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National Repository of Grey Literature 2 records found  Search took 0.00 seconds. 
Excitation-Contraction and Excitation-Transcription Coupling in Vascular Smooth Muscle Cells: Alterations in Experimental Hypertension and Vascular Remodeling
 Misárková, Eliška ; Zicha, Josef (advisor) ; Hock, Miroslav (referee)
Vascular smooth muscle cells (VSMCs) express considerable phenotype plasticity. They are able to change their phenotype in vivo if necessary. It is important to know that during this phenotype switch the expression of transport proteins and channels is modified, which results in significant alteration of Ca2+ signaling in smooth muscle cells. In differentiated cells, which represent contractile phenotype, there are dominant rapid, transient events in intracellular Ca2+ concentration (Ca2+ i), while the resting cytosolic Ca2+ i concentration is low. In differentiated cells these Ca2+ i events are mainly caused by two components of the Ca2+ signalling pathways: 1) extracellular Ca2+ influx via L-type voltage-gated Ca2+ channels (L-type VGCC) in plasma membrane, and 2) depletion of intracellular Ca2+ stores via ryanodin receptors located on sarcoplasmic reticulum. Rapid Ca2+ i oscillations are quickly reduced by numerous Ca2+ ATPases of sarco/endoplasmic reticulum and plasma membrane. Proliferating vascular smooth muscle cells are characterized by a long-lasting Ca2+ i oscillations accompanied by sustained elevation of basal intracellular Ca2+ concentration. During phenotype switch from contractile phenotype to proliferative phenotype there is decreased Ca2+ ATPase activity, and store-operated Ca2+...
Detailed record
Excitation-Contraction and Excitation-Transcription Coupling in Vascular Smooth Muscle Cells: Alterations in Experimental Hypertension and Vascular Remodeling
 Misárková, Eliška ; Zicha, Josef (advisor) ; Hock, Miroslav (referee)
Vascular smooth muscle cells (VSMCs) express considerable phenotype plasticity. They are able to change their phenotype in vivo if necessary. It is important to know that during this phenotype switch the expression of transport proteins and channels is modified, which results in significant alteration of Ca2+ signaling in smooth muscle cells. In differentiated cells, which represent contractile phenotype, there are dominant rapid, transient events in intracellular Ca2+ concentration (Ca2+ i), while the resting cytosolic Ca2+ i concentration is low. In differentiated cells these Ca2+ i events are mainly caused by two components of the Ca2+ signalling pathways: 1) extracellular Ca2+ influx via L-type voltage-gated Ca2+ channels (L-type VGCC) in plasma membrane, and 2) depletion of intracellular Ca2+ stores via ryanodin receptors located on sarcoplasmic reticulum. Rapid Ca2+ i oscillations are quickly reduced by numerous Ca2+ ATPases of sarco/endoplasmic reticulum and plasma membrane. Proliferating vascular smooth muscle cells are characterized by a long-lasting Ca2+ i oscillations accompanied by sustained elevation of basal intracellular Ca2+ concentration. During phenotype switch from contractile phenotype to proliferative phenotype there is decreased Ca2+ ATPase activity, and store-operated Ca2+...
Detailed record

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