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Vascular endothelial growth factor and bladder from a different perspective: not only an angiogenic factor.

Forskningsöversiktsartikel
Författare Berk Burgu
Özgu Aydogdu
Publicerad i Journal of pediatric surgery
Volym 45
Nummer/häfte 2
Sidor 447-52
ISSN 1531-5037
Publiceringsår 2010
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi
Sidor 447-52
Språk en
Länkar dx.doi.org/10.1016/j.jpedsurg.2009....
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Angiogenesis Inducing Agents, pharmacology, Animals, Embryonic Development, genetics, physiology, Female, Humans, Mice, Organogenesis, genetics, physiology, Pregnancy, Urinary Bladder, embryology, Urinary Bladder Neck Obstruction, genetics, physiopathology, Vascular Endothelial Growth Factor A, genetics, physiology, Vascular Endothelial Growth Factor Receptor-1, drug effects, genetics, physiology, Vascular Endothelial Growth Factor Receptor-2, drug effects, genetics, physiology, Vascular Endothelial Growth Factors, genetics, physiology
Ämneskategorier Pediatrik, Urologi och njurmedicin, Klinisk medicin

Sammanfattning

Angiogenesis has a key role for embryonic development and is crucial in several major diseases. Molecular basis of angiogenesis has been widely investigated (J Biochem Mol Biol. 2006;39:469-478, Oncogene. 2000;19:5598-5605). In this review, vascular endothelial growth factor (VEGF) and related receptors and their key roles in embryonic bladder development are discussed. The normal VEGF expression and related angiogenesis pattern of embryonic bladder are highlighted. The VEGF family especially VEGF-A is the major player in angiogenesis as well as many other angiogenic factors and activates 2 tyrosine kinase receptors, VEGFR-1 and VEGFR-2 (J Biochem Mol Biol. 2006;39:469-478). Besides its worthy role in angiogenesis, VEGF-A also seems to participate in normal bladder development (J Urol. 2007;177:1552-1557, Br J Urol Int. 2006;98:217-225). In previous studies, we have shown that exogenous VEGF or hypoxia-induced endogenous upregulation of this protein accelerates the growth of the bladder by detrusor and urothelium hypertrophy and hyperplasia (J Urol. 2007;177:1552-1557, Br J Urol Int. 2006;98:217-225, Dev Biol. 1997;183:139-149, Neurourol Urodyn. 2004;23:342-348). This abrupt role of VEGF on detrusor muscle through a hypoxic pathway may potentially be a part of the solution for many urologic conditions such as remodeling of detrusor muscle in antenatal bladder outlet obstruction.

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