No description available.

No description available.

Thesis (M.S.Ed.)--Baylor University, 2005. / Includes bibliographical references (p. 46-50).

Hydroxymethylgluteryl-CoA reductase inhibitors (statins) are commonly used in the treatment of cardiovascular diseases. These drugs have been shown to induce cell death in various cell types. It is unclear if this is a class effect or a phenomenon specific to certain compounds. We hypothesize that lipophilic statins induce cell death in primary human atrial myofibroblasts (hATMF) whereas hydrophilic statins do not. hATMF were treated with atorvastatin, simvastatin (lipophilic statins) or pravastatin (hydrophilic statin). Cell viability was assessed using MTT assay. Induction of apoptosis and autophagy were estimated with western blot analysis. We found that lipophilic statin treatment of hATMF reduced cell viability in a time and dose-dependent manner and increased expression of apoptotic markers. These effects were not observed with the hydrophilic statin. In conclusion, there are substantial differences between various compounds in the statin family. These differences should be considered when selecting a drug for a particular patient.

There is emerging evidence to suggest that cardiac myofibroblasts (CMyfbs) participating in cardiac fibrosis represent a heterogeneous population in origin. We hypothesized that bone marrow derived mesenchymal stem cells (MSCs) readily adopt a myofibroblastic phenotype in culture. We assessed and compared human primary MSCs and human CMyfbs with respect to their phenotypic and functional characteristics by examining their gene expression profile, ability to contract collagen gels, and ability to synthesize collagen. We also examined the role of non-muscle myosin II (NMMII) in modulating the myofibroblast function using siRNA and blebbistatin to inhibit NMMII activity. The data revealed that MSCs adopt a myofibroblastic phenotype in culture and demonstrate the capability to contract collagen gels and synthesize collagen similar to human CMyfbs. Inhibition of NMMII activity with blebbistatin completely inhibits gel contractility without affecting cell viability. Thus, MSCs exhibit similar physiological and functional characteristics as CMyfbs, and may contribute to cardiac fibrosis.

Hydroxymethylgluteryl-CoA reductase inhibitors (statins) are commonly used in the treatment of cardiovascular diseases. These drugs have been shown to induce cell death in various cell types. It is unclear if this is a class effect or a phenomenon specific to certain compounds. We hypothesize that lipophilic statins induce cell death in primary human atrial myofibroblasts (hATMF) whereas hydrophilic statins do not. hATMF were treated with atorvastatin, simvastatin (lipophilic statins) or pravastatin (hydrophilic statin). Cell viability was assessed using MTT assay. Induction of apoptosis and autophagy were estimated with western blot analysis. We found that lipophilic statin treatment of hATMF reduced cell viability in a time and dose-dependent manner and increased expression of apoptotic markers. These effects were not observed with the hydrophilic statin. In conclusion, there are substantial differences between various compounds in the statin family. These differences should be considered when selecting a drug for a particular patient.

There is emerging evidence to suggest that cardiac myofibroblasts (CMyfbs) participating in cardiac fibrosis represent a heterogeneous population in origin. We hypothesized that bone marrow derived mesenchymal stem cells (MSCs) readily adopt a myofibroblastic phenotype in culture. We assessed and compared human primary MSCs and human CMyfbs with respect to their phenotypic and functional characteristics by examining their gene expression profile, ability to contract collagen gels, and ability to synthesize collagen. We also examined the role of non-muscle myosin II (NMMII) in modulating the myofibroblast function using siRNA and blebbistatin to inhibit NMMII activity. The data revealed that MSCs adopt a myofibroblastic phenotype in culture and demonstrate the capability to contract collagen gels and synthesize collagen similar to human CMyfbs. Inhibition of NMMII activity with blebbistatin completely inhibits gel contractility without affecting cell viability. Thus, MSCs exhibit similar physiological and functional characteristics as CMyfbs, and may contribute to cardiac fibrosis.

Thesis (Ph. D.)--Tartu University, 2004. / "The purpose of the study was to compare the reflection of destruction of myofibrils on the ultrastructural level and changes in myofibrillar proteins in slow-twitch and fast-twitch skeletal muscle and their fibre types in case of volume-overtrained and glucocorticoid caused myopathy." --p. 22.

No description available.

Previous investigations have indicated that shoulder stiffness was related with the degree of inflammation and the number of myofibroblasts in subacromial bursa tissue of rotator cuff lesions. But the interaction mechanism between inflammatory cytokines and myofibroblasts induced shoulder stiffness has not been fully explored. The purpose of this research is to study the effect of IL-1 £] on myofibroblasts in rotator cuff lesions with shoulder stiffness. Myofibroblasts from subacromial bursa tissue of rotator cuff lesions were cultured with or without IL-1 £]. The gene and protein expression of £\-smooth muscle actin (£\-SMA) and prolyl 4-hydroxylase (PH-4) were determined. The results showed that high levels of PH-4 and low levels of £\-SMA were expressed in myofibroblasts cultured with IL-1 £]. PH-4 gene had higher expression in tissue of stiff patients than non-stiff patients, but £\-SMA gene expression had no significant difference. According to the results, myofibroblasts cultured with extra IL-1 £] showed increased PH-4 expression and decreased £\-SMA expression. This indicates myofibroblasts might transdifferentiate into fibroblasts via IL-1 £] effect.