Regulation of calcium stores in normal and diabetic endothelial cells

Simple item page
dc.creatorSanka, Shankar Chittaranjan
dc.date.accessioned2016-11-14T23:09:24Z
dc.date.available2011-02-18T23:39:54Z
dc.date.available2016-11-14T23:09:24Z
dc.date.issued2000-12
dc.degree.departmentTTUHSC -- Molecular Biophysics
dc.description.abstractCytosolic Ca^^ ([Ca^^]*'^^) mediates many cellular ftinctions, e.g.. cell growth, motility, secretion, etc. In many cell types, ion transport processes appear to be dependent on metabolism of glucose for maximal activity. In certain cell types, a strict coupling between glycolysis and the acfivity of Endoplasmic Reticulum Ca^"-ATPases (SERCA). involved in regulating Ca^^ homeostasis, has been suggested. In diabetes, glucose homeostasis is altered. We hypothesize that Ca^^ homeostasis in microvascular endothelial cells from diabetic animals is altered due to a dysfunction of glycolysis coupling the activity of SERCA. We further hypothesize that endosomal/lysosomal (E/L) compartments exhibiting SERCA are involved in this dysfunction. Our data indicated that agonist stimulation (ATP, vasopressin, angiotensin-II)elicited [Ca^"]^^* increases (independent of extracellular Ca^^) that were larger in endothelial cells from diabetic than from normal animals. Simultaneous measurements of [Ca^^]'^^' and Ca^^ in E/L compartments ([Ca^^]^) using fluorescence spectroscopy, indicated that E/L compartments released Ca^^ following agonist-stimulation. The magnitude of the Ca'* release was significantly larger in microvascular endothelial cells from diabetic rats. SERCA inhibitors elicited Ca^^ releases from E/L compartments in both normal and diabetic models. The magnitude of the [Ca^^]^ release was however similar among normal and diabetic cells. Immunocytochemical experiments demonstrated that 60% of E/L compartments exhibited SERCA. These data indicate that (a) E/L compartments are important for Ca^^ homeostasis in microvascular endothelial cells from both normal and diabetic models; (b) Ca^^ regulation in E/L compartments is different in cells from a diabefic model, (c) the compartment involved in altered Ca'* homeostasis in diabetes is unknown.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttp://hdl.handle.net/2346/20360en_US
dc.language.isoeng
dc.publisherTexas Tech Universityen_US
dc.rights.availabilityUnrestricted.
dc.subjectSignal transductionen_US
dc.subjectVascularen_US
dc.subjectEndotheliumen_US
dc.subjectCa(2+)-Transporting ATPaseen_US
dc.subjectType I diabetesen_US
dc.subjectDiabetes mellitusen_US
dc.subjectHomeostasisen_US
dc.subjectCalcium channelsen_US
dc.subjectCalciumen_US
dc.titleRegulation of calcium stores in normal and diabetic endothelial cells
dc.typeThesis

Files

Collections

Texas Tech University