateral Artery Segments Exposed to Reversed Flow Direction
OBJECTIVE—Collateral arteriogenesis, the growth of existing arterial vessels to a larger diameter, is a fundamental adaptive response that is often critical for the perfusion and survival of tissues downstream of chronic arterial occlusion(s). Shear stress regulates arteriogenesis; however, the arte...
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Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2015-11, Vol.35 (11), p.2354-2365 |
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creator | Heuslein, Joshua L Meisner, Joshua K Li, Xuanyue Song, Ji Vincentelli, Helena Leiphart, Ryan J Ames, Elizabeth G Blackman, Brett R Price, Richard J |
description | OBJECTIVE—Collateral arteriogenesis, the growth of existing arterial vessels to a larger diameter, is a fundamental adaptive response that is often critical for the perfusion and survival of tissues downstream of chronic arterial occlusion(s). Shear stress regulates arteriogenesis; however, the arteriogenic significance of reversed flow direction, occurring in numerous collateral artery segments after femoral artery ligation, is unknown. Our objective was to determine if reversed flow direction in collateral artery segments differentially regulates endothelial cell signaling and arteriogenesis.
APPROACH AND RESULTS—Collateral segments experiencing reversed flow direction after femoral artery ligation in C57BL/6 mice exhibit increased pericollateral macrophage recruitment, amplified arteriogenesis (30% diameter and 2.8-fold conductance increases), and remarkably permanent (12 weeks post femoral artery ligation) remodeling. Genome-wide transcriptional analyses on human umbilical vein endothelial cells exposed to reversed flow conditions mimicking those occurring in vivo yielded 10-fold more significantly regulated transcripts, as well as enhanced activation of upstream regulators (nuclear factor κB [NFκB], vascular endothelial growth factor, fibroblast growth factor-2, and transforming growth factor-β) and arteriogenic canonical pathways (protein kinase A, phosphodiesterase, and mitogen-activated protein kinase). Augmented expression of key proarteriogenic molecules (Kruppel-like factor 2 [KLF2], intercellular adhesion molecule 1, and endothelial nitric oxide synthase) was also verified by quantitative real-time polymerase chain reaction, leading us to test whether intercellular adhesion molecule 1 or endothelial nitric oxide synthase regulate amplified arteriogenesis in flow-reversed collateral segments in vivo. Interestingly, enhanced pericollateral macrophage recruitment and amplified arteriogenesis was attenuated in flow-reversed collateral segments after femoral artery ligation in intercellular adhesion molecule 1 mice; however, endothelial nitric oxide synthase mice showed no such differences.
CONCLUSIONS—Reversed flow leads to a broad amplification of proarteriogenic endothelial signaling and a sustained intercellular adhesion molecule 1–dependent augmentation of arteriogenesis. Further investigation of the endothelial mechanotransduction pathways activated by reversed flow may lead to more effective and durable therapeutic options for arterial occlus |
doi_str_mv | 10.1161/ATVBAHA.115.305775 |
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APPROACH AND RESULTS—Collateral segments experiencing reversed flow direction after femoral artery ligation in C57BL/6 mice exhibit increased pericollateral macrophage recruitment, amplified arteriogenesis (30% diameter and 2.8-fold conductance increases), and remarkably permanent (12 weeks post femoral artery ligation) remodeling. Genome-wide transcriptional analyses on human umbilical vein endothelial cells exposed to reversed flow conditions mimicking those occurring in vivo yielded 10-fold more significantly regulated transcripts, as well as enhanced activation of upstream regulators (nuclear factor κB [NFκB], vascular endothelial growth factor, fibroblast growth factor-2, and transforming growth factor-β) and arteriogenic canonical pathways (protein kinase A, phosphodiesterase, and mitogen-activated protein kinase). Augmented expression of key proarteriogenic molecules (Kruppel-like factor 2 [KLF2], intercellular adhesion molecule 1, and endothelial nitric oxide synthase) was also verified by quantitative real-time polymerase chain reaction, leading us to test whether intercellular adhesion molecule 1 or endothelial nitric oxide synthase regulate amplified arteriogenesis in flow-reversed collateral segments in vivo. Interestingly, enhanced pericollateral macrophage recruitment and amplified arteriogenesis was attenuated in flow-reversed collateral segments after femoral artery ligation in intercellular adhesion molecule 1 mice; however, endothelial nitric oxide synthase mice showed no such differences.
