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Adult Stem Cell Plasticity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Others confirmed these results using untreated MSC in different animal models. MSC expanded and chemically labeled in culture integrated into cardiac muscle when injected into healthy myocardium.108 Labeled cells were aligned in intercalated disks, exhibited myocyte morphology, and stained positively for connexin 43. The presence of this component of gap junctions indicates that the donor-derived cells were electrically coupled to the endogenous myocardium. When human MSC, transfected with the LacZ gene, were injected into the uninjured myocardium of immunodeficient mice, LacZ+ cells were found within four days.109 Although these did not initially express protein markers of cardiac muscle, after fourteen days, donor cells were rod shaped and aligned with other cardiomyocytes, had increased in size, and expressed desmin, cardiac troponin T, α-actinin, phospholamban, and β-myosin heavy chain. Unfortunately, engraftment rates were low in both these studies; only about 1 LacZ+ cell per tissue section was found by Toma et al.
Applications of the revolving motor
Published in Peixuan Guo, Zhengyi Zhao, Biomotors: Linear, Rotation, and Revolution Motion Mechanisms, 2017
The concept described here for high efficient viral inhibition may have an impact in antiviral therapy by introducing dominant negative proteins (Lee et al., 2014) or inactive mutant proteins into the cell, either by intracellular expression using viral vectors for gene delivery or direct introduction of proteins into cell (Trottier et al., 1996; Chen et al., 1997; Fang et al., 2014; Shu et al., 2015). This involves the incorporation of mutant protein subunits into a multimeric complex identified as drug target. If a multimeric complex is identified with high stoichiometry and K = 1 due to the sequential action of the homomeric subunits, then incorporating one mutant subunit into the complex would inactivate the complex completely. Since the viral machine is composed of Z subunits, one drugged subunit per complex would only work when the intracellular drug concentration is high. But if the strategy is to apply a dominant negative protein, such as the dominant negative phospholamban in cardiac gene therapy (Lee et al., 2014), then more augmented effect of the mutant protein subunits will be expected as the Z value increases.
In-Vivo Imaging of Transgene Expression Using the Herpesviral Thymidine Kinase Reporter Gene
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Frank M. Bengel, Sanjiv S. Gambhir
Treatment of heart failure is another scenario for gene therapy, where it is close to entering clinical trials (10). Molecular targets for restitution of contractile function in the failing heart include interventions in calcium homeostasis [e.g., overexpression of sarcoplasmic reticulum Ca-ATPase (SERCA) to increase contraction and relaxation velocity, or inhibition of phospholamban to increase SERCA levels (11,12)], in β-adrenergic signal transduction [e.g., β-receptor overexpression to increase contractility, or inhibition of β-adrenoceptor kinases to reduce receptor desensitization (13)] and in the cascade of apoptotic cell death [e.g., overexpression of the antiapoptotic factor Bcl-2 (14)].
Cardiac contractility modulation for the treatment of moderate to severe HF
Published in Expert Review of Medical Devices, 2021
CCM has been found to phosphorylate the protein phospholamban which, in its unphosphorylated state, acts to inhibit the function of SERCA2a. Once phosphorylated, phospholamban dissociates from SERCA2a and its ability to pump calcium back into the SR is increased, thus improving calcium reuptake into the SR.