Dataset Information

Atrial ERK1/2 activation in the embryo leads to incomplete Septal closure: a novel mouse model of atrial Septal defect.

ABSTRACT: BACKGROUND:MEK1 mutation and activated MAPK signaling has been found in patients with RASopathies and abnormal cardiac development. Previous studies have suggested that regulation of fetal MAPK signaling is essential for normal cardiac development. We investigated the effect of active MEK1 overexpression on fetal atrial septal development. METHODS AND RESULTS:An inducible double transgenic (DTg) mouse model was developed in which cardiac-specific fetal expression of a constitutively active form of human MEK1 (aMEK1) was induced primarily in the atrium via the withdrawal of doxycycline from the drinking water of pregnant mice. Atrial septal defect (ASD) was found in 51% (23/45) of DTg mice. Fifty-two percent (12/23) of ASD mice died before weaning, and surviving ASD mice exhibited hypertrophic hearts with enlarged right atria and decreased fractional shorting (40?±?2% vs. 48?±?0%, p?

SUBMITTER: Yeh CC

PROVIDER: S-EPMC5702213 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Atrial ERK1/2 activation in the embryo leads to incomplete Septal closure: a novel mouse model of atrial Septal defect.

Yeh Che-Chung CC Fan Yanying Y Yang Yi-Lin YL Mann Michael J MJ

Journal of biomedical science 20171124 1

<h4>Background</h4>MEK1 mutation and activated MAPK signaling has been found in patients with RASopathies and abnormal cardiac development. Previous studies have suggested that regulation of fetal MAPK signaling is essential for normal cardiac development. We investigated the effect of active MEK1 overexpression on fetal atrial septal development.<h4>Methods and results</h4>An inducible double transgenic (DTg) mouse model was developed in which cardiac-specific fetal expression of a constitutive ...[more]

PMID: 29178881

Similar Datasets

Project description:INTRODUCTION:Change in migraine headache (MH)-preexisting MH change or development of de novo MH-are known potential complications following percutaneous closure of atrial septal defect (ASD), but consensus on a causal trigger remains elusive. OBJECTIVES:To expose potential MH triggers linked, mainly by timing and occurrence, to the emergence of de novo MH or change in preexisting MH subsequent to percutaneous ASD closure (pASDC). METHODS:The literature was systematically searched for studies available in English reporting MH status after pASDC published between January 1, 1990 and November 15, 2015. We determined the number and percentage of patients experiencing MH status change within 7?days post procedure and the cumulative total by final follow-up (Mdn?=?12?months). RESULTS:Twenty-five studies met the inclusion criteria, which accounted for a total of 1,646 pASDC patients. Pre-procedure MH prevalence was 8% (126/1,646). Change in preexisting MH occurred in a total of 72% (91/126), 12% (11/91) within 7-days after pASDC; within follow-up MH improved in 14% (18/126), resolved in 37% (47/126), but persisted in 63% (79/126). De novo MH incidence ranged between 10 (153/1,520) and 18.3% (153/836); 34% incipience (52/153) was within 7-days of pASDC; females accounted for 80% (63/79) of gender differentiated cases; of type distinguished cases, 42% (51/122) were MH without aura (MO) and 58% (71/122) were MH with aura (MA); MH improved in 10% (16/153), resolved in 24% (37/153) but persisted beyond final follow-up in 76% (116/153). Antiplatelet agents were effective modulators of MH in 44% (11/25) studies. Possible adverse MH-predisposing traits were scarce: larger ASD size reported in ~2% (39/1,646) of patients experiencing de novo MH or preexisting MH exacerbation; short aortic rim reported in three de novo MH patients; allergic response to occluder nickel alloy in four patients with MH status change from baseline (de novo or preexisting MH change not specified). INTERPRETATION:Early intensification of MH status change but later amelioration (virtually paralleling stages of endothelialization), relatively high efficacy of antiplatelet agents, and the emergence of MA as the dominant de novo MH type favor proinflammatory triggers of MH status change after pASDC.

Dataset Information

Atrial ERK1/2 activation in the embryo leads to incomplete Septal closure: a novel mouse model of atrial Septal defect.

Publications

Atrial ERK1/2 activation in the embryo leads to incomplete Septal closure: a novel mouse model of atrial Septal defect.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure