<i>Bmp2</i> and <i>Bmp4</i> genetically interact to support multiple aspects of mouse development including functional heart development

Uchimura, Takashi; Komatsu, Yoshihiro; Tanaka, Momo; McCann, Kelly L.; Mishina, Yuji

doi:10.1002/dvg.20511

Cited by 51 publications

(48 citation statements)

References 55 publications

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“…Several studies revealed that there was interaction between BMP2 and BMP4. 16,17 We found that BMP4 treatment did not affect BMP2 protein expression in cardiomyocytes ( Figure S11C). …”

Section: Bmp4 Induces Cardiomyocyte Hypertrophy and Apoptosis Throughmentioning

confidence: 92%

Bone Morphogenetic Protein-4 Mediates Cardiac Hypertrophy, Apoptosis, and Fibrosis in Experimentally Pathological Cardiac Hypertrophy

et al. 2013

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Identifying the key factor mediating pathological cardiac hypertrophy is critically important for developing the strategy to protect against heart failure. Bone morphogenetic protein-4 (BMP4) is a mechanosensitive and proinflammatory gene. In this study, we investigated the role of BMP4 in cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. The in vivo pathological cardiac hypertrophy models were induced by pressure-overload and angiotensin (Ang) II constant infusion in mice, and the in vitro model was induced by Ang II exposure to cultured cardiomyocytes. The expression of BMP4 increased in pressure overload, Ang II constant infusion-induced pathological cardiac hypertrophy, but not in swimming exercise-induced physiological cardiac hypertrophy in mice. BMP4 expression also increased in Ang II–induced cardiomyocyte hypertrophy in vitro. In turn, BMP4 induced cardiomyocyte hypertrophy, apoptosis, and cardiac fibrosis, and these pathological consequences were inhibited by the treatment with BMP4 inhibitors noggin and DMH1. Moreover, Ang II–induced cardiomyocyte hypertrophy was inhibited by BMP4 inhibitors. The underlying mechanism that BMP4-induced cardiomyocyte hypertrophy and apoptosis was through increasing NADPH oxidase 4 expression and reactive oxygen species-dependent pathways. Lentivirus-mediated overexpression of BMP4 recapitulated hypertrophy and apoptosis in cultured cardiomyocytes. BMP4 inhibitor DMH1 inhibited pressure overload–induced cardiac hypertrophy in mice in vivo. The plasma BMP4 level of heart failure patients was increased compared with that of subjects without heart failure. In summary, we conclude that BMP4 is a mediator and novel therapeutic target for pathological cardiac hypertrophy.

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“…Several studies revealed that there was interaction between BMP2 and BMP4. 16,17 We found that BMP4 treatment did not affect BMP2 protein expression in cardiomyocytes ( Figure S11C). …”

Section: Bmp4 Induces Cardiomyocyte Hypertrophy and Apoptosis Throughmentioning

confidence: 92%

Bone Morphogenetic Protein-4 Mediates Cardiac Hypertrophy, Apoptosis, and Fibrosis in Experimentally Pathological Cardiac Hypertrophy

et al. 2013

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“…40 Both genes are highly conserved, with over 90% similarity in mature proteins. 41 There is also a possible biological explanation for height in infants/children in early childhood by PTPN7. PTPN7 is a member of the PTP family.…”

Section: Discussionmentioning

confidence: 99%

Genetic variants that affect length/height in infancy/early childhood in Vietnamese-Korean families

et al. 2010

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To identify genetic factors that influence height in infancy/early childhood , a family-based genome-wide association study was conducted using 269 888 single-nucleotide polymorphisms (SNPs) in 165 families composed of a Korean father, a Vietnamese mother and Vietnamese-Korean offspring in the International Marriage-based Immigrant Cohort in Korea. In a single-SNP-based analysis, the six SNPs in or near genes MAF, MAGI2, BMP4 and PTPN7 showed consistent suggestive associations at all height standard deviation scores using Korean, World Health Organization and Vietnamese growth references. Analyzing the haplotypes for the genes, haplotype blocks were found to be significantly associated with height. Similar to the results of a contiguous haplotype analysis using tag SNPs as above, noncontiguous haplotypes of variable length also showed a significant association near the suspected loci. Our result suggests that height during infancy/early childhood may be regulated by genetic variations that differ from those of adults.

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“…In a similar work, it has been observed that ECs are also involved during the early stages of pancreas development [20] . Another research work indicated that signals from myocardium, such as those exerted by bone morphogenetic protein-2 (BMP-2), can promote epithelial-mesenchymal transformation mediated by ECs [24,29] . In the kidney, VEGF, bFGF, and PDGF coordinate cellular differentiation, proliferation, and migration [30] .…”

Section: Endothelium As An Endocrine Organmentioning

confidence: 99%

Endothelium-derived essential signals involved in pancreas organogenesis

Talavera-Adame

Dafoe

2015

WJEM

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Endothelial cells (ECs) are essential for pancreas differentiation, endocrine specification, and endocrine function. They are also involved in the physiopathology of type 1 and type 2 diabetes. During embryogenesis, aortic ECs provide specific factors that maintain the expression of key genes for pancreas development such as pancreatic and duodenal homeobox-1. Other unknown factors are also important for pancreatic endocrine specification and formation of insulin-producing beta cells. Endocrine precursors proliferate interspersed with ductal cells and exocrine precursors and, at some point of development, these endocrine precursors migrate to pancreatic mesenchyme and start forming the islets of Langerhans. By the end of the gestation and close to birth, these islets contain immature beta cells with the capacity to express vascular endothelial growth factor and therefore to recruit ECs from the surrounding microenvironment. ECs in turn produce factors that are essential to maintain insulin secretion in pancreatic beta cells. Once assembled, a cross talk between endocrine cells and ECs maintain the integrity of islets toward an adequate function during the whole life of the adult individual. This review will focus in the EC role in the differentiation and maturation of pancreatic beta cells during embryogenesis as well as the current knowledge about the involvement of endothelium to derive pancreatic beta cells in vitro from mouse or human pluripotent stem cells.

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Bmp2 and Bmp4 genetically interact to support multiple aspects of mouse development including functional heart development

Cited by 51 publications

References 55 publications

Bone Morphogenetic Protein-4 Mediates Cardiac Hypertrophy, Apoptosis, and Fibrosis in Experimentally Pathological Cardiac Hypertrophy

Bone Morphogenetic Protein-4 Mediates Cardiac Hypertrophy, Apoptosis, and Fibrosis in Experimentally Pathological Cardiac Hypertrophy

Genetic variants that affect length/height in infancy/early childhood in Vietnamese-Korean families

Endothelium-derived essential signals involved in pancreas organogenesis

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