Developmental Biology: Myocardial Atrial Chambers Study

Subject: Sciences
Pages: 2
Words: 327
Reading time:
2 min

Intra-organ communication is necessary for the growth and development of organs. Biochemical signalling is involved in communication in the heart through molecules such as BMPs, Wnts, FGFs. Conversely, cell-to-cell communication occurs through the Ephrin, Notch, or Neuregulin/ErbB2 pathways. However, the mode of communication that synchronizes the growth of the endocardium and myocardium is not known. It has been shown that endocardial chambers in zebrafish develop by multiplication without accretion of cells or interactions at any boundary.

Conversely, accretion of cells to the chamber extremities and changes in cell size are responsible for myocardial development. The study “Biomechanical Signaling Within the Developing Zebrafish Heart Attunes Endocardial Growth to Myocardial Chamber Dimensions” by Bornhorst et al. compared the outcomes of two genetic conditions that altered the measurements of the myocardial atrial chambers. The specific conditions were the loss of Nkx2.5 or a surge in the expression of Wnt8a.

Antisense oligonucleotide morpholinos (MO) were injected into the zebrafish lines to knock down targeted genes. Heat shock was used to conduct the transgenic overexpression of the Wnt8a gene coupled to a green fluorescent protein as a tagging moiety. Immunohistochemical studies were conducted on embryos at the correct developmental stage, followed by measurement of cell propagation, cell size and tension of endocardial tissue.

The outcomes suggested the existence of intra-organ communication machinery between the myocardium and endocardium that harmonised the growth of heart tissues in the course of cardiac ballooning. A signal involving the enlargement of the myocardial chamber was conveyed to the endocardium, leading to an increase in junctional forces within the endocardium. The authors proposed that Cadherin-5 transduced these signals by the nuclear localisation of a transcription factor known as Yap 1, which led to endocardial proliferation. The authors concluded that the expansion of the myocardial chamber causes the growth of the endocardium and that relaxing the tension of the myocardium stops this growth.