Tumor necrosis factor-α and the early vein graft
Background Tumor necrosis factor-α (TNF-α) has been implicated in the blood vessel wall response to hemodynamic forces. We hypothesized that TNF-α activity drives neointimal hyperplasia (NIH) during vein graft arterialization and that anti-TNF-α therapy would inhibit NIH. Methods Rabbits underwent b...
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| description | Background Tumor necrosis factor-α (TNF-α) has been implicated in the blood vessel wall response to hemodynamic forces. We hypothesized that TNF-α activity drives neointimal hyperplasia (NIH) during vein graft arterialization and that anti-TNF-α therapy would inhibit NIH. Methods Rabbits underwent bilateral vein grafting using jugular vein. All distal branches except the occipital artery were unilaterally ligated to create distinct flow environments between the bilateral grafts. Vein grafts were harvested sequentially up to 28 days for TNF-α messenger RNA (mRNA) quantitation. In separate experiments, animals received short-term or long-term dosing with pegylated soluble TNF-α type I receptor (PEG sTNF-RI) or vehicle. After 14 to 28 days, grafts were analyzed for morphometry, proliferation, apoptosis, and PEG sTNF-RI distribution. Results Quantitative mRNA assay (TaqMan) revealed shear-dependent ( P < .001) and time-dependent ( P < .001) TNF-α expression. TNF-α induction was maximal at day 1 and gradually decreased over time, but was persistently elevated even 4 weeks later ( P < .001). Low shear (associated with increased NIH) resulted in significantly higher TNF-α mRNA expression ( P = .03). PEG sTNF-RI was found in high concentrations in the serum and localized to NIH. The high-flow and low-flow vein grafts from treated animals demonstrated similar volumes of NIH compared with controls. PEG-sTNF-RI had only modest impact on vascular wall cell turnover, as reflected by terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling ( P = .064) and anti-Ki-67 ( P = .12) assays. Conclusions Placement of a vein into the arterial circulation acutely upregulates TNF-α; this expression level correlates with the degree of subsequent NIH. Pharmacologic interruption of this signaling pathway has no significant impact on NIH or wall cellular proliferation/apoptosis, suggesting that early vein graft adaptations can proceed via TNF-α–independent mechanisms. |
| doi_str_mv | 10.1016/j.jvs.2006.08.049 |
| format | Article |
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Keith, MD</creator><creatorcontrib>Jiang, Zhihua, MD, PhD ; Shukla, Ankur, BS ; Miller, Brett L., BS ; Espino, Derek R., BS ; Tao, Ming, MD ; Berceli, Scott A., MD, PhD ; Ozaki, C. Keith, MD</creatorcontrib><description>Background Tumor necrosis factor-α (TNF-α) has been implicated in the blood vessel wall response to hemodynamic forces. We hypothesized that TNF-α activity drives neointimal hyperplasia (NIH) during vein graft arterialization and that anti-TNF-α therapy would inhibit NIH. Methods Rabbits underwent bilateral vein grafting using jugular vein. All distal branches except the occipital artery were unilaterally ligated to create distinct flow environments between the bilateral grafts. Vein grafts were harvested sequentially up to 28 days for TNF-α messenger RNA (mRNA) quantitation. In separate experiments, animals received short-term or long-term dosing with pegylated soluble TNF-α type I receptor (PEG sTNF-RI) or vehicle. After 14 to 28 days, grafts were analyzed for morphometry, proliferation, apoptosis, and PEG sTNF-RI distribution. Results Quantitative mRNA assay (TaqMan) revealed shear-dependent ( P < .001) and time-dependent ( P < .001) TNF-α expression. TNF-α induction was maximal at day 1 and gradually decreased over time, but was persistently elevated even 4 weeks later ( P < .001). Low shear (associated with increased NIH) resulted in significantly higher TNF-α mRNA expression ( P = .03). PEG sTNF-RI was found in high concentrations in the serum and localized to NIH. The high-flow and low-flow vein grafts from treated animals demonstrated similar volumes of NIH compared with controls. PEG-sTNF-RI had only modest impact on vascular wall cell turnover, as reflected by terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling ( P = .064) and anti-Ki-67 ( P = .12) assays. Conclusions Placement of a vein into the arterial circulation acutely upregulates TNF-α; this expression level correlates with the degree of subsequent NIH. Pharmacologic interruption of this signaling pathway has no significant impact on NIH or wall cellular proliferation/apoptosis, suggesting that early vein graft adaptations can proceed via TNF-α–independent mechanisms.