@article{BornhorstXiaNakajimaetal.2019,
  author    = {Bornhorst, Dorothee and Xia, Peng and Nakajima, Hiroyuki and Dingare, Chaitanya and Herzog, Wiebke and Lecaudey, Virginie and Mochizuki, Naoki and Heisenberg, Carl-Philipp and Yelon, Deborah and Abdelilah-Seyfried, Salim},
  title     = {Biomechanical signaling within the developing zebrafish heart attunes endocardial growth to myocardial chamber dimensions},
  series = {Nature Communications},
  volume    = {10},
  journal   = {Nature Communications},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {2041-1723},
  doi       = {10.1038/s41467-019-12068-x},
  pages     = {10},
  year      = {2019},
  abstract  = {Intra-organ communication guides morphogenetic processes that are essential for an organ to carry out complex physiological functions. In the heart, the growth of the myocardium is tightly coupled to that of the endocardium, a specialized endothelial tissue that lines its interior. Several molecular pathways have been implicated in the communication between these tissues including secreted factors, components of the extracellular matrix, or proteins involved in cell-cell communication. Yet, it is unknown how the growth of the endocardium is coordinated with that of the myocardium. Here, we show that an increased expansion of the myocardial atrial chamber volume generates higher junctional forces within endocardial cells. This leads to biomechanical signaling involving VE-cadherin, triggering nuclear localization of the Hippo pathway transcriptional regulator Yap1 and endocardial proliferation. Our work suggests that the growth of the endocardium results from myocardial chamber volume expansion and ends when the tension on the tissue is relaxed.},
  language  = {en}
}
@article{UribeRamadassDograetal.2018,
  author    = {Uribe, Veronica and Ramadass, Radhan and Dogra, Deepika and Rasouli, S. Javad and Gunawan, Felix and Nakajima, Hiroyuki and Chiba, Ayano and Reischauer, Sven and Mochizuki, Naoki and Stainier, Didier Y. R.},
  title     = {In vivo analysis of cardiomyocyte proliferation during trabeculation},
  series = {Development : Company of Biologists},
  volume    = {145},
  journal   = {Development : Company of Biologists},
  number    = {14},
  publisher = {Company biologists LTD},
  address   = {Cambridge},
  issn      = {0950-1991},
  doi       = {10.1242/dev.164194},
  pages     = {12},
  year      = {2018},
  abstract  = {Cardiomyocyte proliferation is crucial for cardiac growth, patterning and regeneration; however, few studies have investigated the behavior of dividing cardiomyocytes in vivo. Here, we use time-lapse imaging of beating hearts in combination with the FUCCI system to monitor the behavior of proliferating cardiomyocytes in developing zebrafish. Confirming in vitro observations, sarcomere disassembly, as well as changes in cell shape and volume, precede cardiomyocyte cytokinesis. Notably, cardiomyocytes in zebrafish embryos and young larvae mostly divide parallel to the myocardial wall in both the compact and trabecular layers, and cardiomyocyte proliferation is more frequent in the trabecular layer. While analyzing known regulators of cardiomyocyte proliferation, we observed that the Nrg/ErbB2 and TGF beta signaling pathways differentially affect compact and trabecular layer cardiomyocytes, indicating that distinct mechanisms drive proliferation in these two layers. In summary, our data indicate that, in zebrafish, cardiomyocyte proliferation is essential for trabecular growth, but not initiation, and set the stage to further investigate the cellular and molecular mechanisms driving cardiomyocyte proliferation in vivo.},
  language  = {en}
}