Category: 321673-30-7

Min, Arim published the artcileNOX2-Derived ROS-Mediated Surface Translocation of BLT1 Is Essential for Exocytosis in Human Eosinophils Induced by LTB₄, Computed Properties of 321673-30-7, the publication is International Archives of Allergy and Immunology (2014), 165(1), 40-51, database is CAplus and MEDLINE.

Background: Leukotriene B₄ (LTB₄) is a proinflammatory lipid mediator that elicits eosinophil exocytosis, leading to allergic inflammation. However, the detailed intracellular signaling mechanisms of eosinophil exocytosis induced by LTB₄ are poorly understood. Herein, we report that NADPH oxidase (NOX)2-derived reactive oxygen species (ROS)-mediated BLT1 migration to the cell surface is required for exocytosis in human eosinophils induced by LTB₄. Methods: Peripheral blood eosinophils were purified and stimulated for up to 60 min with LTB₄. The signaling role of NOX2-derived ROS in BLT1-dependent exocytosis in LTB₄-stimulated eosinophils was investigated. Results: Stimulating eosinophils with LTB₄ induced intracellular ROS production and surface upregulation of the exocytosis marker protein CD63 via BLT1-mediated signaling. LTB₄ induced p47^phox phosphorylation and 91^phox expression required for NOX2 activation in a BLT1-dependent manner. Pretreatment with NOX2 inhibitors, but not mitochondria inhibitor, prevented LTB₄-induced ROS generation and exocytosis. At 30 min after stimulation with LTB₄, BLT1 expression at the cell surface was upregulated. LTB₄-triggered surface upregulation of BLT1 was also blocked by inhibition of ROS generation with NOX2 inhibitors. Moreover, stimulation for 30 min with LTB₄ resulted in the interaction of BLT1 with NOX2 by immunoprecipitation LTB₄-induced ROS generation, surface upregulation of BLT1 and exocytosis was also inhibited by pretreatment with a lipid raft disruptor, protein kinase C inhibitor, or Src kinase inhibitor. Conclusion: These results suggest that NOX2-derived ROS-mediated BLT1 trafficking to the cell surface plays a key role in the exocytosis of human eosinophils induced by LTB₄.

International Archives of Allergy and Immunology published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Computed Properties of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Uddin, Mohib published the artcileResolvins: Natural agonists for resolution of pulmonary inflammation, Computed Properties of 321673-30-7, the publication is Progress in Lipid Research (2011), 50(1), 75-88, database is CAplus and MEDLINE.

A review. Inappropriate or excessive pulmonary inflammation can contribute to chronic lung diseases. In health, the resolution of inflammation is an active process that terminates inflammatory responses. The recent identification of endogenous lipid-derived mediators of resolution has provided a window to explore the pathobiol. of inflammatory disease and structural templates for the design of novel pro-resolving therapeutics. Resolvins (resolution-phase interaction products) are a family of pro-resolving mediators that are enzymically generated from essential omega-3 polyunsaturated fatty acids. Two mol. series of resolvins have been characterised, namely E- and D-series resolvins which possess distinct structural, biochem. and pharmacol. properties. Acting as agonists at specific receptors (CMKLR1, BLT1, ALX/FPR2 and GPR32), resolvins can signal for potent counter-regulatory effects on leukocyte functions, including preventing uncontrolled neutrophil swarming, decreasing the generation of cytokines, chemokines and reactive oxygen species and promoting clearance of apoptotic neutrophils from inflamed tissues. Hence, resolvins provide mechanisms for cytoprotection of host tissues to the potentially detrimental effects of unresolved inflammation. This review highlights recent exptl. findings in resolvin research, and the impact of these stereospecific mols. on the resolution of pulmonary inflammation and tissue catabasis.

Progress in Lipid Research published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C6H10F3NO, Computed Properties of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Chen, Mei published the artcileJoint Tissues Amplify Inflammation and Alter Their Invasive Behavior via Leukotriene B₄ in Experimental Inflammatory Arthritis, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Journal of Immunology (2010), 185(9), 5503-5511, database is CAplus and MEDLINE.

