Essential roles of Meltrin β (ADAM19) in heart development

Kurohara, Kazuto; Komatsu, Kouji; Kurisaki, Tomohiro; Masuda, Aki; Irie, Naoki; Asano, Masahide; Sudo, Katsuko; Nabeshima, Yo Ichi; Iwakura, Yoichiro; Sehara-Fujisawa, Atsuko

doi:10.1016/j.ydbio.2003.10.021

Cited by 92 publications

(93 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, a group of genes involved in cardiac development (Gata4 (Kuo et al 1997, Tevosian et al 2002, Adam19 (Kurohara et al 2004), Fgf4, and Fgfr2 (Feldman et al 1995, Wang et al 2005, and Bmp4 (Liu et al 2004, Zakin & De Robertis 2004 are down- Effect of IVF on mouse preimplantation embryo regulated, and Cebpa knock outs show abnormalities in adipogenesis, hematopoiesis, hepatic, and lung morphology and premature death (Flodby et al 1996, Zhang et al 2004. It is possible that these changes are temporary and disappear, but could persist and affect long term development, extending the Barker hypothesis (Barker 1998) to the preimplantation period.…”

Section: Discussionmentioning

confidence: 99%

Effect of in vitro fertilization on gene expression and development of mouse preimplantation embryos

Giritharan¹,

Talbi²,

Donjacour³

et al. 2007

Reproduction

142

127

View full text Add to dashboard Cite

In vitro culture (IVC) of preimplantation mouse embryos is associated with changes in gene expression. It is however, not known if the method of fertilization affects the global pattern of gene expression. We compared gene expression and development of mouse blastocysts produced by in vitro fertilization (IVF) versus blastocysts fertilized in vivo and cultured in vitro from the zygote stage (IVC) versus control blastocysts flushed out of the uterus on post coital day 3.5. The global pattern of gene expression was assessed using the Affymetrix 430 2.0 chip. It appears that each method of fertilization has a unique pattern of gene expression and development. Embryos cultured in vitro had a reduction in the number of trophoblastic cells (IVF 33.5 cells, IVC 39.9 cells, and 49.6 cells in the in vivo group) and, to a lesser degree, of inner cell mass cells (12.8, 11.7, and 13.8 respectively). The inner cell mass nuclei were larger after culture in vitro (140 mm 2 , 113 mm 2 , and 86 mm 2 respectively). Although a high number of genes (1912) was statistically different in the IVF cohort when compared with the in vivo control embryos, the magnitude of the changes in gene expression were low and only a minority of genes (29 genes) was changed more than fourfold. Surprisingly, IVF embryos were different from IVC embryos (3058 genes were statistically different, but only three changed more than fourfold). Proliferation, apoptosis, and morphogenetic pathways are the most common pathways altered after IVC. Overall, IVF and embryo culture have a profound effect on gene expression pattern and phenotype of mouse preimplantation embryos.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of in vitro fertilization on gene expression and development of mouse preimplantation embryos

Giritharan¹,

Talbi²,

Donjacour³

et al. 2007

Reproduction

142

127

View full text Add to dashboard Cite

show abstract

“…This gene may play a role in cell-cell and cell-matrix interactions during spermatogenesis. The myocardial role of Adam3 is not known so far, but Adam10, Adam15 and Adam19 from the same gene family demonstrably show altered expression during cardiomyopathy (Fedak, Moravec, & McCarthy, 2006;Kurohara, Komatsu, Kurisaki, & Masuda, 2004).…”

Section: Gene Expression Alteration Due To Perfusionmentioning

confidence: 99%

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

Faragó

Kocsis

Feher

et al. 2008

Journal of Pharmacological and Toxicological Methods

View full text Add to dashboard Cite

Introduction: Although crystalloid-perfused isolated heart models are widely used in cardiovascular research, there are several limitations of these techniques. Changes in cardiac gene expression pattern due to normoxic perfusion itself have not been studied, despite its potential importance to provide useful information on limitations of this model. Therefore, here we investigated the time-dependent effect of normoxic, normothermic perfusion on global gene expression at mRNA and protein levels. Methods: Hearts from male CFLP mice were perfused according to the Langendorff technique. We assessed relative gene expression changes by DNA microarray analysis of 8000 genes after 0, 60 and 120 min perfusion. Results: Twelve genes exhibited significant up-regulation and 27 showed repression in hearts perfused for 60 or 120 min as compared to 0 min controls. Expression changes of 17 selected genes were verified and an additional 19 genes were examined by real-time quantitative PCR. Genes with altered expression included those coding for Creatin kinase, Lactate dehydrogenase, Voltage-dependent anion channel 1, a Disintegrin and Metalloprotease domain 3, Integrin alpha 7, Long-chain acyl-CoA dehydrogenase, Casein kinase II, Ketohexokinase, Chloride ion current inducer protein, Matrix metalloproteinase 2 and 9, Superoxide dismutases and Nitric oxide synthases, etc. Discussion: Our results show that normoxic crystalloid perfusion itself results in time-dependent changes in cardiac gene expression which should be considered when designing ex vivo perfusion protocols in the mouse heart to mimic cardiac pathologies as many of these genes have been suspected to influence several cardiovascular diseases.

show abstract

“…Most members of ADAM families had been recognized to function in a range of biological processes, including myoblast differentiation and growth factor secretion 7, 8. Later on, several studies revealed that ADAM family also participated in cardiovascular development9, 10, 11, 12, 13 or cardiomyopathies 9, 14, 15, 16. Notably, a previous investigation suggested that ADAM10/12/15/17 expressions were increasing in both human dilated cardiomyopathy and (or) hypertrophic obstructive cardiomyopathy 17.…”

mentioning

confidence: 99%

ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK‐AKT Signaling

Xiang

Luo

et al. 2018

JAHA

View full text Add to dashboard Cite

BackgroundCardiac hypertrophy has been recognized as an important independent risk factor for the development of heart failure and increases the risk of cardiac morbidity and mortality. A disintegrin and metalloprotease 23 (ADAM23), a member of ADAM family, is involved in cancer and neuronal differentiation. Although ADAM23 is expressed in the heart, the role of ADAM23 in the heart and in cardiac diseases remains unknown.Methods and ResultsWe observed that ADAM23 expression is decreased in both failing human hearts and hypertrophic mice hearts. Cardiac‐specific conditional ADAM23‐knockout mice significantly exhibited exacerbated cardiac hypertrophy, fibrosis, and dysfunction, whereas transgenic mice overexpressing ADAM23 in the heart exhibited reduced cardiac hypertrophy in response to pressure overload. Consistent results were also observed in angiotensin II‐induced neonatal rat cardiomyocyte hypertrophy. Mechanistically, ADAM23 exerts anti‐hypertrophic effects by specifically targeting the focal adhesion kinase‐protein kinase B (FAK‐AKT) signaling cascade. Focal adhesion kinase inactivation by inhibitor (PF‐562271) greatly reversed the detrimental effects in ADAM23‐knockout mice subjected to aortic banding.ConclusionAltogether, we identified ADAM23 as a negative regulator of cardiac hypertrophy through inhibiting focal adhesion kinase‐protein kinase B signaling pathway, which could be a promising therapeutic target for this malady.

show abstract

Essential roles of Meltrin β (ADAM19) in heart development

Cited by 92 publications

References 52 publications

Effect of in vitro fertilization on gene expression and development of mouse preimplantation embryos

Effect of in vitro fertilization on gene expression and development of mouse preimplantation embryos

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

ADAM23 in Cardiomyocyte Inhibits Cardiac Hypertrophy by Targeting FAK‐AKT Signaling

Contact Info

Product

Resources

About