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

Liu, Honglei; Zhang, Hongqiao; Forman, Henry Jay

doi:10.1165/rcmb.2006-0297oc

Cited by 41 publications

(24 citation statements)

References 64 publications

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“…However, the role of the PI-PLC is not completely solved, as, in contrast to the previous study, U73122 did not inhibit hypoxia-induced calcium signals in human PASMCs, although a prominent role for TRPC6 was detected in these cells [145]. DAG kinase inhibition or phospholipase C (PLC) activation might be caused by superoxide [152,153]. Moreover, D609 significantly suppressed pulmonary vasoconstriction induced with a generator of superoxide anions [48].…”

Section: Downstream Targets Of Rosmentioning

confidence: 94%

Oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction

et al. 2015

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Number 11 in the series "Physiology in respiratory medicine" Edited by R. Naeije, D. Chemla, A. Vonk-Noordegraaf and A.T. Dinh-Xuan Affiliation: Excellence Cluster Cardiopulmonary System, University of Giessen Lung Center, German Center for Lung Research (DZL), Justus-Liebig-University, Giessen, Germany.Correspondence: Norbert Weissmann, Excellence Cluster Cardiopulmonary System, University of Giessen Lung Center, German Center for Lung Research (DZL), Justus-Liebig-University, 35392 Giessen, Germany. E-mail: Norbert.Weissmann@innere.med.uni-giessen.de ABSTRACT Hypoxic pulmonary vasoconstriction (HPV), also known as the von Euler-Liljestrand mechanism, is an essential response of the pulmonary vasculature to acute and sustained alveolar hypoxia. During local alveolar hypoxia, HPV matches perfusion to ventilation to maintain optimal arterial oxygenation. In contrast, during global alveolar hypoxia, HPV leads to pulmonary hypertension. The oxygen sensing and signal transduction machinery is located in the pulmonary arterial smooth muscle cells (PASMCs) of the pre-capillary vessels, albeit the physiological response may be modulated in vivo by the endothelium. While factors such as nitric oxide modulate HPV, reactive oxygen species (ROS) have been suggested to act as essential mediators in HPV. ROS may originate from mitochondria and/or NADPH oxidases but the exact oxygen sensing mechanisms, as well as the question of whether increased or decreased ROS cause HPV, are under debate. ROS may induce intracellular calcium increase and subsequent contraction of PASMCs via direct or indirect interactions with protein kinases, phospholipases, sarcoplasmic calcium channels, transient receptor potential channels, voltage-dependent potassium channels and L-type calcium channels, whose relevance may vary under different experimental conditions. Successful identification of factors regulating HPV may allow development of novel therapeutic approaches for conditions of disturbed HPV. @ERSpublications ROS originating from mitochondria and/or NADPH oxidases may initiate HPV but exact signalling mechanisms are unclear http://ow.ly/SkaGC

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Section: Downstream Targets Of Rosmentioning

confidence: 94%

Oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction

et al. 2015

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“…At UC Merced, Honglei Liu and Hongqiao Zhang began our studies of the mechanism through which respirable silica activates the production of pro-inflammatory cytokines. Their studies implicated activation of PC-PLC in the signaling [98]. Gayatri Premasekharan, a graduate student working in materials science with Valerie Leppert, took this work further by demonstrating an essential role for surface iron and the role of lipid raft disruption in the mechanism [99].…”

Section: Air Pollutionmentioning

confidence: 99%

Redox signaling: an evolution from free radicals to aging

Forman

2016

Free Radical Biology and Medicine

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“…al. demonstrated TNF-α and IL-1β release following silica was mediated through phosphotidylcholine-specific phospholipase C regulated in a redox-dependent fashion [100]. The inflammatory cytokines most commonly associated with silica-induced free radicals are TNF-α [101,102], IL-1β [100], MIP-1, MIP-2, MCP-1 [103], and IL-8 (following TNF-α priming) [104].…”

Section: Cell-derived Free Radicalsmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

342

242

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Inhalation of the crystalline form of silica is associated with a variety of pathologies from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science researchers looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage (AM) interacts with the inhaled silica particle and the consequences of silicainduced toxicity on the cellular level. Based on experimental results, several rationales have been developed on exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica) triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species (RNS) are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, where silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis is described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

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

Cited by 41 publications

References 64 publications

Oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction

Oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction

Redox signaling: an evolution from free radicals to aging

Silica binding and toxicity in alveolar macrophages

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