Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury
Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current stu...
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| Autor*in: |
Herring, Brian Paul [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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| Anmerkung: |
© Herring et al.; licensee BioMed Central Ltd. 2014 |
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| Übergeordnetes Werk: |
Enthalten in: Journal of angiogenesis research - London : BioMed Central, 2009, 6(2014), 1 vom: 01. Okt. |
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| Übergeordnetes Werk: |
volume:6 ; year:2014 ; number:1 ; day:01 ; month:10 |
| Links: |
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| DOI / URN: |
10.1186/2045-824X-6-21 |
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SPR030902045 |
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| 520 | |a Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. | ||
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| 650 | 4 | |a Neointima |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Smooth muscle α-actin |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Hoggatt, April M |4 aut | |
| 700 | 1 | |a Burlak, Christopher |4 aut | |
| 700 | 1 | |a Offermanns, Stefan |4 aut | |
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10.1186/2045-824X-6-21 doi (DE-627)SPR030902045 (SPR)2045-824X-6-21-e DE-627 ger DE-627 rakwb eng Herring, Brian Paul verfasserin aut Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Herring et al.; licensee BioMed Central Ltd. 2014 Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. Vascular smooth muscle (dpeaa)DE-He213 Neointima (dpeaa)DE-He213 Smooth muscle myosin (dpeaa)DE-He213 Smooth muscle α-actin (dpeaa)DE-He213 Hoggatt, April M aut Burlak, Christopher aut Offermanns, Stefan aut Enthalten in Journal of angiogenesis research London : BioMed Central, 2009 6(2014), 1 vom: 01. Okt. (DE-627)609775553 (DE-600)2516062-X 2040-2384 nnns volume:6 year:2014 number:1 day:01 month:10 https://dx.doi.org/10.1186/2045-824X-6-21 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 6 2014 1 01 10 |
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10.1186/2045-824X-6-21 doi (DE-627)SPR030902045 (SPR)2045-824X-6-21-e DE-627 ger DE-627 rakwb eng Herring, Brian Paul verfasserin aut Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Herring et al.; licensee BioMed Central Ltd. 2014 Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. Vascular smooth muscle (dpeaa)DE-He213 Neointima (dpeaa)DE-He213 Smooth muscle myosin (dpeaa)DE-He213 Smooth muscle α-actin (dpeaa)DE-He213 Hoggatt, April M aut Burlak, Christopher aut Offermanns, Stefan aut Enthalten in Journal of angiogenesis research London : BioMed Central, 2009 6(2014), 1 vom: 01. Okt. (DE-627)609775553 (DE-600)2516062-X 2040-2384 nnns volume:6 year:2014 number:1 day:01 month:10 https://dx.doi.org/10.1186/2045-824X-6-21 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 6 2014 1 01 10 |
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10.1186/2045-824X-6-21 doi (DE-627)SPR030902045 (SPR)2045-824X-6-21-e DE-627 ger DE-627 rakwb eng Herring, Brian Paul verfasserin aut Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Herring et al.; licensee BioMed Central Ltd. 2014 Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. Vascular smooth muscle (dpeaa)DE-He213 Neointima (dpeaa)DE-He213 Smooth muscle myosin (dpeaa)DE-He213 Smooth muscle α-actin (dpeaa)DE-He213 Hoggatt, April M aut Burlak, Christopher aut Offermanns, Stefan aut Enthalten in Journal of angiogenesis research London : BioMed Central, 2009 6(2014), 1 vom: 01. Okt. (DE-627)609775553 (DE-600)2516062-X 2040-2384 nnns volume:6 year:2014 number:1 day:01 month:10 https://dx.doi.org/10.1186/2045-824X-6-21 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 6 2014 1 01 10 |
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10.1186/2045-824X-6-21 doi (DE-627)SPR030902045 (SPR)2045-824X-6-21-e DE-627 ger DE-627 rakwb eng Herring, Brian Paul verfasserin aut Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Herring et al.; licensee BioMed Central Ltd. 2014 Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. Vascular smooth muscle (dpeaa)DE-He213 Neointima (dpeaa)DE-He213 Smooth muscle myosin (dpeaa)DE-He213 Smooth muscle α-actin (dpeaa)DE-He213 Hoggatt, April M aut Burlak, Christopher aut Offermanns, Stefan aut Enthalten in Journal of angiogenesis research London : BioMed Central, 2009 6(2014), 1 vom: 01. Okt. (DE-627)609775553 (DE-600)2516062-X 2040-2384 nnns volume:6 year:2014 number:1 day:01 month:10 https://dx.doi.org/10.1186/2045-824X-6-21 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 6 2014 1 01 10 |
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10.1186/2045-824X-6-21 doi (DE-627)SPR030902045 (SPR)2045-824X-6-21-e DE-627 ger DE-627 rakwb eng Herring, Brian Paul verfasserin aut Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Herring et al.; licensee BioMed Central Ltd. 2014 Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. Vascular smooth muscle (dpeaa)DE-He213 Neointima (dpeaa)DE-He213 Smooth muscle myosin (dpeaa)DE-He213 Smooth muscle α-actin (dpeaa)DE-He213 Hoggatt, April M aut Burlak, Christopher aut Offermanns, Stefan aut Enthalten in Journal of angiogenesis research London : BioMed Central, 2009 6(2014), 1 vom: 01. Okt. (DE-627)609775553 (DE-600)2516062-X 2040-2384 nnns volume:6 year:2014 number:1 day:01 month:10 https://dx.doi.org/10.1186/2045-824X-6-21 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 6 2014 1 01 10 |
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Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. 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previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury |
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Previously differentiated medial vascular smooth muscle cells contribute to neointima formation following vascular injury |
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Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. © Herring et al.; licensee BioMed Central Ltd. 2014 |
| abstractGer |
Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. © Herring et al.; licensee BioMed Central Ltd. 2014 |
| abstract_unstemmed |
Background The origins of neointimal smooth muscle cells that arise following vascular injury remains controversial. Studies have suggested that these cells may arise from previously differentiated medial vascular smooth muscle cells, resident stem cells or blood born progenitors. In the current study we examined the contribution of the previously differentiated vascular smooth muscle cells to the neointima that forms following carotid artery ligation. Methods We utilized transgenic mice harboring a cre recombinase-dependent reporter gene (mTmG). These mice express membrane targeted tandem dimer Tomato (mTomato) prior to cre-mediated excision and membrane targeted EGFP (mEGFP) following excision. The mTmG mice were crossed with transgenic mice expressing either smooth muscle myosin heavy chain (Myh11) or smooth muscle α-actin (Acta2) driven tamoxifen regulated cre recombinase. Following treatment of adult mice with tamoxifen these mice express mEGFP exclusively in differentiated smooth muscle cells. Subsequently vascular injury was induced in the mice by carotid artery ligation and the contribution of mEGFP positive cells to the neointima determined. Results Analysis of the cellular composition of the neointima that forms following injury revealed that mEGFP positive cells derived from either Mhy11 or Acta2 tagged medial vascular smooth muscle cells contribute to the majority of neointima formation (79 ± 17% and 81 ± 12%, respectively). Conclusion These data demonstrate that the majority of the neointima that forms following carotid ligation is derived from previously differentiated medial vascular smooth muscle cells. © Herring et al.; licensee BioMed Central Ltd. 2014 |
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Hoggatt, April M Burlak, Christopher Offermanns, Stefan |
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