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
Hauptverfasser: Heuslein, Joshua L, Meisner, Joshua K, Li, Xuanyue, Song, Ji, Vincentelli, Helena, Leiphart, Ryan J, Ames, Elizabeth G, Blackman, Brett R, Price, Richard J
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container_end_page 2365
container_issue 11
container_start_page 2354
container_title Arteriosclerosis, thrombosis, and vascular biology
container_volume 35
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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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><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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