In Vivo Remodelling of Vascularizing Engineered Tissues
Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue....
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Chamberlain, M. Dean [verfasserIn] West, Michael E. D. [verfasserIn] Lam, Gabrielle C. [verfasserIn] Sefton, Michael V. [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Annals of biomedical engineering - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1972, 43(2014), 5 vom: 09. Okt., Seite 1189-1200 |
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| Übergeordnetes Werk: |
volume:43 ; year:2014 ; number:5 ; day:09 ; month:10 ; pages:1189-1200 |
| Links: |
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| DOI / URN: |
10.1007/s10439-014-1146-x |
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| Katalog-ID: |
SPR010061487 |
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| 520 | |a Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue. The characteristics and dynamics of this response are slowly being elucidated, especially as they are modulated by the complex interaction between the biomaterial and cellular components of the tissue constructs and the host. This process has elements that are similar to both wound healing and tumour development, and its features are illustrated by reference to the bottom-up generation of a tissue using modular constructs. These modular constructs consist of mesenchymal stromal cells (MSC) embedded in endothelial cell (EC)-covered collagen gel rods that are a few hundred microns in size. Particular attention is paid to the role of hypoxia and macrophage recruitment, as well as the paracrine effects of the MSC and EC in this host response. | ||
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| 650 | 4 | |a HIF-1α |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Angiogenesis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Mesenchymal stromal cells |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Myeloid cells |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Macrophages |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a M1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a M2 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Host response |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a West, Michael E. D. |e verfasserin |4 aut | |
| 700 | 1 | |a Lam, Gabrielle C. |e verfasserin |4 aut | |
| 700 | 1 | |a Sefton, Michael V. |e verfasserin |4 aut | |
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10.1007/s10439-014-1146-x doi (DE-627)SPR010061487 (SPR)s10439-014-1146-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.09 bkl Chamberlain, M. Dean verfasserin aut In Vivo Remodelling of Vascularizing Engineered Tissues 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue. The characteristics and dynamics of this response are slowly being elucidated, especially as they are modulated by the complex interaction between the biomaterial and cellular components of the tissue constructs and the host. This process has elements that are similar to both wound healing and tumour development, and its features are illustrated by reference to the bottom-up generation of a tissue using modular constructs. These modular constructs consist of mesenchymal stromal cells (MSC) embedded in endothelial cell (EC)-covered collagen gel rods that are a few hundred microns in size. Particular attention is paid to the role of hypoxia and macrophage recruitment, as well as the paracrine effects of the MSC and EC in this host response. Hypoxia (dpeaa)DE-He213 HIF-1α (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Mesenchymal stromal cells (dpeaa)DE-He213 Myeloid cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 M1 (dpeaa)DE-He213 M2 (dpeaa)DE-He213 Host response (dpeaa)DE-He213 West, Michael E. D. verfasserin aut Lam, Gabrielle C. verfasserin aut Sefton, Michael V. verfasserin aut Enthalten in Annals of biomedical engineering Dordrecht [u.a.] : Springer Science + Business Media B.V, 1972 43(2014), 5 vom: 09. Okt., Seite 1189-1200 (DE-627)270424792 (DE-600)1477155-X 1573-9686 nnns volume:43 year:2014 number:5 day:09 month:10 pages:1189-1200 https://dx.doi.org/10.1007/s10439-014-1146-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.09 ASE AR 43 2014 5 09 10 1189-1200 |
| spelling |
10.1007/s10439-014-1146-x doi (DE-627)SPR010061487 (SPR)s10439-014-1146-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.09 bkl Chamberlain, M. Dean verfasserin aut In Vivo Remodelling of Vascularizing Engineered Tissues 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue. The characteristics and dynamics of this response are slowly being elucidated, especially as they are modulated by the complex interaction between the biomaterial and cellular components of the tissue constructs and the host. This process has elements that are similar to both wound healing and tumour development, and its features are illustrated by reference to the bottom-up generation of a tissue using modular constructs. These modular constructs consist of mesenchymal stromal cells (MSC) embedded in endothelial cell (EC)-covered collagen gel rods that are a few hundred microns in size. Particular attention is paid to the role of hypoxia and macrophage recruitment, as well as the paracrine effects of the MSC and EC in this host response. Hypoxia (dpeaa)DE-He213 HIF-1α (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Mesenchymal stromal cells (dpeaa)DE-He213 Myeloid cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 M1 (dpeaa)DE-He213 M2 (dpeaa)DE-He213 Host response (dpeaa)DE-He213 West, Michael E. D. verfasserin aut Lam, Gabrielle C. verfasserin aut Sefton, Michael V. verfasserin aut Enthalten in Annals of biomedical engineering Dordrecht [u.a.] : Springer Science + Business Media B.V, 1972 43(2014), 5 vom: 09. Okt., Seite 1189-1200 (DE-627)270424792 (DE-600)1477155-X 1573-9686 nnns volume:43 year:2014 number:5 day:09 month:10 pages:1189-1200 https://dx.doi.org/10.1007/s10439-014-1146-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.09 ASE AR 43 2014 5 09 10 1189-1200 |
