3,4,5-Trihydroxycinnamic acid attenuates lipopolysaccharide (LPS)-induced acute lung injury via downregulating inflammatory molecules and upregulating HO-1/AMPK activation

Lee, Jae Won; Wang, Chun; Kwon, Ok‐Kyoung; Park, Hyun Ah; Lim, Yourim; Lee, Jae-Hyeon; Kim, Doo-Young; Kim, Jung Hee; Lee, Hyeong‐Kyu; Ryu, Hyung Won; Oh, Sei‐Ryang; Ahn, Ki Hoon

doi:10.1016/j.intimp.2018.08.015

Cited by 28 publications

(25 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CXCL8 is a widely studied proinflammatory chemokine that acts as a chemoattractant for neutrophils, and gingival fibroblasts actively participate in the production of this chemokine . Recently, decreased expression of CXCL8 was associated with the upregulation of HO‐1 expression and p‐AMPK activation in human airway epithelial cells . Thus, we investigated if HO‐1 and p‐AMPK are affected by IL‐1β in HGFs.…”

Section: Resultsmentioning

confidence: 98%

“…Therefore, the anti‐inflammatory effects of HO‐1 seem to be associated with A2A/A2B‐receptor signaling. HO‐1 has also shown to have a protective role in the attenuation of nuclear factor‐κB activation in in vivo and in vitro models of acute lung injury . Interestingly, HO‐1 controls the expression of immunoregulatory cytokines during infection, favoring pathogen survival in the host .…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown a connection between adenosine and the enzyme HO-1 29,35 which is known to be involved in the suppression of inflammatory response. 13 In a murine model of pulmonary inflammation, the activation of HO-1 significantly decreased polymorphonuclear leukocyte (PMN) F I G U R E 5 Adenosine generated from eATP breakdown through the action of CD73 can dampen IL-1 -induced CXCL8 secretion.…”

Section: Discussionmentioning

confidence: 99%

“…HO-1 has also shown to have a protective role in the attenuation of nuclear factor-B activation in in vivo and in vitro models of acute lung injury. 29 Interestingly, HO-1 controls the expression of immunoregulatory cytokines during infection, favoring pathogen survival in the host. 36 Indeed, HO-1 is a stress-responsive enzyme important for defense against oxidant-induced injury during inflammatory processes and is highly inducible by various stimuli, such as lipopolysaccharide, cytokines, heat shock, heavy metals, oxidants, and its substrate heme.…”

Section: Discussionmentioning

confidence: 99%

“…19 Recently, decreased expression of CXCL8 was associated with the upregulation of HO-1 expression and p-AMPK activation in human airway epithelial cells. 29 Thus, we investigated if HO-1 and p-AMPK are affected by IL-1 in HGFs. As shown in Figure 3, increased levels of both HO-1 (Figs.…”

Section: Extracellular Atp Attenuates Il-1 -Induced Cxcl8 Secretion Amentioning

confidence: 99%

See 4 more Smart Citations

CD73‐dependent adenosine dampens interleukin‐1β–induced CXCL8 production in gingival fibroblasts: Association with heme oxygenase‐1 and adenosine monophosphate‒activated protein kinase

Ramos-Junior

Pedram

Lee

et al. 2019

Journal of Periodontology

View full text Add to dashboard Cite

Background During inflammation, stressed or infected cells can release adenosine triphosphate (ATP) to the extracellular medium, which can be hydrolyzed to adenosine by ectonucleotidases such as ectonucleoside triphosphate diphosphohydrolase 1 (CD39) and 5′‐nucleotidase (CD73). The role of CD73 in the modulation of cytokine release by human gingival fibroblasts (HGFs) remains underexplored. Here, we investigated whether CD73‐mediated hydrolysis of extracellular ATP (eATP) could affect interleukin (IL)‐1β‐induced CXCL8 secretion. Methods The levels of mRNA expression of adenosine receptors, CD39 and CD73 of periodontitis samples were retrieved from a public database. Moreover, HGF mRNA levels were measured by quantitative reverse transcription‐polymerase chain reaction (RT‐qPCR) after 3, 6, or 24 hours of IL‐1β stimulation. IL‐1β‐induced CXCL8 protein levels were measured after pretreatment with 100‐µM eATP in the presence or absence of CD73 inhibitor. The effect of eATP degradation to adenosine on CXCL8 levels was investigated using agonist and antagonist of adenosine receptors. Results Levels of CD39, CD73, and adenosine receptor mRNA were differentially modulated by IL‐1β. ATP pretreatment impaired IL‐1β‐induced CXCL8 secretion and required activation of heme oxygenase‐1 (HO‐1) and phosphorylated adenosine monophosphate‒activated protein kinase (pAMPK). The inhibition of CD73 or the inhibition of adenosine receptors abrogated the ATP effect on CXCL8 secretion. Conclusions CD73‐generated adenosine dampens IL‐1β‐induced CXCL8 in HGFs and involves HO‐1 and pAMPK signaling. These results imply that CD73 is a negative regulator of the inflammatory microenvironment, suggesting that this ectoenzyme could be involved in the generation of deficient CXCL8 gradient in chronic inflammation.

show abstract

Section: Resultsmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Extracellular Atp Attenuates Il-1 -Induced Cxcl8 Secretion Amentioning

confidence: 99%

See 3 more Smart Citations

CD73‐dependent adenosine dampens interleukin‐1β–induced CXCL8 production in gingival fibroblasts: Association with heme oxygenase‐1 and adenosine monophosphate‒activated protein kinase

Ramos-Junior

Pedram

Lee

et al. 2019

Journal of Periodontology

View full text Add to dashboard Cite

show abstract

Ellipticine blocks synergistic effects of IL-17A and TNF-α in epithelial cells and alleviates severe acute pancreatitis-associated acute lung injury

Mulati

et al. 2020

Biochemical Pharmacology

View full text Add to dashboard Cite

Novel regulators and targets of redox signaling in pulmonary vasculature

Daneva

Laubach

Sonkusare

2019

Current Opinion in Physiology

View full text Add to dashboard Cite

Dysregulated redox signaling in pulmonary vasculature is central to the development of pulmonary arterial hypertension (PAH) and lung injury. Modulators of reactive oxygen species (ROS) production and downstream signaling targets are critical for mediating the physiological or pathological effects of ROS. Understanding the complex interactions between the modulators and signaling targets of ROS is essential for developing novel strategies to prevent or attenuate lung pathologies. In this review, we discuss recent studies on the modulators and targets of ROS in pulmonary endothelial and smooth muscle cells, their cellular effects, and the disease conditions associated with dysregulated redox signaling.

show abstract

3,4,5-Trihydroxycinnamic acid attenuates lipopolysaccharide (LPS)-induced acute lung injury via downregulating inflammatory molecules and upregulating HO-1/AMPK activation

Cited by 28 publications

References 39 publications

CD73‐dependent adenosine dampens interleukin‐1β–induced CXCL8 production in gingival fibroblasts: Association with heme oxygenase‐1 and adenosine monophosphate‒activated protein kinase

CD73‐dependent adenosine dampens interleukin‐1β–induced CXCL8 production in gingival fibroblasts: Association with heme oxygenase‐1 and adenosine monophosphate‒activated protein kinase

Ellipticine blocks synergistic effects of IL-17A and TNF-α in epithelial cells and alleviates severe acute pancreatitis-associated acute lung injury

Novel regulators and targets of redox signaling in pulmonary vasculature

Contact Info

Product

Resources

About