Mechanisms by which mesenchymal-derived tissue lineages participate in amplifying and perpetuating synovial inflammation in arthritis have been relatively underinvestigated and are therefore poorly understood. Elucidating these processes is likely to provide new insights into the pathogenesis of multiple diseases. Leukotriene B₄ (LTB₄) is a potent proinflammatory lipid mediator that initiates and amplifies synovial inflammation in the K/BxN model of arthritis. We sought to elucidate mechanisms by which mesenchymal-derived fibroblast-like synoviocytes (FLSs) perpetuate synovial inflammation. We focused on the abilities of FLSs to contribute to LTB₄ synthesis and to respond to LTB₄ within the joint. Using a series of bone marrow chimeras generated from 5-lipoxygenase^-/- and leukotriene A₄ (LTA₄) hydrolase^-/- mice, we demonstrate that FLSs generate sufficient levels of LTB₄ production through transcellular metabolism in K/BxN serum-induced arthritis to drive inflammatory arthritis. FLSs-which comprise the predominant lineage populating the synovial lining-are competent to metabolize exogenous LTA₄ into LTB₄ ex vivo. Stimulation of FLSs with TNF increased their capacity to generate LTB₄ 3-fold without inducing the expression of LTA₄ hydrolase protein. Moreover, LTB₄ (acting via LTB₄ receptor 1) was found to modulate the migratory and invasive activity of FLSs in vitro and also promote joint erosion by pannus tissue in vivo. Our results identify novel roles for FLSs and LTB₄ in joints, placing LTB₄ regulation of FLS biol. at the center of a previously unrecognized amplification loop for synovial inflammation and tissue pathol.

Journal of Immunology published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Sasaki, Fumiyuki published the artcileBiochemical and immunological characterization of a novel monoclonal antibody against mouse leukotriene B4 receptor 1, Synthetic Route of 321673-30-7, the publication is PLoS One (2017), 12(9), e0185133/1-e0185133/19, database is CAplus and MEDLINE.

Leukotriene B4 (LTB4) receptor 1 (BLT1) is a G protein-coupled receptor expressed in various leukocyte subsets; however, the precise expression of mouse BLT1 (mBLT1) has not been reported because a mBLT1 monoclonal antibody (mAb) has not been available. In this study, we present the successful establishment of a hybridoma cell line (clone 7A8) that produces a high-affinity mAb for mBLT1 by direct immunization of BLT1-deficient mice with mBLT1-overexpressing cells. The specificity of clone 7A8 was confirmed using mBLT1- overexpressing cells and mouse peripheral blood leukocytes that endogenously express BLT1. Clone 7A8 did not cross-react with human BLT1 or other G protein-coupled receptors, including human chemokine (C-X-C motif) receptor 4. The 7A8 mAb binds to the second extracellular loop of mBLT1 and did not affect LTB4 binding or intracellular calcium mobilization by LTB4. The 7A8 mAb pos. stained Gr-1-pos. granulocytes, CD11b-pos. granulocytes/monocytes, F4/80-pos. monocytes, CCR2-high and CCR2-low monocyte subsets in the peripheral blood and a CD4-pos. T cell subset, Th1 cells differentiated in vitro from naive CD4-pos. T cells. This mAb was able to detect Gr-1-pos. granulocytes and monocytes in the spleens of naive mice by immunohistochem. Finally, i.p. administration of 7A8 mAb depleted granulocytes and monocytes in the peripheral blood. We have therefore succeeded in generating a high-affinity anti-mBLT1 mAb that is useful for analyzing mBLT1 expression in vitro and in vivo.

PLoS One published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Synthetic Route of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Ichiki, Takako published the artcileReceptor for Advanced Glycation End Products Regulates Leukotriene B₄ Receptor 1 Signaling, SDS of cas: 321673-30-7, the publication is DNA and Cell Biology (2016), 35(12), 747-750, database is CAplus and MEDLINE.

Leukotriene B₄ receptor 1 (BLT1), a high-affinity G protein-coupled receptor (GPCR) for leukotriene B₄ (LTB₄), plays important roles in inflammatory and immune reactions. Although the LTB₄-BLT1 axis is known to promote inflammation, the binding proteins that modulate LTB₄-BLT1 signaling have not been identified. Recently, we discovered that receptor for advanced glycation end products (RAGE) interacts with BLT1 and modulates LTB₄-BLT1 signaling. We propose RAGE as a new class of GPCR modulator and a new target of future GPCR studies.

