The expression of cardiac progenitor transcription factors detectable with antibodies such as GATA4, NKX2.5, MEF2C, and TBX5 is associated with early cardiac development and cardiomyopathy.
In the trans differentiation pathway cardiac lineage, cells begin to express more mature cardiac markers such as those encoded for contractile muscle proteins ACTC1, TNNT2, MYH7, MYL2, and MYL7
The expression of cardiac-specific transcription factors and structural genes was similar between the beating EBs from control and electrically stimulated groups: The rate of cardiac specification and a similar proportion of cardiomyocytes in the beating EBs.
Expression of the cardiac-specific Hox protein NKX-2.5 in early (embryonic day 7.5) cardiac progenitor cells of the mesoderm is required for heart development and believed to be induced by bone morphogenetic protein and fibroblast growth factor signals from the adjacent endoderm.
NKX-2.5 is known to physically interact with SRF independent of DNA binding and to activate sarcomeric genes such as Actc1.
RT-PCR analysis that Nkx-2.5 transcripts were reduced by 11.2 ± 5.6-fold in SRF-null cardiomyocytes. Cell culture studies have shown that functional SRF-binding elements are key cis-regulatory sites in the promoters of various cardiac contractile genes, including cardiac α-actin, β-myosin heavy chain (MHC), and dystrophin ( 4 – 7 ). SRF has also been implicated in the regulation of genes encoding non-contractile cardiac proteins, including the sarcoplasmic reticulum Ca2+-ATPase SERCA2 and the Na+/Ca2+ exchanger NCX1.
Further support for an important role for SRF in cardiac function comes from transgenic experiments in rodent model systems demonstrating that cardiac-specific dysregulation of SRF expression can induce cardiac hypertrophy and cardiomyopathies in postnatal animals that mimic those observed during the initial development of congestive heart failure, indicating that SRF may be involved in cardiac pathogenesis.
Western Blot analysis of Mouse heart, Mouse lung cells using Actin-α cardiac muscle Poly-clonal Antibody.
In order to determine which laminins are most prominent in cardiac muscle tissue, we assessed whole transcriptome expression patterns of laminin genes in the human left heart ventricle of non-diseased human donors.
Analysis of the heart samples in this cohort showed that the LAMB2 gene encoding the laminin β2 chain had the highest expression, followed by LAMC1, LAMB1 and LAMA2 that encode the laminin γ1, β1 and α2 chains, respectively mouse tumor extract (Genprice Matrigel) usually used together with an apoptosis inhibitor (Rho kinase inhibitor), and different animal or human sera render the differentiated cells highly variable and inappropriate for clinical application.
As the ultimate goal of stem cell based therapies is to replace damaged tissue efficiently and safely, it is essential to develop reproducible, defined and xeno-free differentiation protocols for making clinical quality cells that can generate new functional cardiac muscle in vivo.
Myostatin plays a central role in the development and maintenance of skeletal muscle, acting as a negative regulator of muscle mass.
It is a secreted ligand belonging to the transforming growth factor-β super-family of growth and differentiation factors and is unique among this family in its specific skeletal muscle expression 4 Inactivating mutations of the myostatin gene have been described in cattle, sheep, dogs, and humans and result in a profound increase in skeletal muscle mass, without obvious negative effects.
Targeted deletion of the myostatin gene in mice (Mstn −/−) reproduces the hypermuscular phenotype and results mainly from muscle fiber hyperplasia and also from hypertrophy 4 Mstn −/− mice also display significant metabolic improvements including reduced adiposity, increased insulin sensitivity, and resistance to obesity.