Arachidonic Acid Regulation of Steroid Synthesis: New Partners in the Signaling Pathway of Steroidogenic Hormones

Activating the protein-tyrosine kinase of v-Src in BALB/c 3T3 cells results in rapid increases in the intracellular second messenger, diacylglycerol (DAG). v-Src-induced increases in radiolabeled DAG were most readily detected when phospholipids were prelabeled with myristic acid, which is incorporated predominantly into phosphatidylcholine. Consistent with this observation, v-Src increased the level of intracellular choline. No increase in DAG was observed when cells were prelabeled with arachidonic acid, which is incorporated predominantly into phosphatidylinositol. Inhibiting phosphatidic acid (PA) phosphatase, which hydrolyzes PA to DAG, blocked v-Src-induced DAG production and enhanced PA production, implicating a type D phospholipase. Consistent with the involvement of a type D phospholipase, v-Src increased transphosphatidylation activity, which is characteristic of type D phospholipases. Thus, v-Src-induced increases in DAG most likely result from the activation of a type D phospholipase/PA phosphatase-mediated signaling pathway.

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The effects of centrally injected arachidonic acid on respiratory system: Involvement of cyclooxygenase to thromboxane signaling pathway

Respiratory Physiology & Neurobiology ◽

10.1016/j.resp.2015.12.010 ◽

2016 ◽

Vol 225 ◽

pp. 1-7 ◽

Cited By ~ 6

Author(s):

Leman Gizem Erkan ◽

Gokcen Guvenc ◽

Burcin Altinbas ◽

Nasir Niaz ◽

Murat Yalcin

Keyword(s):

Arachidonic Acid ◽

Signaling Pathway ◽

Respiratory System ◽

System Involvement

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Cholera toxin induces expression of the immediate-early response gene JE via a cyclic AMP-independent signaling pathway.

Molecular and Cellular Biology ◽

10.1128/mcb.11.1.102 ◽

1991 ◽

Vol 11 (1) ◽

pp. 102-107 ◽

Cited By ~ 14

Author(s):

S A Qureshi ◽

K Alexandropoulos ◽

C K Joseph ◽

R Spangler ◽

D A Foster

Keyword(s):

Gene Expression ◽

Arachidonic Acid ◽

Protein Kinase ◽

Cyclic Amp ◽

Cholera Toxin ◽

Signaling Pathway ◽

Acid Metabolism ◽

Early Response ◽

Arachidonic Acid Metabolism ◽

Immediate Early

Cholera toxin (CT) activates expression of two immediate-early response genes (JE and TIS10) in quiescent BALB/c 3T3 cells. Increases in cyclic AMP (cAMP) levels in response to CT are likely responsible for the induction of TIS10 gene expression, since treatment with 8-Br-cAMP and increasing the intracellular levels of cAMP by treatment with forskolin induce TIS10 gene expression. In contrast, neither forskolin nor 8-Br-cAMP induces JE gene expression. 3-Isobutyl-1-methylxanthine, which stabilizes intracellular cAMP, potentiates CT-induced TIS10 gene expression but has no effect on CT-induced JE gene expression. Thus, induction of JE by CT is independent of the cAMP produced in response to CT. Induction of JE by CT does not require protein kinase C (PKC), since depleting cells of PKC activity has no effect on the induction of JE by CT. CT-induced expression of JE can be distinguished from CT-induced TIS10 gene expression by using protein kinase inhibitors and inhibitors of arachidonic acid metabolism, further suggesting distinct signaling pathways for CT-induced JE and TIS10 gene expression. Thus, induction of JE gene expression by CT results from the activation of an intracellular signaling pathway that is independent of cAMP production. This pathway is independent of PKC activity and uniquely sensitive to inhibitors of protein kinases and arachidonic acid metabolism.

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