CONCLUSIONS—Reversed flow leads to a broad amplification of proarteriogenic endothelial signaling and a sustained intercellular adhesion molecule 1–dependent augmentation of arteriogenesis. Further investigation of the endothelial mechanotransduction pathways activated by reversed flow may lead to more effective and durable therapeutic options for arterial occlusive diseases.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/ATVBAHA.115.305775</identifier><identifier>PMID: 26338297</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Animals ; Arteries - metabolism ; Arteries - pathology ; Arteries - physiopathology ; Blood Flow Velocity ; Cells, Cultured ; Collateral Circulation ; Disease Models, Animal ; Femoral Artery - physiopathology ; Femoral Artery - surgery ; Gene Expression Regulation ; Hindlimb ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - metabolism ; Ischemia - genetics ; Ischemia - metabolism ; Ischemia - pathology ; Ischemia - physiopathology ; Ligation ; Macrophages - metabolism ; Male ; Mechanotransduction, Cellular ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Skeletal - blood supply ; Neovascularization, Physiologic ; NF-kappa B - genetics ; NF-kappa B - metabolism ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Regional Blood Flow ; Stress, Mechanical ; Time Factors ; Vascular Remodeling</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2015-11, Vol.35 (11), p.2354-2365</ispartof><rights>2015 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3945-63fc373c956a696ad289471e1e5e418085aa9264b1f1c7e23d08803d0d7ff1ec3</citedby><cites>FETCH-LOGICAL-c3945-63fc373c956a696ad289471e1e5e418085aa9264b1f1c7e23d08803d0d7ff1ec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26338297$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Heuslein, Joshua L</creatorcontrib><creatorcontrib>Meisner, Joshua K</creatorcontrib><creatorcontrib>Li, Xuanyue</creatorcontrib><creatorcontrib>Song, Ji</creatorcontrib><creatorcontrib>Vincentelli, Helena</creatorcontrib><creatorcontrib>Leiphart, Ryan J</creatorcontrib><creatorcontrib>Ames, Elizabeth G</creatorcontrib><creatorcontrib>Blackman, Brett R</creatorcontrib><creatorcontrib>Price, Richard J</creatorcontrib><title>Mechanisms of Amplified Arteriogenesis in Collateral Artery Segments Exposed to Reversed Flow Direction</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—Collateral arteriogenesis, the growth of existing arterial vessels to a larger diameter, is a fundamental adaptive response that is often critical for the perfusion and survival of tissues downstream of chronic arterial occlusion(s). Shear stress regulates arteriogenesis; however, the arteriogenic significance of reversed flow direction, occurring in numerous collateral artery segments after femoral artery ligation, is unknown. Our objective was to determine if reversed flow direction in collateral artery segments differentially regulates endothelial cell signaling and arteriogenesis.
APPROACH AND RESULTS—Collateral segments experiencing reversed flow direction after femoral artery ligation in C57BL/6 mice exhibit increased pericollateral macrophage recruitment, amplified arteriogenesis (30% diameter and 2.8-fold conductance increases), and remarkably permanent (12 weeks post femoral artery ligation) remodeling. Genome-wide transcriptional analyses on human umbilical vein endothelial cells exposed to reversed flow conditions mimicking those occurring in vivo yielded 10-fold more significantly regulated transcripts, as well as enhanced activation of upstream regulators (nuclear factor κB [NFκB], vascular endothelial growth factor, fibroblast growth factor-2, and transforming growth factor-β) and arteriogenic canonical pathways (protein kinase A, phosphodiesterase, and mitogen-activated protein kinase). Augmented expression of key proarteriogenic molecules (Kruppel-like factor 2 [KLF2], intercellular adhesion molecule 1, and endothelial nitric oxide synthase) was also verified by quantitative real-time polymerase chain reaction, leading us to test whether intercellular adhesion molecule 1 or endothelial nitric oxide synthase regulate amplified arteriogenesis in flow-reversed collateral segments in vivo. Interestingly, enhanced pericollateral macrophage recruitment and amplified arteriogenesis was attenuated in flow-reversed collateral segments after femoral artery ligation in intercellular adhesion molecule 1 mice; however, endothelial nitric oxide synthase mice showed no such differences.
