Both hMECs and hESCs upregulated expression of cardiac markers upon differentiation, but they exclusively expressed genes for myosin light chain (Myl2, Myl7) and myosin heavy chain (Myh6), respectively.
Cazorla, O. et al. Differential expression of cardiac titin isoforms and modulation of cellular stiffness.
(E) Cardiomyocytes differentiated from cryopreserved H1 hESC: top panel, colony of beating cardiomyocytes; lower panels, expression of cardiac marker TNNT2.
Expression of cardiac genes for calcium cycling increased in PBFT and coincided with broader vertical and thermal niche utilization.
Total RNA was analysed by Pico-drop (Perkin Elmer), electrophoresis and used for RT-PCR and qRT-PCR to evaluate the relative expression of cardiac miRs.
Cardiomyocyte-specific deletion of Bmal1 leads to a similar lengthening of QRS and QTc intervals, which was ascribed to aberrant expression of cardiac ion channels Scn5a and Kcnh2 59, 59.
Slides were visualized using LSM-700 confocal microscope, and the expression of cardiac markers was quantified using Imaris software and at least 5 images of each type of scaffold.
These functional enhancements are associated with increased expression of cardiac myosin light chain-2v, cardiac troponin I and integrin alpha-7.
This result was confirmed by Troponin-T immunostaining, the expression of cardiac genes (i.e., Tnnt2, Nkx2-5, Actc1ctc1), and beating analysis of the EBs.
These nanofibers were characterized by SEM, FT-IR, tensile testing and cell culture studies for the normal expression of cardiac proteins.
The expression of cardiac specific protein (cardiac troponin I) and genes of differentiating cardiomyocytes is analyzed by immunofluorescence and RT-PCR.
