TLR4 activation of TRPC6-dependent calcium signaling mediates endotoxin-induced lung vascular permeability and inflammation

Tauseef, Mohammad; Knezevic, Nebojsa; Chava, Koteswara R.; Smith, Monica; Sukriti, Sukriti; Gianaris, Nicholas; Obukhov, Alexander G.; Vogel, Stephen M.; Schraufnagel, Dean E.; Dietrich, Alexander; Birnbaumer, Lutz; Malik, Asrar B.; Mehta, Dolly

doi:10.1083/jcb1992oia2

Cited by 35 publications

(82 citation statements)

References 13 publications

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“…In addition, TRPC channels have been reported to be associated with the production of proinflammatory cytokines and inflammation. 27,28 A very recent study has demonstrated that TLR4 activation of TRPC6-dependent Ca 2+ signaling mediates endotoxin-induced lung vascular permeability and inflammation. 27 Strikingly, except NOD2-mediated Ca 2+ signaling directly contributing to cytoskeleton rearrangement and podocyte apoptosis, our preliminary results indicate that knockdown of TRPC6 can also attenuate NOD2-induced production of proinflammatory mediators in podocytes (data not shown).…”

Section: Discussionmentioning

confidence: 99%

“…27,28 A very recent study has demonstrated that TLR4 activation of TRPC6-dependent Ca 2+ signaling mediates endotoxin-induced lung vascular permeability and inflammation. 27 Strikingly, except NOD2-mediated Ca 2+ signaling directly contributing to cytoskeleton rearrangement and podocyte apoptosis, our preliminary results indicate that knockdown of TRPC6 can also attenuate NOD2-induced production of proinflammatory mediators in podocytes (data not shown). Therefore, it is very possible that NOD2-mediated Ca 2+ signaling and its proinflammatory action may build a signaling network to modulate related signaling in producing renal injury in hHcys.…”

Section: Discussionmentioning

confidence: 99%

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Novel Role of NOD2 in Mediating Ca ²⁺ Signaling

Han

Wang

et al. 2013

Hypertension

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Novel Role of NOD2 in Mediating Ca ²⁺ Signaling

Han

Wang

et al. 2013

Hypertension

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“…Recently, we showed that TRPC6 plays a key role in signaling both LPS-induced lung vascular permeability and inflammation. 83 Tauseef et al 83 showed that LPS resulted in DAG production, which activated TRPC6. Activated TRPC6 induced MYLK activity that, by stimulating actomyosin cross-bridging, mediates endothelial cell contraction, leading to increased lung vascular permeability.…”

Section: +mentioning

confidence: 99%

Mechanisms Regulating Endothelial Permeability

et al. 2014

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The endothelial monolayer partitioning underlying tissue from blood components in the vessel wall maintains tissue fluid balance and host defense through dynamically opening intercellular junctions. Edemagenic agonists disrupt endothelial barrier function by signaling the opening of the intercellular junctions leading to the formation of protein-rich edema in the interstitial tissue, a hallmark of tissue inflammation that, if left untreated, causes fatal diseases, such as acute respiratory distress syndrome. In this review, we discuss how intercellular junctions are maintained under normal conditions and after stimulation of endothelium with edemagenic agonists. We have focused on reviewing the new concepts dealing with the alteration of adherens junctions after inflammatory stimulus.

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“…LPS also significantly (p < 0.05) increased the inflammatory cells. As impaired vascular barrier function is critical in the pathogenesis of ARDS (26,27), we investigated whether CTCE protects barrier integrity in LPS-induced ARDS. We found that CTCE decreased LPS-induced protein, inflammatory cell, cytokine and chemokine levels in BAL as well as lung permeability and alveolar edema.…”

Section: Ctce Decreased Lps-induced Pulmonary Vascular Leak and Inflamentioning

confidence: 99%