CONCLUSIONS—Reversed flow leads to a broad amplification of proarteriogenic endothelial signaling and a sustained intercellular adhesion molecule 1–dependent augmentation of arteriogenesis. Further investigation of the endothelial mechanotransduction pathways activated by reversed flow may lead to more effective and durable therapeutic options for arterial occlusive diseases.</description><subject>Animals</subject><subject>Arteries - metabolism</subject><subject>Arteries - pathology</subject><subject>Arteries - physiopathology</subject><subject>Blood Flow Velocity</subject><subject>Cells, Cultured</subject><subject>Collateral Circulation</subject><subject>Disease Models, Animal</subject><subject>Femoral Artery - physiopathology</subject><subject>Femoral Artery - surgery</subject><subject>Gene Expression Regulation</subject><subject>Hindlimb</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Ischemia - genetics</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - pathology</subject><subject>Ischemia - physiopathology</subject><subject>Ligation</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mechanotransduction, Cellular</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Neovascularization, Physiologic</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Regional Blood Flow</subject><subject>Stress, Mechanical</subject><subject>Time Factors</subject><subject>Vascular Remodeling</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kDtv2zAUhYmiQZ3XH-hQcOyihG9Ko-omcQAHAdokq0BTVzZbSnRJuU7-fRjI7ZiF98FzDi4-hD5TckGpopf1w9O3elHnQV5wIrWWH9AxlUwUQnH1MfdEV4VUgs3QSUq_CCGCMfIJzZjivGSVPkbrO7AbM7jUJxw6XPdb7zoHLa7jCNGFNQyQXMJuwPPgvclL46fPF_wT1j0MY8JXz9uQsmkM-Af8hfjWX_uwx99dBDu6MJyho874BOeHeooer68e5otieX9zO6-XheWVkIXineWa20oqoyplWlZWQlOgIEHQkpTSmIopsaIdtRoYb0lZkvy2uusoWH6Kvk652xj-7CCNTe-ShXz5AGGXGqqZFlwxJrKUTVIbQ0oRumYbXW_iS0NJ8wa4OQDOg2wmwNn05ZC_W_XQ_rf8I5oFahLsg8-Q0m-_20NsNmD8uHkv-RXWmoh6</recordid><startdate>201511</startdate><enddate>201511</enddate><creator>Heuslein, Joshua L</creator><creator>Meisner, Joshua K</creator><creator>Li, Xuanyue</creator><creator>Song, Ji</creator><creator>Vincentelli, Helena</creator><creator>Leiphart, Ryan J</creator><creator>Ames, Elizabeth G</creator><creator>Blackman, Brett R</creator><creator>Price, Richard J</creator><general>American Heart Association, Inc</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></search><sort><creationdate>201511</creationdate><title>Mechanisms of Amplified Arteriogenesis in Collateral Artery Segments Exposed to Reversed Flow Direction</title><author>Heuslein, Joshua L ; Meisner, Joshua K ; Li, Xuanyue ; Song, Ji ; Vincentelli, Helena ; Leiphart, Ryan J ; Ames, Elizabeth G ; Blackman, Brett R ; Price, Richard J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3945-63fc373c956a696ad289471e1e5e418085aa9264b1f1c7e23d08803d0d7ff1ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Arteries - metabolism</topic><topic>Arteries - pathology</topic><topic>Arteries - physiopathology</topic><topic>Blood Flow Velocity</topic><topic>Cells, Cultured</topic><topic>Collateral Circulation</topic><topic>Disease Models, Animal</topic><topic>Femoral Artery - physiopathology</topic><topic>Femoral Artery - surgery</topic><topic>Gene Expression Regulation</topic><topic>Hindlimb</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Ischemia - genetics</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - pathology</topic><topic>Ischemia - physiopathology</topic><topic>Ligation</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Mechanotransduction, Cellular</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Neovascularization, Physiologic</topic><topic>NF-kappa B - genetics</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Regional Blood Flow</topic><topic>Stress, Mechanical</topic><topic>Time Factors</topic><topic>Vascular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Heuslein, Joshua L</creatorcontrib><creatorcontrib>Meisner, Joshua K</creatorcontrib><creatorcontrib>Li, Xuanyue</creatorcontrib><creatorcontrib>Song, Ji</creatorcontrib><creatorcontrib>Vincentelli, Helena</creatorcontrib><creatorcontrib>Leiphart, Ryan J</creatorcontrib><creatorcontrib>Ames, Elizabeth G</creatorcontrib><creatorcontrib>Blackman, Brett R</creatorcontrib><creatorcontrib>Price, Richard