Further purification and partial characterization of the rat lung cytoplasmic factors modulating adenylate cyclase activity in plasma membrane

Nijjar, M. S.; Khangura, B. S.

doi:10.1007/bf00225654

Cited by 4 publications

(1 citation statement)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Earlier studies had suggested that a cytosolic cyclase-activating factor might be involved in regulating the changes in P-adrenergic responsiveness during red cell maturation (Shane et al, 1985a,b). A variety of such factors have been described previously in other tissues (Sahyoun et al, 1983;Nijjar and Khangura, 1988). Our findings are compatible with the assumption that the target of this cytosolic factor is either the ing MEL cells in the postfusion period proba 1 ly cannot catalytic subunit of the cyclase or the a-subunit of the stimulatory G protein.…”

Section: Camp Responses In Reticulocyte-mel Cell Hybridssupporting

confidence: 92%

Analysis by cell hybridization of mechanisms that regulate β‐Adrenergic responses in reticulocytes and in differentiating erythroid cells

Porzig

Moudry

Montandon

1991

Journal Cellular Physiology

View full text Add to dashboard Cite

In intact reticulocytes, but not in fragmented membranes, the loss of adenylate cyclase activity during cell maturation followed a biphasic time course. A rapid phase (t1/2 approximately 2 h) during which the initial activity was reduced by 40-50% was followed by a slow phase with t1/2 close to 3 days. The fast decay seemed to occur on the adenylate cyclase level since (-)isoprenaline- or forskolin-stimulated activities behaved similarly and bacterial toxin-monitored Gs and Gi proteins remained stable. The mechanism of the initial decrease in hormonal responsiveness was further analysed in hybrid cells prepared by fusing reticulocytes with Friend erythroleukemia (MEL) cells. The hybrids contained reticulocyte-derived beta-adrenoceptors and MEL cell-derived adenylate cyclase and G proteins. Fusion of reticulocytes to native MEL cells caused adenylate cyclase activity to drop by 30% at 2 h and 45% at 18 h after fusion. By contrast, hybrids prepared after dimethylsulfoxide-induced differentiation of MEL cells showed stable or increasing rates of receptor-coupled cAMP formation between 2 and 18 h after fusion, concomitant with the enhanced activity of the Gs protein in these cells. A cyclase-stimulating factor present in the cytosol of MEL cells and of reticulocytes appeared not to be involved in short-term regulation of hormonal responsiveness. We conclude that the strength of beta-adrenergic responses in erythroid progenitor cells is primarily regulated by modulating G protein-mediated receptor cyclase coupling while reticulocytes, during early maturation, seem to rely on direct inactivation of adenylate cyclase, probably via a cytosolic proteolytic pathway.

show abstract

Section: Camp Responses In Reticulocyte-mel Cell Hybridssupporting

confidence: 92%

Analysis by cell hybridization of mechanisms that regulate β‐Adrenergic responses in reticulocytes and in differentiating erythroid cells

Porzig

Moudry

Montandon

1991

Journal Cellular Physiology

View full text Add to dashboard Cite

show abstract

Relationship between the cytoplasmic activator of adenylate cyclase and glycogen metabolism in rat lung

1988

View full text Add to dashboard Cite

The role of cytoplasmic activator of adenylate cyclase in rat lung metabolism was investigated. Mouse adrenal tumor (MAT) cells undergo differentiation in response to choleratoxin which acts through cyclic AMP. The activator of adenylate cyclase from rat lung also produced cyclic AMP in a disrupted MAT cell preparation. However, unlike choleratoxin, it did not induce MAT cell differentiation in whole cells. These results suggest impermeability of MAT cells, and possibly other cells, to the activator. Thus, means of altering activator activity in lung cytoplasm were sought, and changes in activator activity were related to lung glycogen. Adrenalectomy (ADX) in rats led to a reduction in activator activity that was accompanied by an elevation in lung glycogen. Dexamethasone treatment of adrenalectomized rats reversed both of these effects. Streptozotocin-induced diabetes in rats elevated activator activity and lowered lung glycogen. Insulin treatment of the diabetic rats restored activator activity to the normal control values. Preweaning of rats on day 16 instead of day 22 increased activator activity on the 19th day over the controls and there was a concomitant decrease in lung glycogen. Feeding the separated pups with homogenized milk restored glycogen and activator activity to the control values. These results indicate that activator activity in rat lung cytoplasm was dependent on the circulating levels of cortisol and insulin, and that there appeared to be an inverse relationship between activator activity and glycogen level in rat lungs.

show abstract

Effects of premature weaning and diet on lung growth and appearance of adenylate cyclase activator in rat lung

Nijjar

Hatch

1991

Mol Cell Biochem

View full text Add to dashboard Cite

Early weaning of rat pups on day 16 to semi-ground Purina chow food and drinking water, ad libitum, delayed growth of body and lungs, and the appearance of adenylate cyclase activator (ACA) in lung after day 22. However, early weaning of pups to either milk or a gel diet containing semi-ground Purina chow food, agarose gel, water (30:1:69, w/w), and drinking water, restored lung and body growth and the appearance of ACA to control values. Early weaning of pups to dry semi-ground Purina chow food and drinking water also induced a transient rise in ACA on day 19. This early rise in ACA was completely absent in pups weaned on day 16 to milk, whereas it persisted in pups weaned similarly to a gel diet. Interestingly, lung glycogen decreased on day 19 in pups weaned early to dry semi-ground Purina chow food without (group 2) or with triiodothyronine administration (group 3), and on day 25 after normal weaning on day 22 (Nijjar, M.S. Biochim. Biophys. Acta 586: 464-472, 1979). These data indicate 1) that reduced food intake (starvation) in pups weaned on day 16 to dry semi-ground Purina chow food was responsible for the delayed growth of body and lung, and the delayed appearance of ACA in lung after day 22, and 2) that a change in diet from milk to Purina chow food and associated alterations in hormones, possibly cortisol and insulin, were responsible for the appearance of ACA in rat lung.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Further purification and partial characterization of the rat lung cytoplasmic factors modulating adenylate cyclase activity in plasma membrane

Cited by 4 publications

References 25 publications

Analysis by cell hybridization of mechanisms that regulate β‐Adrenergic responses in reticulocytes and in differentiating erythroid cells

Analysis by cell hybridization of mechanisms that regulate β‐Adrenergic responses in reticulocytes and in differentiating erythroid cells

Relationship between the cytoplasmic activator of adenylate cyclase and glycogen metabolism in rat lung

Effects of premature weaning and diet on lung growth and appearance of adenylate cyclase activator in rat lung

Contact Info

Product

Resources

About