Publication

Endoglin haploinsufficiency attenuates radiation-induced deterioration of kidney function in mice

Scharpfenecker, M., Floot, B., Russell, N. S., Coppes, R. P. & Stewart, F. A., Sep-2013, In : Radiotherapy and Oncology. 108, 3, p. 464-468 5 p.

Research output: Contribution to journalArticleAcademicpeer-review

  • Marion Scharpfenecker
  • Ben Floot
  • Nicola S. Russell
  • Rob P. Coppes
  • Fiona A. Stewart

Background and Purpose: Endoglin is a transforming growth receptor beta (TGF-beta) co-receptor, which plays a crucial role in the development of late normal tissue damage. Mice with halved endoglin levels (Eng(+/-) mice) develop less inflammation, vascular damage and fibrosis after kidney irradiation compared to their wild type littermates (Eng(+/+) mice). This study was aimed at investigating whether reduced tissue damage in Eng(+/-) mice also results in superior kidney function.

Material and Methods: Kidneys of Eng(+/+) and Eng(+/-) mice were irradiated with a single dose of 14 Gy. Functional kidney parameters and kidney histology were analysed at 20, 30 and 40 weeks after irradiation.

Results: Eng(+/-) mice displayed improved kidney parameters (haematocrit, BUN) compared to Eng(+/+) mice at 40 weeks after irradiation. Irradiation of Eng(+/+) kidneys damaged the vascular network and led to an increase in PDGFR-beta positive cells, indicative of fibrosis-promoting myofibroblasts. Compared to Eng(+/+) kidneys, vascular perfusion and number of PDGFR-beta positive cells were reduced in Eng(+/-) control mice; however, this did not further deteriorate after irradiation.

Conclusions: Taken together, we show that not only kidney morphology, but also kidney function is improved after irradiation in Eng(+/-) compared to Eng(+/+) mice. (C) 2013 Elsevier Ireland Ltd. All rights reserved. Radiotherapy and Oncology 108 (2013) 464-468

Original languageEnglish
Pages (from-to)464-468
Number of pages5
JournalRadiotherapy and Oncology
Volume108
Issue number3
Publication statusPublished - Sep-2013

    Keywords

  • Endoglin, Pericytes, Vasculature, Perfusion, Fibrosis, Kidney, HEREDITARY HEMORRHAGIC TELANGIECTASIA, ANGIOGENESIS, FIBROSIS, PERICYTES, GROWTH, INJURY, MODEL

ID: 5992954