DNA and Cell Biology published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, SDS of cas: 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Chou, Richard C. published the artcileLipid-Cytokine-Chemokine Cascade Drives Neutrophil Recruitment in a Murine Model of Inflammatory Arthritis, Safety of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Immunity (2010), 33(2), 266-278, database is CAplus and MEDLINE.

A large and diverse array of chemoattractants control leukocyte trafficking, but how these apparently redundant signals collaborate in vivo is still largely unknown. We previously demonstrated an absolute requirement for the lipid chemoattractant leukotriene B₄ (LTB₄) and its receptor BLT1 for neutrophil recruitment into the joint in autoantibody-induced arthritis. We now demonstrate that BLT1 is required for neutrophils to deliver IL-1 into the joint to initiate arthritis. IL-1-expressing neutrophils amplify arthritis through the production of neutrophil-active chemokines from synovial tissue cells. CCR1 and CXCR2, two neutrophil chemokine receptors, operate nonredundantly to sequentially control the later phase of neutrophil recruitment into the joint and mediate all neutrophil chemokine activity in the model. Thus, we have uncovered a complex sequential relationship involving unique contributions from the lipid mediator LTB₄, the cytokine IL-1, and CCR1 and CXCR2 chemokine ligands that are all absolutely required for effective neutrophil recruitment into the joint.

Immunity published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Safety of [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Ren, Kun published the artcileQuercetin induces the selective uptake of HDL-cholesterol via promoting SR-BI expression and the activation of the PPARγ/LXRα pathway, SDS of cas: 321673-30-7, the publication is Food & Function (2018), 9(1), 624-635, database is CAplus and MEDLINE.

Reverse cholesterol transport (RCT) is the process to deliver cholesterol to the liver for further excretion and involves scavenger receptor class B type I (SR-BI)-mediated selective lipid uptake (SLU) from high-d. lipoprotein cholesterol (HDL-C). The up-regulation of hepatic SR-BI expression accelerates HDL-C clearance in circulation and impedes the development of atherosclerosis (AS). In the present study, we explored the modulation of hepatic SR-BI expression and SR-BI-mediated SLU by quercetin, a natural flavonoid compound in the diet with a favorable role in cardiovascular disorders. We found that quercetin significantly increased the expression level of SR-BI in HepG2 cells in a concentration- and time-dependent manner. Besides, quercetin had stimulatory effects on the binding of 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate (Dil)-labeled HDL to hepatocytes and ¹²⁵I/³H-CE-HDL association Treatment with small interfering RNA (siRNA) or SR-BI specific inhibitor, BLT-1, inhibited quercetin-induced Dil-HDL binding and selective HDL-C uptake. Treatment with quercetin increased both proliferator-activated receptor γ (PPARγ) and liver X receptor α (LXRα) levels. Addnl., the quercetin-induced expression of SR-BI, Dil-HDL binding and the selective uptake of HDL-C were significantly attenuated by treatment with PPARγ siRNA, LXRα siRNA, and their antagonists, resp. In C57BL/6 mice, quercetin administration potently increased SR-BI, PPARγ and LXRα levels and lipid accumulation in the liver. Altogether, our results suggest that quercetin-induced up-regulation of SR-BI and subsequent lipid uptake in hepatocytes might contribute to its beneficial effects on cholesterol homeostasis and atherogenesis.

Food & Function published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, SDS of cas: 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Rahabi, Mouna published the artcileDivergent Roles for Macrophage C-type Lectin Receptors, Dectin-1 and Mannose Receptors, in the Intestinal Inflammatory Response, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Cell Reports (2020), 30(13), 4386-4398.e5, database is CAplus and MEDLINE.

Colonic macrophages are considered to be major effectors of inflammatory bowel diseases (IBDs) and the control of gut inflammation through C-type lectin receptors is an emerging concept. We show that during colitis, the loss of dectin-1 on myeloid cells prevents intestinal inflammation, while the lack of mannose receptor (MR) exacerbates it. A marked increase in dectin-1 expression in dextran sulfate sodium (DSS)-exposed MR-deficient mice supports the critical contribution of dectin-1 to colitis outcome. Dectin-1 is crucial for Ly6C^highCCR2^high monocyte population enrichment in the blood and their recruitment to inflamed colon as precursors of inflammatory macrophages. Dectin-1 also promotes inflammasome-dependent interleukin-1β (IL-1β) secretion through leukotriene B4 production Interestingly, colonic inflammation is associated with a concomitant overexpression of dectin-1/CCL2/LTA4H and downregulation of MR on macrophages from IBD patients. Thus, MR and dectin-1 on macrophages are important mucosal inflammatory regulators that contribute to the intestinal inflammation.

