title: Augmented cardiac hypertrophy in response to pressure overload in mice lacking ELTD1.
abstract: BACKGROUND
  Epidermal growth factor (EGF), latrophilin and seven transmembrane domain-containing protein 1 (ELTD1) is developmentally upregulated in the heart. Little is known about the relationship between ELTD1 and cardiac diseases. Therefore, we aimed to clarify the role of ELTD1 in pressure overload-induced cardiac hypertrophy.
  
  
  RESULTS
  C57BL/6J wild-type (WT) mice and ELTD1-knockout (KO) mice were subjected to left ventricular pressure overload by descending aortic banding (AB). KO mice exhibited more unfavorable cardiac remodeling than WT mice 28 days post AB; this remodeling was characterized by aggravated cardiomyocyte hypertrophy, thickening of the ventricular walls, dilated chambers, increased fibrosis, and blunted systolic and diastolic cardiac function. Analysis of signaling pathways revealed enhanced extracellular signal-regulated kinase (ERK) and the c-Jun amino-terminal kinase (JNK) phosphorylation in response to ELTD1 deletion.
  
  
  CONCLUSIONS
  ELTD1 deficiency exacerbates cardiac hypertrophy and cardiac function induced by AB-induced pressure overload by promoting both cardiomyocyte hypertrophy and cardiac fibrosis. These effects are suggested to originate from the activation of the ERK and JNK pathways, suggesting that ELTD1 is a potential target for therapies that prevent the development of cardiac disease.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, People's Republic of China.
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Xiao
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
authors.forename: Rui
authors.initials: R
authors.lastname: Zhang
authors.forename: Guangpu
authors.initials: G
authors.lastname: Fan
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Dingsheng
authors.initials: D
authors.lastname: Jiang
authors.forename: Hongliang
authors.initials: H
authors.lastname: Li
mesh_terms: D000818:Animals; D001483:Base Sequence; D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D016022:Case-Control Studies; D017931:DNA Primers / Q000235:genetics; D005355:Fibrosis; D006333:Heart Failure / Q000378:metabolism; D006801:Humans; D020935:MAP Kinase Signaling System; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D032383:Myocytes, Cardiac / Q000473:pathology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism / Q000502:physiology
chemical_list: C428324:ADGRL4 protein, human; D017931:DNA Primers; D043562:Receptors, G-Protein-Coupled; D051057:Proto-Oncogene Proteins c-akt