Adenosine Formation and Release by Embryonic Chick Neurons and Glia in Cell Culture

Meghji, Parviz; Tuttle, Jeremy B.; Rubio, Rafael

doi:10.1111/j.1471-4159.1989.tb09252.x

Cited by 90 publications

(68 citation statements)

References 45 publications

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“…DNA was assayed in similar cell suspensions after sonication, using a standard curve based on calf thymus DNA (Sigma) and Hoechst 33258, as published previously. 20 …”

Section: Cell Culturesmentioning

confidence: 99%

Nerve growth factor synthesis in vascular smooth muscle.

Creedon

Tuttle

1991

Hypertension

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Details of the interdependent, trophic relation between smooth muscle and its neural innervation are not well known despite suggestions that neural influences may contribute significantly to hypertensive and other cardiovascular disease. Vascular smooth muscle is a major target of innervation by neurons of the sympathetic nervous system. Sympathetic neurons depend on a constant supply of the potent neurotrophic peptide nerve growth factor. Nerve growth factor regulates an impressive list of neuronal and perhaps muscle properties, yet its source in vessels and the determinants of its synthesis are not known. We have taken advantage of the cytoarchitecture of the aorta to demonstrate that vascular smooth muscle cells synthesize nerve growth factor. The survival of cultured sympathetic neurons is supported in a nerve growth factor-dependent manner by co-culture with pure rat aortic vascular smooth muscle cells. Furthermore, pure smooth muscle cell cultures contain nerve growth factorspecific messenger RNA. Levels of messenger nucleic acid coding for nerve growth factor in smooth muscle are regulated by contractile agonists (angiotensin II, arginine vasopressin) and the adrenergic agonist phenylephrine. This suggests a link between muscle activity and growth factor production. Secretion of nerve growth factor protein by vascular smooth muscle was measured using a sensitive two-site immunoassay. Secretion is highest during muscle growth. Secretion is elevated by angiotensin II and arginine vasopression but slightly inhibited by phenylephrine. These results suggest that cultured vascular smooth muscle can serve as a useful model in which to study the cellular regulation of trophic factor synthesis in health and disease. (Hypertension 1991;18:730-741)

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“…DNA was assayed in similar cell suspensions after sonication, using a standard curve based on calf thymus DNA (Sigma) and Hoechst 33258, as published previously. 20 …”

Section: Cell Culturesmentioning

confidence: 99%

Nerve growth factor synthesis in vascular smooth muscle.

Creedon

Tuttle

1991

Hypertension

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“…Adenine nucleotide measurement by HPLC ATP, ADP, and AMP levels of the cybrids were measured using anion-exchange HPLC (Meghji et al, 1989). Recovery of the adenine nucleotide contents from cells was in excess of 90% (Shryock et al, 1986).…”

Section: Methodsmentioning

confidence: 99%

Calcium Homeostasis and Reactive Oxygen Species Production in Cells Transformed by Mitochondria from Individuals with Sporadic Alzheimer’s Disease

Sheehan

Swerdlow

Miller³

et al. 1997

J. Neurosci.

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242

140

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Alzheimer's disease (AD) is associated with defects in mitochondrial function. Mitochondrial-based disturbances in calcium homeostasis, reactive oxygen species (ROS) generation, and amyloid metabolism have been implicated in the pathophysiology of sporadic AD. The cellular consequences of mitochondrial dysfunction, however, are not known. To examine these consequences, mitochondrially transformed cells (cybrids) were created from AD patients or disease-free controls. Mitochondria from platelets were fused to 0 cells created by depleting the human neuroblastoma line SH-SY5Y of its mitochondrial DNA (mtDNA). AD cybrids demonstrated a 52% decrease in electron transport chain (ETC) complex IV activity but no difference in complex I activity compared with control cybrids or SH-SY5Y cells. This mitochondrial dysfunction suggests a transferable mtDNA defect associated with AD. ROS generation was elevated in the AD cybrids. AD cybrids also displayed an increased basal cytosolic calcium concentration and enhanced sensitivity to inositol-1,4,5-triphosphate (InsP 3 )-mediated release. Furthermore, they recovered more slowly from an elevation in cytosolic calcium induced by the InsP 3 agonist carbachol. Mitochondrial calcium buffering plays a major role after this type of perturbation. ␤-amyloid (25-35) peptide delayed the initiation of calcium recovery to a carbachol challenge and slowed the recovery rate. Nerve growth factor reduced the carbachol-induced maximum and moderated the recovery kinetics. Succinate increased ETC activity and partially restored the AD cybrid recovery rate. These subtle alterations in calcium homeostasis and ROS generation might lead to increased susceptibility to cell death under circumstances not ordinarily toxic.

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“…Initially, it is difficult to reconcile the involvement of adenosine in the PHH of LC neurons with the blockade of this response by a low Ca2P-high Mg2+ medium. Metabolic damage leads to an increased formation of intracellular adenosine, which then leaves the cells via a nucleotide transporter (Meghji, Tuttle & Rubio, 1989). This efflux of adenosine is Ca2+ independent.…”

Section: Hypoxic Hyperpolarization (Hh) and Posthypoxic Hyperpolarizamentioning

confidence: 99%