The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
VEGF-dependent plasticity of fenestrated capillaries in the normal adult microvasculature
Abstract
Unlike during development, blood vessels in the adult are generally thought not to require VEGF for normal function. However, VEGF is a survival factor for many tumor vessels, and there are clues that some normal blood vessels may also depend on VEGF. In this study, we sought to identify which, if any, vascular beds in adult mice depend on VEGF for survival. Mice were treated with a small-molecule VEGF receptor (VEGFR) tyrosine kinase inhibitor or soluble VEGFRs for 1–3 wk. Blood vessels were assessed using immunohistochemistry or scanning or transmission electron microscopy. In a study of 17 normal organs after VEGF inhibition, we found significant capillary regression in pancreatic islets, thyroid, adrenal cortex, pituitary, choroid plexus, small-intestinal villi, and epididymal adipose tissue. The amount of regression was dose dependent and varied from organ to organ, with a maximum of 68% in thyroid, but was less in normal organs than in tumors in RIP-Tag2-transgenic mice or in Lewis lung carcinoma. VEGF-dependent capillaries were fenestrated, expressed high levels of both VEGFR-2 and VEGFR-3, and had normal pericyte coverage. Surviving capillaries in affected organs had fewer fenestrations and less VEGFR expression. All mice appeared healthy, but distinct physiological changes, including more efficient blood glucose handling, accompanied some regimens of VEGF inhibition. Strikingly, most capillaries in the thyroid grew back within 2 wk after cessation of treatment for 1 wk. Our findings of VEGF dependency of normal fenestrated capillaries and rapid regrowth after regression demonstrate the plasticity of the adult microvasculature.
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Bevacizumab plus Irinotecan, Fluorouracil, and Leucovorin for Metastatic Colorectal Cancer
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VEGF-Trap: A VEGF blocker with potent antitumor effects
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Self-citationLeptin induces vascular permeability and synergistically stimulates angiogenesis with FGF-2 and VEGF
Cao, R., Brakenhielm, E., Wahlestedt, C., Thyberg, J., & Cao, Y. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.101564798 · Cited by 446
Cited by
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Mechanisms of adverse effects of anti-VEGF therapy for cancer
Kamba, T., & McDonald, D. M. (2007) · British Journal of Cancer · doi:10.1038/sj.bjc.6603813 · Cited by 990
Self-citationFERRARA, N., DAMICO, L., SHAMS, N., LOWMAN, H., & KIM, R. (2006) · Retina · doi:10.1097/01.iae.0000242842.14624.e7 · Cited by 849
Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia
Herrmann, J. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-020-0348-1 · Cited by 747
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Metadata
- Authors
- Kamba, T., Tam, B. Y. Y., Hashizume, H., Haskell, A., Sennino, B., Mancuso, M. R., Norberg, S. M., O'Brien, S. M., Davis, R. B., Gowen, L. C., Anderson, K. D., Thurston, G., Joho, S., Springer, M. L., Kuo, C. J., & McDonald, D. M.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2006-02
- Volume
- 290
- Issue
- 2
- Pages
- H560-H576
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2132272301
- Cited by
- 775
- References
- 8
- FWCI
- 15.56
- Type
- journal article
- Language
- en
- Open access
- closed
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- Kamba, T., Tam, B. Y. Y., Hashizume, H., Haskell, A., Sennino, B., Mancuso, M. R., Norberg, S. M., O'Brien, S. M., Davis, R. B., Gowen, L. C., Anderson, K. D., Thurston, G., Joho, S., Springer, M. L., Kuo, C. J., & McDonald, D. M. (2006). VEGF-dependent plasticity of fenestrated capillaries in the normal adult microvasculature. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00133.2005
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