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10.1007/s10439-014-1146-x doi (DE-627)SPR010061487 (SPR)s10439-014-1146-x-e DE-627 ger DE-627 rakwb eng 610 ASE 44.09 bkl Chamberlain, M. Dean verfasserin aut In Vivo Remodelling of Vascularizing Engineered Tissues 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue. The characteristics and dynamics of this response are slowly being elucidated, especially as they are modulated by the complex interaction between the biomaterial and cellular components of the tissue constructs and the host. This process has elements that are similar to both wound healing and tumour development, and its features are illustrated by reference to the bottom-up generation of a tissue using modular constructs. These modular constructs consist of mesenchymal stromal cells (MSC) embedded in endothelial cell (EC)-covered collagen gel rods that are a few hundred microns in size. Particular attention is paid to the role of hypoxia and macrophage recruitment, as well as the paracrine effects of the MSC and EC in this host response. Hypoxia (dpeaa)DE-He213 HIF-1α (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Mesenchymal stromal cells (dpeaa)DE-He213 Myeloid cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 M1 (dpeaa)DE-He213 M2 (dpeaa)DE-He213 Host response (dpeaa)DE-He213 West, Michael E. D. verfasserin aut Lam, Gabrielle C. verfasserin aut Sefton, Michael V. verfasserin aut Enthalten in Annals of biomedical engineering Dordrecht [u.a.] : Springer Science + Business Media B.V, 1972 43(2014), 5 vom: 09. Okt., Seite 1189-1200 (DE-627)270424792 (DE-600)1477155-X 1573-9686 nnns volume:43 year:2014 number:5 day:09 month:10 pages:1189-1200 https://dx.doi.org/10.1007/s10439-014-1146-x lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.09 ASE AR 43 2014 5 09 10 1189-1200 |
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Chamberlain, M. Dean @@aut@@ West, Michael E. D. @@aut@@ Lam, Gabrielle C. @@aut@@ Sefton, Michael V. @@aut@@ |
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610 ASE 44.09 bkl In Vivo Remodelling of Vascularizing Engineered Tissues Hypoxia (dpeaa)DE-He213 HIF-1α (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Mesenchymal stromal cells (dpeaa)DE-He213 Myeloid cells (dpeaa)DE-He213 Macrophages (dpeaa)DE-He213 M1 (dpeaa)DE-He213 M2 (dpeaa)DE-He213 Host response (dpeaa)DE-He213 |
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in vivo remodelling of vascularizing engineered tissues |
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In Vivo Remodelling of Vascularizing Engineered Tissues |
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Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue. The characteristics and dynamics of this response are slowly being elucidated, especially as they are modulated by the complex interaction between the biomaterial and cellular components of the tissue constructs and the host. This process has elements that are similar to both wound healing and tumour development, and its features are illustrated by reference to the bottom-up generation of a tissue using modular constructs. These modular constructs consist of mesenchymal stromal cells (MSC) embedded in endothelial cell (EC)-covered collagen gel rods that are a few hundred microns in size. Particular attention is paid to the role of hypoxia and macrophage recruitment, as well as the paracrine effects of the MSC and EC in this host response. |
| abstractGer |
Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue. The characteristics and dynamics of this response are slowly being elucidated, especially as they are modulated by the complex interaction between the biomaterial and cellular components of the tissue constructs and the host. This process has elements that are similar to both wound healing and tumour development, and its features are illustrated by reference to the bottom-up generation of a tissue using modular constructs. These modular constructs consist of mesenchymal stromal cells (MSC) embedded in endothelial cell (EC)-covered collagen gel rods that are a few hundred microns in size. Particular attention is paid to the role of hypoxia and macrophage recruitment, as well as the paracrine effects of the MSC and EC in this host response. |
| abstract_unstemmed |
Abstract A critical aspect of creating vascularized tissues is the remodelling that occurs in vivo, driven in large part by the host response to the tissue construct. Rather than a simple inflammatory response, a beneficial tissue remodelling response results in the formation of vascularised tissue. The characteristics and dynamics of this response are slowly being elucidated, especially as they are modulated by the complex interaction between the biomaterial and cellular components of the tissue constructs and the host. This process has elements that are similar to both wound healing and tumour development, and its features are illustrated by reference to the bottom-up generation of a tissue using modular constructs. These modular constructs consist of mesenchymal stromal cells (MSC) embedded in endothelial cell (EC)-covered collagen gel rods that are a few hundred microns in size. Particular attention is paid to the role of hypoxia and macrophage recruitment, as well as the paracrine effects of the MSC and EC in this host response. |
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| title_short |
In Vivo Remodelling of Vascularizing Engineered Tissues |
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https://dx.doi.org/10.1007/s10439-014-1146-x |
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| author2 |
West, Michael E. D. Lam, Gabrielle C. Sefton, Michael V. |
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| doi_str |
10.1007/s10439-014-1146-x |
| up_date |
2024-07-03T13:43:04.534Z |
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| score |
7.3996735 |