Regulation of Cytosolic Phospholipase A2 in Arachidonic Acid Release of Rat-Liver Macrophages

Ambs, Petra; Baccarini, Manuela; Schwende, H.; Fitzke, Edith; Dieter, Peter

doi:10.1007/978-1-4899-1813-0_71

Cited by 7 publications

(7 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These data clearly indicate the critical role of cPLA 2 in the ET-1 induction of TXA 2 from KCs from both sham and BDL animals. In addition, these data support previous reports of the critical role of calcium in the activation of cPLA 2 in KCs (28).…”

Section: Discussionsupporting

confidence: 91%

“…Stimulation of Gi coupled receptors have been reported to lead to the phosphorylation of cPLA 2 and release of AA via the activation of p38 MAPK and ERK1/2, although the intermediates involved in the activation of p38 have not been fully elucidated (38)(39)(40)(41)(42)(43)(44)(45)(46)(47). KCs express ET (B) receptors coupled to Gq/G11 and Gi proteins (48)(49)(50)(51), and several reports have supported the initial findings by Qui et al of the requirements of both a transient increase in calcium and phosphorylation of ser505, via p38 MAPK or ERK1/2, for the full activation of cPLA 2 and AA release in macrophages (28,34,35).…”

Section: Introductionmentioning

confidence: 88%

See 1 more Smart Citation

Altered Endothelin-1 Signaling in Production of Thromboxane A2 in Kupffer Cells from Bile Duct Ligated Rats

Miller

Zhang

2009

Cell Mol Immunol

View full text Add to dashboard Cite

Kupffer cells (KCs), the liver resident macrophages accounting for 80-90% of the total population of fixed tissue macrophages in the body, not only play a key role in host defense via removing particulate materials from the portal circulation, but may also contribute to the pathogenesis of various liver diseases. We have previously demonstrated that KCs play an important role in controlling portal hypertension and hepatocellular injury via releasing thromboxane A 2 (TXA 2 ) in early fibrosis induced by one-week bile duct ligation (BDL). Production of TXA 2 is controlled by cytosolic phospholipase A 2 (cPLA 2 ) that is activated by the interaction of entothelin-1 (ET-1) with its G-protein coupled ET receptor B (ETBR). However, the signaling pathways that contribute to the ET-1-induced activation of cPLA 2

show abstract

Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 88%

Altered Endothelin-1 Signaling in Production of Thromboxane A2 in Kupffer Cells from Bile Duct Ligated Rats

Miller

Zhang

2009

Cell Mol Immunol

View full text Add to dashboard Cite

show abstract

“…33 In macrophages, Ca 2+ regulates PGE 2 production by activating cPLA 2 to promote the release of AA. 11,12 In pituitary cells, Ca 2+ also exerts its role on COX-2 expression by activating CaMKs to induce the activation of c/EBPb, which is one of the two most important transcript factors that are essential for both basal transcription and the induction of COX-2. 20,21 In the present study, we found that Ca 2+ could also regulate COX-2 expression and PGE 2 production by activating CaMKII to induce the activation of CREB, the other important transcript factor that is essential for both basal transcription and the induction of COX-2, in primary rat peritoneal macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 For AA release, the activation of calcium-dependent cytosolic phospholipase A2 (cPLA 2 ) plays an essential role, which catalyses the hydrolysis of membrane phospholipid into AA. 11,12 In turn, COX-2 converts AA into PGE 2 .…”

Section: Introductionmentioning

confidence: 99%

Calcium/calmodulin‐dependent protein kinase II regulates cyclooxygenase‐2 expression and prostaglandin E₂ production by activating cAMP‐response element‐binding protein in rat peritoneal macrophages

Zhou

Yang

2014

Immunology

View full text Add to dashboard Cite

SummaryProstaglandin E 2 (PGE 2 ) is an important inducer of inflammation, which is also closely linked to the progress of tumours. In macrophages, PGE 2 production is regulated by arachidonic acid release and cyclooxygenase-2 (COX-2) expression. In the present study, we found that COX-2 expression can be achieved by activating Ca 2+ /Calmodulin (CaM)-dependent protein kinase II (CaMKII) and cAMP-response element-binding protein (CREB) in rat peritoneal macrophages. Our results indicated that lipopolysaccharide and PMA could elicit the transient increase of the concentration of intracellular free calcium ions ([Ca 2+ ] i ), which induced activation of CaMKs with the presence of CaM. The subtype of CaMKs, CaMKII, then triggered the activation of CREB, which elevated COX-2 expression and PGE 2 production in a chronological order. These results suggested that Ca 2+ /CaM-dependent CaMKII plays an important role in mediating COX-2 expression and PGE 2 production by activating CREB in macrophages. The study also provides more useful information to clarify the mechanism of calcium regulation of PGE 2 production, which plays an essential role in inflammation and cancers.

show abstract

“…Mast cells are not involved (5), and there is no evidence that the other cell types are implicated. C5aR 1 is a G-protein-linked receptor that acts by increasing intracellular inositol-1,4,5-triphosphate and Ca 2ϩ (47), rapidly activating cyclooxygenase (COX)-1-catalyzed PGE 2 production (2,40,46,47). COX-1 is constitutive, functionally coupled mainly with cytosolic PGE 2 synthase (PGES) and therefore prepared to quickly synthesize PGE 2 (55).…”

