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Physiol. Genomics 31: 53-62, 2007. First published June 5, 2007; doi:10.1152/physiolgenomics.00026.2007 Free Article
1094-8341/07 $8.00
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Received 6 February 2007; accepted in final form 23 May 2007.
Physiological Genomics 31:53-62 (2007)
1094-8341/07 $8.00 © 2007 American Physiological Society

Fgl2 deficiency causes neonatal death and cardiac dysfunction during embryonic and postnatal development in mice

Junwu Mu7, Dawei Qu7, Agata Bartczak5, M. James Phillips5, Justin Manuel5, Wei He5, Cheryl Koscik5, Michael Mendicino5, Li Zhang5, David A. Clark5, David R. Grant5, Peter H. Backx2,3,4,6, Gary A. Levy2,5 and S. Lee Adamson1,3,4,7

1 Departments of Obstetrics and Gynecology, University of Toronto, Toronto, Ontario, Canada
2 Department of Medicine, University of Toronto, Toronto, Ontario, Canada
3 Department of Physiology, University of Toronto, Toronto, Ontario, Canada
4 Heart and Stroke/Richard Lewar Centre, University of Toronto, Toronto, Ontario, Canada
5 Multi-Organ Transplant Program, Toronto, Ontario, Canada
6 Cardiology, University Health Network, Toronto, Ontario, Canada
7 Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada

We hypothesized that cardiac dysfunction was responsible for the high perinatal lethality that we previously reported in fibrinogen-like protein 2 (Fgl2) knockout (KO) mice. We therefore used ultrasound biomicroscopy to assess left ventricular (LV) cardiac structure and function during development in Fgl2 KO and wild-type (WT) mice. The only deaths observed between embryonic day (E)8.5 (onset of heart beating) and postnatal day (P)28 (weaning) were within 3 days after birth, when 33% of Fgl2 KO pups died. Histopathology and Doppler assessments suggested that death was due to acute congestive cardiac failure without evidence of valvular or other obvious cardiac structural abnormalities. Heart rates in Fgl2 KO embryos were significantly reduced at E8.5 and E17.5, and irregular heart rhythms were significantly more common in Fgl2 KO (21/26) than WT (2/21) embryos at E13.5. Indexes of systolic and/or diastolic cardiac function were also abnormal in KO mice at E13.5 and E17.5, in postnatal mice studied at P1, and in KO mice surviving to P28. M-mode analysis showed no difference in LV diastolic chamber dimension, although posterior wall thickness was thinner at P7 and P28 in Fgl2 KO mice. We conclude that Fgl2 deficiency is not associated with obvious structural cardiac defects but is associated with a high incidence of neonatal death as well as contractile dysfunction and rhythm abnormalities during embryonic and postnatal development in mice.

mutant; knockout; embryo; newborn; ultrasound biomicroscopy; mouse; echocardiography; fibrinogen-like protein 2; fibroleukin






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