Cardiac tissue engineering aims to create cardiac tissue constructs that recapitulate the structure and function of the native heart. This approach has been widely used for creating myocardial implants for regenerative medicine, and more recently, for developing in vitro cardiotoxicity screening assays. However, once the engineered myocardial tissues are implanted or subjected to pharmacological stimuli, their performance should be monitored. Currently, there is no biomaterial that promotes functional tissues assembly while providing real‐time information about their function, in situ. In this study, the piezoelectric phenomenon is sought to be exploited, to measure the contractions generated by engineered cardiac tissues. A poly‐(vinylidene fluoride) (PVDF)‐based electrospun fiber scaffold is developed, and it is hypothesized that the contractions of cardiomyocytes in the scaffold will induce mechanical deformations, which will result in measurable electric voltage. The PVDF scaffolds are characterized and optimized for supporting formation of aligned, functional, cardiac tissues. The scaffolds' function is then validated as sensors for tissue contraction and it is demonstrated that they can sense contractions of tissues constructed from as few as 5 × 105 cardiomyocytes. Furthermore, it is demonstrated that human induced pluripotent stem cells can be directly seeded and differentiated to cardiomyocytes, and then mature over the course of 40 days on the PVDF fiber scaffolds.

No abstract

Three dimensional (3D) printing of heart patches usually provides the ability to precisely control cell location in 3D space. Here, one‐step 3D printing of cardiac patches with built‐in soft and stretchable electronics is reported. The tissue is simultaneously printed using three distinct bioinks for the cells, for the conducting parts of the electronics and for the dielectric components. It is shown that the hybrid system can withstand continuous physical deformations as those taking place in the contracting myocardium. The electronic patch is flexible, stretchable, and soft, and the electrodes within the printed patch are able to monitor the function of the engineered tissue by providing extracellular potentials. Furthermore, the system allowed controlling tissue function by providing electrical stimulation for pacing. It is envisioned that such transplantable patches may regain heart contractility and allow the physician to monitor the implant function as well as to efficiently intervene from afar when needed.

Background: Wnt signaling pathways are taking a part in regulation of cell fate decisions in normal and cancerous cells. In some cancer types, a transition from canonical to non-canonical Wnt signaling pathways was identifi ed, a phenomenon, that in return led to increase proliferation, invasiveness and metastasis. Methods: In the current in vitro study we investigated the infl uence of MSCs, co-cultured in direct and indirect contact with OS cells, on the role of Wnt signaling pathways and tumor aggressiveness. Sub-populations were separated using Boyden chambers. Gene expression profi les were determined by qPCR. Results: The results revealed that interactions with MSCs increased migration and invasion capacities along with OS proliferation. Moreover, canonical Wnt signaling activity was low in OS, and co-culture with MSC. However, MSCs did not trigger a switch between the canonical to the no-canonical Wnt pathways. In addition, a more aggressive OS sub-population tend to undergo a transition towards the non-canonical pathway. Moreover, this aggressive subtype presented cancer stem-cells like characteristic. Conclusions: We submit that the progression in OS aggressiveness is attributed to a transition in Wnt signaling from canonical to non-canonical pathways, although MSCs are likely to take a part during the tumor progression, in the case of OS, they did not affect the Wnt switch. These complex tumor promoting interactions may be found in the natural and tumorigenic bone microenvironment. A better understanding of the molecular signaling mechanisms involved in the tumor development and metastasis may contribute to development of new cancer therapies.