Section: Discussionmentioning

confidence: 99%

LPS-activated complement, not LPS per se, triggers the early release of PGE₂by Kupffer cells

Perlik¹,

Li²,

Goorha³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

The intravenous injection of LPS rapidly evokes fever. We have hypothesized that its onset is mediated by prostaglandin (PG)E2 quickly released by Kupffer cells (Kc). LPS, however, does not stimulate PGE2 production by Kc as rapidly as it induces fever; but complement (C) activated by LPS could be the exciting agent. To test this hypothesis, we injected LPS (2 or 8 g/kg) or cobra venom factor (CVF, an immediate activator of the C cascade that depletes its substrate, ultimately causing hypocomplementemia; 25 U/animal) into the portal vein of anesthetized guinea pigs and measured the appearance of PGE2, TNF-␣, IL-1␤, and IL-6 in the inferior vena cava (IVC) over the following 60 min. LPS (at both doses) and CVF induced similar rises in PGE2 within the first 5 min after treatment; the rises in PGE2 due to CVF returned to control in 15 min, whereas PGE2 rises due to LPS increased further, then stabilized. LPS given 3 h after CVF to the same animals also elevated PGE2, but after a 30-to 45-min delay. CVF per se did not alter basal PGE2 and cytokine levels and their responses to LPS. These in vivo effects were substantiated by the in vitro responses of primary Kc from guinea pigs to C (0.116 U/ml) and LPS (200 ng/ml). These results indicate that LPS-activated C rather than LPS itself triggers the early release of PGE2 by Kc. liver; fever; portal vein cannulation; cobra venom factor; pyrogenic cytokines FEVER DEVELOPS QUICKLY AFTER the intravenous bolus administration of a pyrogenic dose of LPS to conscious guinea pigs, rats, and other species, but the afferent mechanism that induces this response is controversial. It is generally thought that it is mediated by pyrogenic cytokines produced secondarily in response to the LPS challenge, rather than by its direct action. Tumor necrosis factor-␣ (TNF-␣), IL-1␤, and IL-6 are the major cytokines implicated in this response (9). There is, however, a temporal disconnect between the first appearance of these cytokines and the onset of the febrile response to intravenous LPS; that is, fever appears within 10 -15 min (13, 51) whereas TNF-␣, the first cytokine to appear, is not detectable until 30 min after LPS treatment (18,23,24,39). This temporal discrepancy is less evident after the intraperitoneal administration of low to moderate doses of LPS, when the latency of fever onset is ϳ60 min but becomes evident also when higher doses are administered, when the onset latency approaches that after intravenous LPS (7).We have shown previously that the onsets of the febrile responses to intravenous and intraperitoneal LPS are correlated with the appearance of LPS in the liver's Kupffer cells (Kc) (31), the body's principal clearinghouse of LPS (16,34,45) and source of pyrogenic cytokines (10). As cytokines are not constitutively expressed by Kc and their de novo production occurs after some delay (32), we and others have proposed, to account for the promptness of the febrile response to intravenous LPS, that the peripheral pyrogenic signal could be transmitted to the preoptic-anterior...

show abstract

Regulation of Cytosolic Phospholipase A2 in Arachidonic Acid Release of Rat-Liver Macrophages

Cited by 7 publications

References 11 publications

Altered Endothelin-1 Signaling in Production of Thromboxane A2 in Kupffer Cells from Bile Duct Ligated Rats

Altered Endothelin-1 Signaling in Production of Thromboxane A2 in Kupffer Cells from Bile Duct Ligated Rats

Calcium/calmodulin‐dependent protein kinase II regulates cyclooxygenase‐2 expression and prostaglandin E₂ production by activating cAMP‐response element‐binding protein in rat peritoneal macrophages

LPS-activated complement, not LPS per se, triggers the early release of PGE₂by Kupffer cells

Contact Info

Product

Resources

About

Regulation of Cytosolic Phospholipase A2 in Arachidonic Acid Release of Rat-Liver Macrophages

Cited by 7 publications

References 11 publications

Altered Endothelin-1 Signaling in Production of Thromboxane A2 in Kupffer Cells from Bile Duct Ligated Rats

Altered Endothelin-1 Signaling in Production of Thromboxane A2 in Kupffer Cells from Bile Duct Ligated Rats

Calcium/calmodulin‐dependent protein kinase II regulates cyclooxygenase‐2 expression and prostaglandin E2 production by activating cAMP‐response element‐binding protein in rat peritoneal macrophages

LPS-activated complement, not LPS per se, triggers the early release of PGE2by Kupffer cells

Contact Info

Product

Resources

About

Calcium/calmodulin‐dependent protein kinase II regulates cyclooxygenase‐2 expression and prostaglandin E₂ production by activating cAMP‐response element‐binding protein in rat peritoneal macrophages

LPS-activated complement, not LPS per se, triggers the early release of PGE₂by Kupffer cells