</description><identifier>ISSN: 0741-5214</identifier><identifier>EISSN: 1097-6809</identifier><identifier>DOI: 10.1016/j.jvs.2006.08.049</identifier><identifier>PMID: 17210403</identifier><identifier>CODEN: JVSUES</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Apoptosis - physiology ; Biological and medical sciences ; Blood Vessel Prosthesis ; Cell Proliferation ; Dermatology ; Disease Models, Animal ; Emergency and intensive care: renal failure. Dialysis management ; Graft Survival ; Hyperplasia - metabolism ; Hyperplasia - pathology ; Intensive care medicine ; Jugular Veins - metabolism ; Jugular Veins - pathology ; Jugular Veins - transplantation ; Male ; Medical sciences ; Rabbits ; Receptors, Tumor Necrosis Factor, Type I - pharmacology ; Recombinant Proteins - pharmacology ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Surgery ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Time Factors ; Tumor Necrosis Factor Decoy Receptors - pharmacology ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Tumors of the skin and soft tissue. Premalignant lesions ; Tunica Intima - pathology ; Up-Regulation ; Vascular surgery: aorta, extremities, vena cava. Surgery of the lymphatic vessels</subject><ispartof>Journal of vascular surgery, 2007, Vol.45 (1), p.169-176</ispartof><rights>The Society for Vascular Surgery</rights><rights>2007 The Society for Vascular Surgery</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-f287b9a3f761ef47da3b91674cb60cf91fc4095f47b0f674135c2039380acbbd3</citedby><cites>FETCH-LOGICAL-c479t-f287b9a3f761ef47da3b91674cb60cf91fc4095f47b0f674135c2039380acbbd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jvs.2006.08.049$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,778,782,3539,4012,27906,27907,27908,45978</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19961638$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17210403$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Zhihua, MD, PhD</creatorcontrib><creatorcontrib>Shukla, Ankur, BS</creatorcontrib><creatorcontrib>Miller, Brett L., BS</creatorcontrib><creatorcontrib>Espino, Derek R., BS</creatorcontrib><creatorcontrib>Tao, Ming, MD</creatorcontrib><creatorcontrib>Berceli, Scott A., MD, PhD</creatorcontrib><creatorcontrib>Ozaki, C. Keith, MD</creatorcontrib><title>Tumor necrosis factor-α and the early vein graft</title><title>Journal of vascular surgery</title><addtitle>J Vasc Surg</addtitle><description>Background Tumor necrosis factor-α (TNF-α) has been implicated in the blood vessel wall response to hemodynamic forces. We hypothesized that TNF-α activity drives neointimal hyperplasia (NIH) during vein graft arterialization and that anti-TNF-α therapy would inhibit NIH. Methods Rabbits underwent bilateral vein grafting using jugular vein. All distal branches except the occipital artery were unilaterally ligated to create distinct flow environments between the bilateral grafts. Vein grafts were harvested sequentially up to 28 days for TNF-α messenger RNA (mRNA) quantitation. In separate experiments, animals received short-term or long-term dosing with pegylated soluble TNF-α type I receptor (PEG sTNF-RI) or vehicle. After 14 to 28 days, grafts were analyzed for morphometry, proliferation, apoptosis, and PEG sTNF-RI distribution. Results Quantitative mRNA assay (TaqMan) revealed shear-dependent ( P < .001) and time-dependent ( P < .001) TNF-α expression. TNF-α induction was maximal at day 1 and gradually decreased over time, but was persistently elevated even 4 weeks later ( P < .001). Low shear (associated with increased NIH) resulted in significantly higher TNF-α mRNA expression ( P = .03). PEG sTNF-RI was found in high concentrations in the serum and localized to NIH. The