RGD Reference Report - Localized expression of angiopoietin 1 and 2 may explain unique characteristics of the rat testicular microvasculature. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Localized expression of angiopoietin 1 and 2 may explain unique characteristics of the rat testicular microvasculature.

Authors: Haggstrom Rudolfsson, S  Johansson, A  Franck Lissbrant, I  Wikstrom, P  Bergh, A 
Citation: Haggstrom Rudolfsson S, etal., Biol Reprod 2003 Oct;69(4):1231-7. Epub 2003 May 28.
RGD ID: 1304385
Pubmed: PMID:12773423   (View Abstract at PubMed)
DOI: DOI:10.1095/biolreprod.102.013375   (Journal Full-text)

The testicular vasculature is unique in several ways. The unfenestrated endothelial cells constitute one part of the blood-testis barrier, and testicular microvessels are normally resistant to inflammation mediators. At the same time that angiogenic factors and inflammation mediators are constitutively produced, the proportion of proliferating endothelial cells is considerably higher than in other organs, but new blood vessels are not formed. Hormonal stimulation of the testis with hCG increase endothelial cell proliferation, vascular permeability, and sensitivity to locally injected inflammation mediators. In the present study, we examined whether local expression of angiopoietin (ang) 1, an inhibitor of vascular leakage and sprouting angiogenesis, and its antagonist, ang 2, could be involved in establishing this vascular phenotype. Using reverse transcription-polymerase chain reaction and immunohistochemistry, we demonstrate that testicular vascular endothelial growth factor-A (VEGF-A), ang 1, ang 2, and the ang-receptor tie 2 are expressed in the testis and that hormonal stimulation with hCG is accompanied by increased expression of VEGF-A and ang 2. The ang 1 protein is expressed in testicular microvessels under basal conditions, and it is largely unaffected after hCG stimulation. Expression of ang 2 in microvessels, in contrast, is low under basal conditions and is up-regulated by hCG. Intratesticular injection of human recombinant ang 1 protein inhibits hCG-induced increase in vascular permeability. Injection of ang 2 in the testis increases endothelial cell proliferation and the volume of the interstitial space. We therefore suggest that ang 1 stabilizes testicular microvessels under basal conditions and that a shift in this balance caused by increased ang 2, together with increased VEGF-A, allows vascular leakage, high endothelial cell proliferation, and presumably, vascular growth after hormonal stimulation.

Objects referenced in this article
Gene Angpt1 angiopoietin 1 Rattus norvegicus

Additional Information