J</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><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Heuslein, Joshua L</au><au>Meisner, Joshua K</au><au>Li, Xuanyue</au><au>Song, Ji</au><au>Vincentelli, Helena</au><au>Leiphart, Ryan J</au><au>Ames, Elizabeth G</au><au>Blackman, Brett R</au><au>Price, Richard J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of Amplified Arteriogenesis in Collateral Artery Segments Exposed to Reversed Flow Direction</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2015-11</date><risdate>2015</risdate><volume>35</volume><issue>11</issue><spage>2354</spage><epage>2365</epage><pages>2354-2365</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><abstract>OBJECTIVE—Collateral arteriogenesis, the growth of existing arterial vessels to a larger diameter, is a fundamental adaptive response that is often critical for the perfusion and survival of tissues downstream of chronic arterial occlusion(s). Shear stress regulates arteriogenesis; however, the arteriogenic significance of reversed flow direction, occurring in numerous collateral artery segments after femoral artery ligation, is unknown. Our objective was to determine if reversed flow direction in collateral artery segments differentially regulates endothelial cell signaling and arteriogenesis.
APPROACH AND RESULTS—Collateral segments experiencing reversed flow direction after femoral artery ligation in C57BL/6 mice exhibit increased pericollateral macrophage recruitment, amplified arteriogenesis (30% diameter and 2.8-fold conductance increases), and remarkably permanent (12 weeks post femoral artery ligation) remodeling. Genome-wide transcriptional analyses on human umbilical vein endothelial cells exposed to reversed flow conditions mimicking those occurring in vivo yielded 10-fold more significantly regulated transcripts, as well as enhanced activation of upstream regulators (nuclear factor κB [NFκB], vascular endothelial growth factor, fibroblast growth factor-2, and transforming growth factor-β) and arteriogenic canonical pathways (protein kinase A, phosphodiesterase, and mitogen-activated protein kinase). Augmented expression of key proarteriogenic molecules (Kruppel-like factor 2 [KLF2], intercellular adhesion molecule 1, and endothelial nitric oxide synthase) was also verified by quantitative real-time polymerase chain reaction, leading us to test whether intercellular adhesion molecule 1 or endothelial nitric oxide synthase regulate amplified arteriogenesis in flow-reversed collateral segments in vivo. Interestingly, enhanced pericollateral macrophage recruitment and amplified arteriogenesis was attenuated in flow-reversed collateral segments after femoral artery ligation in intercellular adhesion molecule 1 mice; however, endothelial nitric oxide synthase mice showed no such differences.
CONCLUSIONS—Reversed flow leads to a broad amplification of proarteriogenic endothelial signaling and a sustained intercellular adhesion molecule 1–dependent augmentation of arteriogenesis. Further investigation of the endothelial mechanotransduction pathways activated by reversed flow may lead to more effective and durable therapeutic options for arterial occlusive diseases.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>26338297</pmid><doi>10.1161/ATVBAHA.115.305775</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Arteries - metabolism Arteries - pathology Arteries - physiopathology Blood Flow Velocity Cells, Cultured Collateral Circulation Disease Models, Animal Femoral Artery - physiopathology Femoral Artery - surgery Gene Expression Regulation Hindlimb Human Umbilical Vein Endothelial Cells - metabolism Humans Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - metabolism Ischemia - genetics Ischemia - metabolism Ischemia - pathology Ischemia - physiopathology Ligation Macrophages - metabolism Male Mechanotransduction, Cellular Mice, Inbred C57BL Mice, Knockout Muscle, Skeletal - blood supply Neovascularization, Physiologic NF-kappa B - genetics NF-kappa B - metabolism Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism Regional Blood Flow Stress, Mechanical Time Factors Vascular Remodeling |
title | Mechanisms of Amplified Arteriogenesis in Collateral Artery Segments Exposed to Reversed Flow Direction |
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