high-flow and low-flow vein grafts from treated animals demonstrated similar volumes of NIH compared with controls. PEG-sTNF-RI had only modest impact on vascular wall cell turnover, as reflected by terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling ( P = .064) and anti-Ki-67 ( P = .12) assays. Conclusions Placement of a vein into the arterial circulation acutely upregulates TNF-α; this expression level correlates with the degree of subsequent NIH. Pharmacologic interruption of this signaling pathway has no significant impact on NIH or wall cellular proliferation/apoptosis, suggesting that early vein graft adaptations can proceed via TNF-α–independent mechanisms.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Blood Vessel Prosthesis</subject><subject>Cell Proliferation</subject><subject>Dermatology</subject><subject>Disease Models, Animal</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Graft Survival</subject><subject>Hyperplasia - metabolism</subject><subject>Hyperplasia - pathology</subject><subject>Intensive care medicine</subject><subject>Jugular Veins - metabolism</subject><subject>Jugular Veins - pathology</subject><subject>Jugular Veins - transplantation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Rabbits</subject><subject>Receptors, Tumor Necrosis Factor, Type I - pharmacology</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Surgery</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor Decoy Receptors - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumors of the skin and soft tissue. Premalignant lesions</subject><subject>Tunica Intima - pathology</subject><subject>Up-Regulation</subject><subject>Vascular surgery: aorta, extremities, vena cava. Surgery of the lymphatic vessels</subject><issn>0741-5214</issn><issn>1097-6809</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kd-K1TAQh4Mo7nH1AbyR3uhd60yTJg2CsCz-gwUvXMG7kKYTTe1p16Q9cB7LF_GZTDkHFrzwKjD5fjPJN4w9R6gQUL4equGQqhpAVtBWIPQDtkPQqpQt6IdsB0pg2dQoLtiTlAYAxKZVj9kFqhpBAN8xvF33cywmcnFOIRXeumWO5Z_fhZ36YvlBBdk4HosDhan4Hq1fnrJH3o6Jnp3PS_b1_bvb64_lzecPn66vbkonlF5KX7eq05Z7JZG8UL3lnUaphOskOK_ROwG6yTcd-FxG3rgauOYtWNd1Pb9kr0597-L8a6W0mH1IjsbRTjSvychWoKh1k0E8gdsXUiRv7mLY23g0CGbzZAaTPZnNk4HWZE858-LcfO321N8nzmIy8PIM2OTs6KOdXEj3nNYSJW8z9-bEUVZxCBRNcoEmR32I5BbTz-G_z3j7T9qNYQp54E86UhrmNU7ZsUGTagPmy7bQbZ8gARsU3_hf38GZmQ</recordid><startdate>2007</startdate><enddate>2007</enddate><creator>Jiang, Zhihua, MD, PhD</creator><creator>Shukla, Ankur, BS</creator><creator>Miller, Brett L., BS</creator><creator>Espino, Derek R., BS</creator><creator>Tao, Ming, MD</creator><creator>Berceli, Scott A., MD, PhD</creator><creator>Ozaki, C. Keith, MD</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><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></search><sort><creationdate>2007</creationdate><title>Tumor necrosis factor-α and the early vein graft</title><author>Jiang, Zhihua, MD, PhD ; Shukla, Ankur, BS ; Miller, Brett L., BS ; Espino, Derek R., BS ; Tao, Ming, MD ; Berceli, Scott A., MD, PhD ; Ozaki, C. Keith, MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-f287b9a3f761ef47da3b91674cb60cf91fc4095f47b0f674135c2039380acbbd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Blood Vessel Prosthesis</topic><topic>Cell Proliferation</topic><topic>Dermatology</topic><topic>Disease Models, Animal</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Graft Survival</topic><topic>Hyperplasia - metabolism</topic><topic>Hyperplasia - pathology</topic><topic>Intensive care medicine</topic><topic>Jugular Veins - metabolism</topic><topic>Jugular Veins - pathology</topic><topic>Jugular Veins - transplantation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Rabbits</topic><topic>Receptors, Tumor Necrosis Factor, Type I - pharmacology</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Surgery</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Time Factors</topic><topic>Tumor Necrosis Factor Decoy Receptors - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumors of the skin and soft tissue. Premalignant lesions</topic><topic>Tunica Intima - pathology</topic><topic>Up-Regulation</topic><topic>Vascular surgery: aorta, extremities, vena cava. Surgery of the lymphatic vessels</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Zhihua, MD, PhD</creatorcontrib><creatorcontrib>Shukla, Ankur, BS</creatorcontrib><creatorcontrib>Miller, Brett L., BS</creatorcontrib><creatorcontrib>Espino, Derek R., BS</creatorcontrib><creatorcontrib>Tao, Ming, MD</creatorcontrib><creatorcontrib>Berceli, Scott A., MD, PhD</creatorcontrib><creatorcontrib>Ozaki, C. Keith, MD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><jtitle>Journal of vascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Zhihua, MD, PhD</au><au>Shukla, Ankur, BS</au><au>Miller, Brett L., BS</au><au>Espino, Derek R., BS</au><au>Tao, Ming, MD</au><au>Berceli, Scott A., MD, PhD</au><au>Ozaki, C. Keith, MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor necrosis factor-α and the early vein graft</atitle><jtitle>Journal of vascular surgery</jtitle><addtitle>J Vasc Surg</addtitle><date>2007</date><risdate>2007</risdate><volume>45</volume><issue>1</issue><spage>169</spage><epage>176</epage><pages>169-176</pages><issn>0741-5214</issn><eissn>1097-6809</eissn><coden>JVSUES</coden><abstract>Background Tumor necrosis factor-α (TNF-α) has been implicated in the blood vessel wall response to hemodynamic forces. We hypothesized that TNF-α activity drives neointimal hyperplasia (NIH) during vein graft arterialization and that anti-TNF-α therapy would inhibit NIH. Methods Rabbits underwent bilateral vein grafting using jugular vein. All distal branches except the occipital artery were unilaterally ligated to create distinct flow environments between the bilateral grafts. Vein grafts were harvested sequentially up to 28 days for TNF-α messenger RNA (mRNA) quantitation. In separate experiments, animals received short-term or long-term dosing with pegylated soluble TNF-α type I receptor (PEG sTNF-RI) or vehicle. After 14 to 28 days, grafts were analyzed for morphometry, proliferation, apoptosis, and PEG sTNF-RI distribution. Results Quantitative mRNA assay (TaqMan) revealed shear-dependent ( P < .001) and time-dependent ( P < .001) TNF-α expression. TNF-α induction was maximal at day 1 and gradually decreased over time, but was persistently elevated even 4 weeks later ( P < .001). Low shear (associated with increased NIH) resulted in significantly higher TNF-α mRNA expression ( P = .03). PEG sTNF-RI was found in high concentrations in the serum and localized to NIH. The high-flow and low-flow vein grafts from treated animals demonstrated similar volumes of NIH compared with controls. PEG-sTNF-RI had only modest impact on vascular wall cell turnover, as reflected by terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling ( P = .064) and anti-Ki-67 ( P = .12) assays. Conclusions Placement of a vein into the arterial circulation acutely upregulates TNF-α; this expression level correlates with the degree of subsequent NIH. Pharmacologic interruption of this signaling pathway has no significant impact on NIH or wall cellular proliferation/apoptosis, suggesting that early vein graft adaptations can proceed via TNF-α–independent mechanisms.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>17210403</pmid><doi>10.1016/j.jvs.2006.08.049</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Apoptosis - physiology Biological and medical sciences Blood Vessel Prosthesis Cell Proliferation Dermatology Disease Models, Animal Emergency and intensive care: renal failure. Dialysis management Graft Survival Hyperplasia - metabolism Hyperplasia - pathology Intensive care medicine Jugular Veins - metabolism Jugular Veins - pathology Jugular Veins - transplantation Male Medical sciences Rabbits Receptors, Tumor Necrosis Factor, Type I - pharmacology Recombinant Proteins - pharmacology Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Surgery Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Time Factors Tumor Necrosis Factor Decoy Receptors - pharmacology Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumors of the skin and soft tissue. Premalignant lesions Tunica Intima - pathology Up-Regulation Vascular surgery: aorta, extremities, vena cava. Surgery of the lymphatic vessels |
| title | Tumor necrosis factor-α and the early vein graft |
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