Lipoteichoic acid induces prostaglandin E2 release and cyclooxygenase-2 synthesis in rat cortical neuronal cells: Involvement of PKCε and ERK activation

Wu, Hsueh Hsia; Hsieh, Wen Shyang; Yang, Yi Yuan; Tsai, Ming-Chuan

doi:10.1016/j.lfs.2006.01.004

Cited by 13 publications

(11 citation statements)

References 23 publications

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“…Many reagents have been reported to increase PC-PLC activity, including growth factors such as insulin (20); cytokines such as TNF-␣ (21, 43), IFN-␥ (44), and IL-4 (22); LPS (16); prostaglandin F2␣ (23); endothelin-1 (24); and others (17,45,46). In this study we found that PC-PLC was also activated by silica in alveolar macrophages (Figure 2).…”

Section: Discussionmentioning

confidence: 99%

“…PC-PLC has been reported to be involved in NF-B activation and cytokine production (16,17). To study whether PC-PLC is involved in the silica-caused inflammatory response, we investigated the effect of D609, a purportedly specific inhibitor of PC-PLC, which we verified inhibited the catalytic activity, on the release of TNF-␣ and IL-1␤, two critical cytokines involved in silica-associated inflammation.…”

Section: Involvement Of Pc-plc In Silica-induced Production Of Cytokimentioning

confidence: 99%

“…Recent studies demonstrated that phosphatidylcholinespecific phospholipase C (PC-PLC) may be involved in the activation of NF-B signaling pathway and the release of inflammatory molecules (16,17). PC-PLC hydrolyzes phosphatidylcholine to phosphorycholine and diacylglycerol (DAG), an activator of most protein kinase C (PKC) isoforms.…”

Section: Clinical Relevancementioning

confidence: 99%

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Silica Induces Macrophage Cytokines through Phosphatidylcholine-Specific Phospholipase C with Hydrogen Peroxide

Liu

Zhang

Forman

2007

Am J Respir Cell Mol Biol

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Silica particle-associated inflammation is implicated in the genesis of several pulmonary diseases, including silicosis and lung cancer. In this study we investigated the role of phosphatidylcholine-specific phospholipase C (PC-PLC) in silica-stimulated induction of TNF-␣ and IL-1␤ and how PC-PLC activity is regulated by silica in a rat alveolar macrophage model. We demonstrated that inhibition of PC-PLC, which was achieved with tricychodecan-9-yl-xanthate (D609), blocked the silica-stimulated induction of TNF-␣ and IL-1␤ in alveolar macrophage, suggesting that PC-PLC is involved in the silica-associated inflammatory response. PC-PLC activity was increased significantly by silica exposure, and this could be inhibited by MnTBAP, which catalyzes both the dismutation of O 2 .-to O 2 and H 2 O 2 and the dismutation of H 2 O 2 to O 2 and H 2 O, revealing that PC-PLC activity is regulated in a redox-dependent manner. This is further confirmed by the finding that PC-PLC activity was increased by exogenous H 2 O 2 . The intracellular calcium chelator BAPTA blocked the H 2 O 2 -increased PC-PLC activity, while the calcium ionophore, A23187, enhanced PC-PLC activity. The data indicate that PC-PLC plays critical roles in the silica-associated inflammatory response and that PC-PLC is regulated through redox-and calciumdependent manners in alveolar macrophages.

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Section: Discussionmentioning

confidence: 99%

Section: Involvement Of Pc-plc In Silica-induced Production Of Cytokimentioning

confidence: 99%

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Silica Induces Macrophage Cytokines through Phosphatidylcholine-Specific Phospholipase C with Hydrogen Peroxide

Liu

Zhang

Forman

2007

Am J Respir Cell Mol Biol

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“…40 Accumulating evidence has demonstrated that LTA is a potent inducer for COX-2 or PGE 2 production, which contributes to the development of inflammation. 17,21 However, little was known about the molecular mechanisms by LTAand S. aureus-induced cPLA 2 /COX-2-dependent airway inflammation. Here, we showed, for the first time, that cPLA 2 and COX-2 expression and PGE 2 release were increased on stimulation with LTA and S. aureus.…”

Section: Pge 2 Regulates Il-6 Release In Vitro In Htsmcs and Leukocytmentioning

confidence: 99%

“…Several studies have indicated that LTAinduced inflammatory responses are mediated through TLR2-dependent multiple signaling molecules, including MyD88, TRAF6, PI3K/Akt, MAPKs, and NF-B. 7,17,20,21 MyD88 plays a key role in TLR signaling. 5 Our previous study has shown that LTA induces the association of TLR2/MyD88 in HTSMCs.…”

mentioning

confidence: 99%

Cooperation of TLR2 with MyD88, PI3K, and Rac1 in Lipoteichoic Acid–Induced cPLA2/COX-2–Dependent Airway Inflammatory Responses

Lee

Tung

et al. 2010

The American Journal of Pathology

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Phosphatidylcholine‐specific phospholipase C activity and level increase evidently in thromboangitis obliterans

Wang

Jin

et al. 2010

BioFactors

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Thromboangitis obliterans (TAO) is considered to be an inflammatory disease. Previous research has demonstrated that phosphatidylcholine-specific phospholipase C (PC-PLC) plays critical roles in various inflammatory responses. However, the connection between PC-PLC and TAO is undetermined. Therefore, we sought to investigate whether PC-PLC was implicated in TAO. In our study, there were two groups: TAO group and control group. The PC-PLC activity of serum of two groups (16 TAO patients and 11 controls) was detected by PC-PLC activity assay. The level and distribution of PC-PLC in posterior tibial arteries in seven TAO patients and four controls were detected by immunofluorescence staining method. PC-PLC activity increased greatly in serum of TAO patients. Immunofluorescence analysis also revealed an upregulation of PC-PLC in the vascular endothelium of TAO patients. Our data suggest that PC-PLC activity and level increase obviously in TAO patients. Our study may provide new clues for seeking pathogenesis of TAO. Furthermore, it may bring new insights into clinical diagnosis and treatment of TAO.

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Lipoteichoic acid induces prostaglandin E2 release and cyclooxygenase-2 synthesis in rat cortical neuronal cells: Involvement of PKCε and ERK activation

Cited by 13 publications

References 23 publications

Silica Induces Macrophage Cytokines through Phosphatidylcholine-Specific Phospholipase C with Hydrogen Peroxide

Silica Induces Macrophage Cytokines through Phosphatidylcholine-Specific Phospholipase C with Hydrogen Peroxide

Cooperation of TLR2 with MyD88, PI3K, and Rac1 in Lipoteichoic Acid–Induced cPLA2/COX-2–Dependent Airway Inflammatory Responses

Phosphatidylcholine‐specific phospholipase C activity and level increase evidently in thromboangitis obliterans

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