6 results match your criteria: "The University of Tennessee Center for Health Sciences[Affiliation]"

CaM kinase IIalpha mediates norepinephrine-induced translocation of cytosolic phospholipase A2 to the nuclear envelope.

J Cell Sci

January 2003

Department of Pharmacology and Centers for Connective Tissue Diseases and Vascular Biology, College of Medicine, The University of Tennessee Center for Health Sciences, Memphis, TN 38163, USA.

Several growth factors, hormones and neurotransmitters, including norepinephrine, increase cellular calcium levels, promoting the translocation of cytosolic phospholipase A(2) to the nuclear envelope. This study was conducted to investigate the contributions of the calcium-binding protein calmodulin and of calcium-calmodulin-dependent protein kinase II to cytosolic phospholipase A(2) translocation to the nuclear envelope elicited by norepinephrine in rabbit aortic smooth-muscle cells. Norepinephrine caused cytosolic phospholipase A(2) accumulation around the nuclear envelope as determined from its immunofluorescence; cytosolic phospholipase A(2) translocation was blocked by inhibitors of calmodulin and calcium-calmodulin-dependent protein kinase II or calcium-calmodulin-dependent protein kinase IIalpha antisense oligonucleotide.

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Norepinephrine (NE) and angiotensin II (Ang II), by promoting extracellular Ca2+ influx, increase Ca2+/calmodulin-dependent kinase II (CaMKII) activity, leading to activation of mitogen-activated protein kinase (MAPK) and cytosolic phospholipase A2 (cPLA2), resulting in release of arachidonic acid (AA) for prostacyclin synthesis in rabbit vascular smooth muscle cells. However, the mechanism by which CaMKII activates MAPK is unclear. The present study was conducted to determine the contribution of AA and its metabolites as possible mediators of CaMKII-induced MAPK activation by NE, Ang II, and epidermal growth factor (EGF) in vascular smooth muscle cells.

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Norepinephrine (NE) stimulates release of arachidonic acid (AA) from tissue lipids in blood vessels, which is metabolized via cyclooxygenase, lipoxygenase (LO), and cytochrome P-450 (CYP-450) pathways to biologically active products. Moreover, NE and AA have been shown to stimulate proliferation of vascular smooth muscle cells (VSMCs) of rat aorta. The purpose of this study was to determine the possible contribution of AA and its metabolites to NE-induced mitogenesis in VSMCs of rat aorta and the underlying mechanism of their actions.

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This report describes the coexistence of infectious panniculitis due to Histoplasma capsulatum in three patients with dermatomyositis. In each case, the appearance of panniculitis was the predominant clinical manifestation of histoplasmosis. Oral ulcers, lymphadenopathy, pulmonary infiltrates, hepatosplenomegaly, and other cardinal features of disseminated histoplasmosis were notably absent.

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We have investigated the contribution of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) and mitogen-activated protein kinase (MAP kinase) in norepinephrine (NE)-induced arachidonic acid (AA) release in rabbit aortic vascular smooth muscle cells (VSMC). NE enhanced release of AA via activation of cytosolic phospholipase A2 (cPLA2) but not secretory PLA2 in VSMC prelabeled with [3H]AA. NE (10 microM) enhanced CaM kinase II and MAP kinase activity.

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Early sexual explorations of children that are of a traumatic nature are often labeled by the child as "bad" or "wrong" and subsequently repressed. The guilt that results from the labeling may be intensified at a later date by some other similar incident, and at this time the person may make a binding commitment or promise to God to serve Him in some dutiful way. If, at a later date, these plans to serve God cannot be realized, depression, phobias, or conversion symptomatology may occur, which we have referred to as the Missionary Syndrome.

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