Cell Reports published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Ito, Sohei published the artcileLeukotriene B₄/leukotriene B₄ receptor pathway is involved in hepatic microcirculatory dysfunction elicited by endotoxin, SDS of cas: 321673-30-7, the publication is Shock (2008), 30(1), 87-91, database is CAplus and MEDLINE.

Leukotrienes (LTs), metabolites of arachidonic acid through 5-lipoxygenase (5-LOX), have been known to play a role in leukocyte recruitment. However, the contribution of LTB₄ to liver microcirculatory dysfunction during endotoxemia remains unknown. LTB₄ receptor (BLT1) has been identified as a high-affinity receptor specific for LTB₄. The present study was conducted to examine the roles of LTB₄ and BLT1 in hepatic microcirculatory dysfunction elicited by LPS in mice. The number of leukocytes adhering to the endothelial cells of the hepatic microvessels and perfused sinusoids was determined 4 h after the administration of LPS (0.3 mg/kg, i.v.) to male C57Bl6 mice by in vivo microscopy. A 5-LOX synthase inhibitor, AA-861 (10 or 100 mg/kg, s.c), was administered 30 min before LPS injection. BLT1 knockout mice were used to investigate whether LPS-induced hepatic microcirculatory dysfunction is mediated by BLT1 signaling. The expression of 5-LOX, intercellular adhesion mol. (ICAM) 1, and TNF-α in the liver was measured by real-time reverse-transcriptase-polymerase chain reaction. The administration of LPS caused significant accumulation of leukocyte adhesion to the hepatic microvessels and reduced sinusoidal perfusion when compared with saline-treated mice. The hepatic microcirculatory dysfunction elicited by LPS was minimized in mice pretreated with AA-861 or in BLT1 knockout mice. This was associated with the suppression of hepatic expression of 5-LOX, ICAM-1, and TNF-α. These findings suggest that the LTB₄/BLT1 pathway mediates hepatic microcirculatory dysfunction by enhanced expression of ICAM-1 and TNF-α in a murine model of endotoxemia.

Shock published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, SDS of cas: 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Okuno, Toshiaki published the artcileBiochemical characterization of three BLT receptors in zebrafish, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is PLoS One (2015), 10(3), e0117888/1-e0117888/19, database is CAplus and MEDLINE.

The leukotriene B4 (LTB4) receptor 1 (BLT1) is a high affinity receptor for LTB4, a chemotactic and inflammatory eicosanoid. The LTB4 receptor 2 (BLT2) was originally identified as a low affinity receptor for LTB4, and, more recently, as a high affinity receptor for 12-hydroxyheptadecatrienoic acid (12-HHT). The zebrafish BLT receptors have not been previously identified and the in vivo functions of these receptors have been unknown. In this paper, we describe one zebrafish BLT1-like receptor, Blt1, and two zebrafish BLT2-like receptors, Blt2a and Blt2b. Cells expressing Blt1 exhibited LTB4-induced intracellular [Ca2+] increases, inhibition of cAMP production, ligand-dependent [35S]GTPγS binding, and transforming growth factor-α (TGFα) shedding activity in a dose-dependent manner, similar to human BLT1. Cells expressing Blt2a and Blt2b exhibited 12-HHT- and LTB4-induced intracellular [Ca2+] increases, inhibition of cAMP production, [35S]GTPγS binding, and TGFα shedding activity, with a dose-dependency similar to human BLT2. Reverse transcription (RT)-PCR anal. and whole-mount in situ hybridization revealed that blt1, blt2a, blt2b, zebrafish LTA4 hydrolase (lta4h), and zebrafish 5-lipoxiganase (5lo) are expressed in zebrafish embryos. Knockdown of blt1 by morpholino antisense oligonucleotides resulted in delayed epiboly at gastrulation. Consistently, knockdown of lta4h, an enzyme mediating LTB4 production, induced a phenotype similar to knockdown of blt1. These results suggest that the LTB4-BLT1 axis is involved in epiboly in zebrafish development.

PLoS One published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics