Vascular Endothelial Growth Factor-B Acts as a Coronary Growth Factor in Transgenic Rats Without Inducing Angiogenesis, Vascular Leak, or Inflammation. Bry, M., Kivelä, R., Holopainen, T., Anisimov, A., Tammela, T., Soronen, J., Silvola, J., Saraste, A., Jeltsch, M., Korpisalo, P., Carmeliet, P., Lemström, K. B., Shibuya, M., Ylä-Herttuala, S., Alhonen, L., Mervaala, E., Andersson, L. C., Knuuti, J., & Alitalo, K. Circulation, 122(17):1725–1733, October, 2010. ![Vascular Endothelial Growth Factor-B Acts as a Coronary Growth Factor in Transgenic Rats Without Inducing Angiogenesis, Vascular Leak, or Inflammation [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Background—Vascular endothelial growth factor-B (VEGF-B) binds to VEGF receptor-1 and neuropilin-1 and is abundantly expressed in the heart, skeletal muscle, and brown fat. The biological function of VEGF-B is incompletely understood. Methods and Results—Unlike placenta growth factor, which binds to the same receptors, adeno-associated viral delivery of VEGF-B to mouse skeletal or heart muscle induced very little angiogenesis, vascular permeability, or inflammation. As previously reported for the VEGF-B167 isoform, transgenic mice and rats expressing both isoforms of VEGF-B in the myocardium developed cardiac hypertrophy yet maintained systolic function. Deletion of the VEGF receptor-1 tyrosine kinase domain or the arterial endothelial Bmx tyrosine kinase inhibited hypertrophy, whereas loss of VEGF-B interaction with neuropilin-1 had no effect. Surprisingly, in rats, the heart-specific VEGF-B transgene induced impressive growth of the epicardial coronary vessels and their branches, with large arteries also seen deep inside the subendocardial myocardium. However, VEGF-B, unlike other VEGF family members, did not induce significant capillary angiogenesis, increased permeability, or inflammatory cell recruitment. Conclusions—VEGF-B appears to be a coronary growth factor in rats but not in mice. The signals for the VEGF-B–induced cardiac hypertrophy are mediated at least in part via the endothelium. Because cardiomyocyte damage in myocardial ischemia begins in the subendocardial myocardium, the VEGF-B–induced increased arterial supply to this area could have therapeutic potential in ischemic heart disease.
@article{bry_vascular_2010,
title = {Vascular {Endothelial} {Growth} {Factor}-{B} {Acts} as a {Coronary} {Growth} {Factor} in {Transgenic} {Rats} {Without} {Inducing} {Angiogenesis}, {Vascular} {Leak}, or {Inflammation}},
volume = {122},
issn = {0009-7322, 1524-4539},
url = {http://circ.ahajournals.org/content/122/17/1725},
doi = {10.1161/CIRCULATIONAHA.110.957332},
abstract = {Background—Vascular endothelial growth factor-B (VEGF-B) binds to VEGF receptor-1 and neuropilin-1 and is abundantly expressed in the heart, skeletal muscle, and brown fat. The biological function of VEGF-B is incompletely understood.
Methods and Results—Unlike placenta growth factor, which binds to the same receptors, adeno-associated viral delivery of VEGF-B to mouse skeletal or heart muscle induced very little angiogenesis, vascular permeability, or inflammation. As previously reported for the VEGF-B167 isoform, transgenic mice and rats expressing both isoforms of VEGF-B in the myocardium developed cardiac hypertrophy yet maintained systolic function. Deletion of the VEGF receptor-1 tyrosine kinase domain or the arterial endothelial Bmx tyrosine kinase inhibited hypertrophy, whereas loss of VEGF-B interaction with neuropilin-1 had no effect. Surprisingly, in rats, the heart-specific VEGF-B transgene induced impressive growth of the epicardial coronary vessels and their branches, with large arteries also seen deep inside the subendocardial myocardium. However, VEGF-B, unlike other VEGF family members, did not induce significant capillary angiogenesis, increased permeability, or inflammatory cell recruitment.
Conclusions—VEGF-B appears to be a coronary growth factor in rats but not in mice. The signals for the VEGF-B–induced cardiac hypertrophy are mediated at least in part via the endothelium. Because cardiomyocyte damage in myocardial ischemia begins in the subendocardial myocardium, the VEGF-B–induced increased arterial supply to this area could have therapeutic potential in ischemic heart disease.},
language = {en},
number = {17},
urldate = {2015-04-30},
journal = {Circulation},
author = {Bry, Maija and Kivelä, Riikka and Holopainen, Tanja and Anisimov, Andrey and Tammela, Tuomas and Soronen, Jarkko and Silvola, Johanna and Saraste, Antti and Jeltsch, Michael and Korpisalo, Petra and Carmeliet, Peter and Lemström, Karl B. and Shibuya, Masabumi and Ylä-Herttuala, Seppo and Alhonen, Leena and Mervaala, Eero and Andersson, Leif C. and Knuuti, Juhani and Alitalo, Kari},
month = oct,
year = {2010},
pmid = {20937974},
keywords = {Coronary Disease, angiogenesis, hypertrophy},
pages = {1725--1733},
}
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C.","Knuuti, J.","Alitalo, K."],"bibdata":{"bibtype":"article","type":"article","title":"Vascular Endothelial Growth Factor-B Acts as a Coronary Growth Factor in Transgenic Rats Without Inducing Angiogenesis, Vascular Leak, or Inflammation","volume":"122","issn":"0009-7322, 1524-4539","url":"http://circ.ahajournals.org/content/122/17/1725","doi":"10.1161/CIRCULATIONAHA.110.957332","abstract":"Background—Vascular endothelial growth factor-B (VEGF-B) binds to VEGF receptor-1 and neuropilin-1 and is abundantly expressed in the heart, skeletal muscle, and brown fat. The biological function of VEGF-B is incompletely understood. Methods and Results—Unlike placenta growth factor, which binds to the same receptors, adeno-associated viral delivery of VEGF-B to mouse skeletal or heart muscle induced very little angiogenesis, vascular permeability, or inflammation. As previously reported for the VEGF-B167 isoform, transgenic mice and rats expressing both isoforms of VEGF-B in the myocardium developed cardiac hypertrophy yet maintained systolic function. Deletion of the VEGF receptor-1 tyrosine kinase domain or the arterial endothelial Bmx tyrosine kinase inhibited hypertrophy, whereas loss of VEGF-B interaction with neuropilin-1 had no effect. Surprisingly, in rats, the heart-specific VEGF-B transgene induced impressive growth of the epicardial coronary vessels and their branches, with large arteries also seen deep inside the subendocardial myocardium. However, VEGF-B, unlike other VEGF family members, did not induce significant capillary angiogenesis, increased permeability, or inflammatory cell recruitment. Conclusions—VEGF-B appears to be a coronary growth factor in rats but not in mice. The signals for the VEGF-B–induced cardiac hypertrophy are mediated at least in part via the endothelium. Because cardiomyocyte damage in myocardial ischemia begins in the subendocardial myocardium, the VEGF-B–induced increased arterial supply to this area could have therapeutic potential in ischemic heart disease.","language":"en","number":"17","urldate":"2015-04-30","journal":"Circulation","author":[{"propositions":[],"lastnames":["Bry"],"firstnames":["Maija"],"suffixes":[]},{"propositions":[],"lastnames":["Kivelä"],"firstnames":["Riikka"],"suffixes":[]},{"propositions":[],"lastnames":["Holopainen"],"firstnames":["Tanja"],"suffixes":[]},{"propositions":[],"lastnames":["Anisimov"],"firstnames":["Andrey"],"suffixes":[]},{"propositions":[],"lastnames":["Tammela"],"firstnames":["Tuomas"],"suffixes":[]},{"propositions":[],"lastnames":["Soronen"],"firstnames":["Jarkko"],"suffixes":[]},{"propositions":[],"lastnames":["Silvola"],"firstnames":["Johanna"],"suffixes":[]},{"propositions":[],"lastnames":["Saraste"],"firstnames":["Antti"],"suffixes":[]},{"propositions":[],"lastnames":["Jeltsch"],"firstnames":["Michael"],"suffixes":[]},{"propositions":[],"lastnames":["Korpisalo"],"firstnames":["Petra"],"suffixes":[]},{"propositions":[],"lastnames":["Carmeliet"],"firstnames":["Peter"],"suffixes":[]},{"propositions":[],"lastnames":["Lemström"],"firstnames":["Karl","B."],"suffixes":[]},{"propositions":[],"lastnames":["Shibuya"],"firstnames":["Masabumi"],"suffixes":[]},{"propositions":[],"lastnames":["Ylä-Herttuala"],"firstnames":["Seppo"],"suffixes":[]},{"propositions":[],"lastnames":["Alhonen"],"firstnames":["Leena"],"suffixes":[]},{"propositions":[],"lastnames":["Mervaala"],"firstnames":["Eero"],"suffixes":[]},{"propositions":[],"lastnames":["Andersson"],"firstnames":["Leif","C."],"suffixes":[]},{"propositions":[],"lastnames":["Knuuti"],"firstnames":["Juhani"],"suffixes":[]},{"propositions":[],"lastnames":["Alitalo"],"firstnames":["Kari"],"suffixes":[]}],"month":"October","year":"2010","pmid":"20937974","keywords":"Coronary Disease, angiogenesis, hypertrophy","pages":"1725–1733","bibtex":"@article{bry_vascular_2010,\n\ttitle = {Vascular {Endothelial} {Growth} {Factor}-{B} {Acts} as a {Coronary} {Growth} {Factor} in {Transgenic} {Rats} {Without} {Inducing} {Angiogenesis}, {Vascular} {Leak}, or {Inflammation}},\n\tvolume = {122},\n\tissn = {0009-7322, 1524-4539},\n\turl = {http://circ.ahajournals.org/content/122/17/1725},\n\tdoi = {10.1161/CIRCULATIONAHA.110.957332},\n\tabstract = {Background—Vascular endothelial growth factor-B (VEGF-B) binds to VEGF receptor-1 and neuropilin-1 and is abundantly expressed in the heart, skeletal muscle, and brown fat. The biological function of VEGF-B is incompletely understood.\nMethods and Results—Unlike placenta growth factor, which binds to the same receptors, adeno-associated viral delivery of VEGF-B to mouse skeletal or heart muscle induced very little angiogenesis, vascular permeability, or inflammation. As previously reported for the VEGF-B167 isoform, transgenic mice and rats expressing both isoforms of VEGF-B in the myocardium developed cardiac hypertrophy yet maintained systolic function. Deletion of the VEGF receptor-1 tyrosine kinase domain or the arterial endothelial Bmx tyrosine kinase inhibited hypertrophy, whereas loss of VEGF-B interaction with neuropilin-1 had no effect. Surprisingly, in rats, the heart-specific VEGF-B transgene induced impressive growth of the epicardial coronary vessels and their branches, with large arteries also seen deep inside the subendocardial myocardium. However, VEGF-B, unlike other VEGF family members, did not induce significant capillary angiogenesis, increased permeability, or inflammatory cell recruitment.\nConclusions—VEGF-B appears to be a coronary growth factor in rats but not in mice. The signals for the VEGF-B–induced cardiac hypertrophy are mediated at least in part via the endothelium. Because cardiomyocyte damage in myocardial ischemia begins in the subendocardial myocardium, the VEGF-B–induced increased arterial supply to this area could have therapeutic potential in ischemic heart disease.},\n\tlanguage = {en},\n\tnumber = {17},\n\turldate = {2015-04-30},\n\tjournal = {Circulation},\n\tauthor = {Bry, Maija and Kivelä, Riikka and Holopainen, Tanja and Anisimov, Andrey and Tammela, Tuomas and Soronen, Jarkko and Silvola, Johanna and Saraste, Antti and Jeltsch, Michael and Korpisalo, Petra and Carmeliet, Peter and Lemström, Karl B. and Shibuya, Masabumi and Ylä-Herttuala, Seppo and Alhonen, Leena and Mervaala, Eero and Andersson, Leif C. and Knuuti, Juhani and Alitalo, Kari},\n\tmonth = oct,\n\tyear = {2010},\n\tpmid = {20937974},\n\tkeywords = {Coronary Disease, angiogenesis, hypertrophy},\n\tpages = {1725--1733},\n}\n\n","author_short":["Bry, M.","Kivelä, R.","Holopainen, T.","Anisimov, A.","Tammela, T.","Soronen, J.","Silvola, J.","Saraste, A.","Jeltsch, M.","Korpisalo, P.","Carmeliet, P.","Lemström, K. 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