Microchimeric fetal cells are recruited to maternal kidney following injury and activate collagen type I transcription.

Bou-Gharios, George, Amin, Farhana, Hill, Peter, Nakamura, Hiroyuki, Maxwell, Patrick and Fisk, Nicholas M. (2011) Microchimeric fetal cells are recruited to maternal kidney following injury and activate collagen type I transcription.. Cells Tissues Organs, 193 6: 379-392. doi:10.1159/000321172

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Author Bou-Gharios, George
Amin, Farhana
Hill, Peter
Nakamura, Hiroyuki
Maxwell, Patrick
Fisk, Nicholas M.
Title Microchimeric fetal cells are recruited to maternal kidney following injury and activate collagen type I transcription.
Journal name Cells Tissues Organs   Check publisher's open access policy
ISSN 1422-6405
Publication date 2011-05
Year available 2010
Sub-type Article (original research)
DOI 10.1159/000321172
Volume 193
Issue 6
Start page 379
End page 392
Total pages 14
Place of publication Basel, Switzerland
Publisher S. Karger AG
Collection year 2011
Language eng
Formatted abstract
Fetal cells enter the maternal circulation from the early first trimester of pregnancy, where they persist in tissue decades later. We investigated in mice whether fetal microchimeric cells (FMCs) can be detected in maternal kidney, and whether they play a role in kidney homeostasis. FMCs were identified in vivo in two models: one an adaptive model following unilateral nephrectomy, the other an injury via unilateral renal ischaemia reperfusion. Both models were carried out in mothers that had been mated with transgenic mice expressing luciferase transgene under the control of collagen type I, and had given birth to either 1 or 3 litters. FMCs were detected by Y-probe fluorescent in situ hybridization (FISH) and bioluminescence, and the cell number quantified by real-time polymerase chain reaction. In the adaptive model, the remaining kidney showed more cells by all 3 parameters compared with the nephrectomized kidney, while ischaemia reperfusion resulted in higher levels of FMC participation in injured compared to contralateral kidneys. Bioluminescence showed that FMCs switch on collagen type I transcription implicating mesenchymal lineage cells. After injury, Y-probe in situ hydridization was found mainly in the tubular epithelial network. Finally, we compared FMCs with bone marrow cells and found similar dynamics but altered distribution within the kidney. We conclude that FMCs (1) are long-term sequelae of pregnancy and (2) are recruited to the kidney as a result of injury or adaptation, where they activate the transcriptional machinery of matrix proteins.
Copyright © 2010 S. Karger AG, Basel.
Keyword Stem cell trafficking
Fetomaternal haemorrhage
Fetal microchimerism
Tissue repair
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ
Additional Notes Published online: December 11, 2010

Document type: Journal Article
Sub-type: Article (original research)
Collections: UQ Centre for Clinical Research Publications
Official 2011 Collection
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Citation counts: TR Web of Science Citation Count  Cited 5 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 10 times in Scopus Article | Citations
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Created: Thu, 17 Feb 2011, 15:39:18 EST by Caroline Irle on behalf of UQ Centre for Clinical Research