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PPAR‐gamma is required in the myocardium for outflow tract development (699.2)
Author(s) -
Keith Benjamin,
Zhou Lun,
Xie Linglin
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.699.2
Subject(s) - endocardium , ventricle , peroxisome proliferator activated receptor , truncus arteriosus , gene knockdown , heart development , medicine , biology , embryonic stem cell , cardiology , endocrinology , tetralogy of fallot , genetics , heart disease , receptor , cell culture , gene
One‐third of congenital heart defects involve abnormalities in the development of the outflow tract (OFT). In our lab’s previous study, 100% of PPAR‐gamma heterozygote mouse embryos at embryonic day 14.5 (E14.5) showed OFT defects including ventricular septal defects (VSD), overriding aorta (OA), double outlet right ventricle (DORV), and common arterial trunk (CAT). These observations suggested that PPAR‐gamma plays a vital role in the development of the OFT. To identify the destined cell lineage for PPAR‐gamma in a specific cell lineage, we performed cre‐lox recombination technology based genetic study to knockdown PPAR‐gamma in specific cell lineages including the myocardium ( Tnt‐cre ), endocardium ( Tie2‐cre ), and the second heart field (Mef2c‐cre). We found that 33% (2/6) PPAR‐gamma Tnt‐cre/+ embryos at E13.5 had OA, but no OFT defects were observed in either PPAR‐gamma Tie2‐cre/+ or PPAR‐gamma Mef2c‐cre/+ . This data revealed that PPAR‐gamma is required in the myocardium, but not endocardium nor second heart field, for the development of the OFT. Grant Funding Source : Supported by the APS STRIDE summer undergraduate fellowship and the UND faculty seed money