Both interleukin-3 and interleukin-6 are necessary for better ex vivo expansion of CD133+ cells from umbilical cord blood.

Umbilical cord blood (UCB), an ideal source for transplantable hematopoietic stem cells (HSC), is readily available and is rich in progenitor cells. Identification of conditions favoring UCB-HSC ex vivo expansion and of repopulating potential remains a major challenge in hematology. CD133+ cells constitute an earlier, less-differentiated HSC group with a potentially higher engraftment capacity.

FAK signalling mediates NF-kappaB activation by mechanical stress in cardiac myocytes.

Background: Nuclear Factor (NF)-kappaB and Focal Adhesion Kinase (FAK) signalling are implicated in cardiomyocyte hypertrophy. We investigated whether FAK signalling contributed towards NF-kappaB activation by mechanical stress in cardiac myocytes.

Methods: Experiments were performed with pressure overload rat left ventricle and isolated cardiac myocytes from adult rats and isolated neonatal rat ventricular myocytes (NRVMs) underwent in vitro stretching.

ARHGAP21 associates with FAK and PKCzeta and is redistributed after cardiac pressure overload.

ARHGAP21 is highly expressed in the heart, which demonstrates activity over Cdc42 and interacts with proteins of the cytoskeleton and adherent junctions. The main cause of cardiac hypertrophy is mechanical stimulus; therefore we analyzed ARHGAP21 expression after acute mechanical stress in the myocardium and its association with FAK and PKCzeta. We demonstrated that ARHGAP21 is relocated to Z-lines and costameres after pressure overload, and interacts with PKCzeta and FAK in control rats (sham), rats submitted to aortic clamping and spontaneously hypertensive rats (SHR).

MEF2C DNA-binding activity is inhibited through its interaction with the regulatory protein Ki-1/57.

Myocyte enhancer factor (MEF2) are MADS box transcription factors that play important roles in the regulation of myogenesis and morphogenesis of muscle cells. MEF2 proteins are activated by mechanical overload in the heart. In this study, we found the interaction of MEF2C with the regulatory protein Ki-1/57 using yeast two-hybrid system.

Targeting to C-terminal myosin heavy chain may explain mechanotransduction involving focal adhesion kinase in cardiac myocytes.

Focal adhesion kinase (Fak) has been implicated as a signaling molecule involved in the early response of cardiac myocytes to mechanical stress. The mechanism of Fak activation by mechanical stimuli is not clear. In this study, we report the load-induced Fak activation and its association with myosin heavy chain in cardiac myocytes.