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Search results for: Leukotriene B4 Receptor(BLT1 Receptor)

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#34844784   2021/11/26 To Up

The role of immune cells in pulmonary hypertension: Focusing on macrophages.

Pulmonary hypertension (PH) is a life-threatening pathological state with elevated pulmonary arterial pressure, resulting in right ventricular failure and heart functional failure. Analyses of human samples and rodent models of pH support the infiltration of various immune cells, including neutrophils, mast cells, dendritic cells, B-cells, T-cells, and natural killer cells, to the lungs and pulmonary perivascular regions and their involvement in the PH development. There is evidence that macrophages are presented in the pulmonary lesions of pH patients as first-line myeloid leucocytes. Macrophage accumulation and presence, both M1 and M2 phenotypes, is a distinctive hallmark of pH which plays a pivotal role in pulmonary artery remodeling through various cellular and molecular interactions and mechanisms, including CCL2 and CX3CL1 chemokines, adventitial fibroblasts, glucocorticoid-regulated kinase 1 (SGK1), crosstalk with other immune cells, leukotriene B4 (LTB4), bone morphogenetic protein receptor 2 (BMPR2), macrophage migration inhibitory factor (MIF), and thrombospondin-1 (TSP-1). In this paper, we reviewed the molecular mechanisms and the role of immune cells and responses are involved in PH development. We also summarized the polarization of macrophages in response to different stimuli and their pathological role and their infiltration in the lung of pH patients and animal models.
Ping Luo, Bing Qiu

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#34814348   // To Up

Prognostic and immunological value of LTB4R in pan-cancer.

LTB4 receptor 1 (LTB4R), as the high affinity leukotriene B4 receptor, is rapidly revealing its function in malignancies. However, it is still uncertain.
Sidan Long, Shuangshuang Ji, Kunmin Xiao, Peng Xue, Shijie Zhu

1425 related Products with: Prognostic and immunological value of LTB4R in pan-cancer.



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#34803675   2021/11/04 To Up

Berberine Alleviates Insulin Resistance and Inflammation Inhibiting the LTB4-BLT1 Axis.

Chronic low-grade inflammation is recognized as a key pathophysiological mechanism of insulin resistance. Leukotriene B4 (LTB4), a molecule derived from arachidonic acid, is a potent neutrophil chemoattractant. The excessive amount of LTB4 that is combined with its receptor BLT1 can cause chronic low-grade inflammation, aggravating insulin resistance. Berberine (BBR) has been shown to relieve insulin resistance due to its anti-inflammatory properties. However, it is not clear whether BBR could have any effects on the LTB4-BLT1 axis. Using LTB4 to induce Raw264.7 and HepG2 cells, we investigated the effect of BBR on the LTB4-BLT1 axis in the progression of inflammation and insulin resistance. Upon exposure to LTB4, intracellular insulin resistance and inflammation increased in HepG2 cells, and chemotaxis and inflammation response increased in RAW264.7 cells. Interestingly, pretreatment with BBR partially blocked these changes. Our preliminary data show that BBR might act on BLT1, modulating the LTB4-BLT1 axis to alleviate insulin resistance and inflammation. Our study demonstrated that BBR treatment could reduce intracellular insulin resistance and inflammation of hepatic cells, as well as chemotaxis of macrophages induced by LTB4. BBR might interact with BLT1 and alter the LTB4-BLT1 signaling pathway. This mechanism might be a novel anti-inflammatory and anti-diabetic function of BBR.
Minmin Gong, Huiyan Duan, Fan Wu, Yanlin Ren, Jing Gong, Lijun Xu, Fuer Lu, Dingkun Wang

2632 related Products with: Berberine Alleviates Insulin Resistance and Inflammation Inhibiting the LTB4-BLT1 Axis.

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#34784723   2021/11/17 To Up

Macrophage 12(S)-HETE Enhances Angiotensin II-Induced Contraction by a BLT2 (Leukotriene B Type-2 Receptor) and TP (Thromboxane Receptor)-Mediated Mechanism in Murine Arteries.

12/15-LO (12/15-lipoxygenase), encoded by Alox15 gene, metabolizes arachidonic acid to 12(S)-HETE (12-HETE). Macrophages are the major source of 12/15-LO among immune cells, and 12/15-LO plays a crucial role in development of hypertension. Global Alox15- or macrophage-deficient mice are resistant to Ang II (angiotensin II)-induced hypertension. This study tests the hypothesis that macrophage 12(S)-HETE contributes to Ang II-mediated arterial constriction and thus to development of Ang II-induced hypertension. Ang II constricted isolated abdominal aortic and mesenteric arterial rings. 12(S)-HETE (100 nmol/L) alone was without effect; however, it significantly enhanced Ang II-induced constriction. The presence of wild-type macrophages also enhanced the Ang II-induced constriction, while Alox15 macrophages did not. Using this model, pretreatment of aortic rings with inhibitors, receptor agonists/antagonists, or removal of the endothelium, systematically uncovered an endothelium-mediated, Ang II receptor-2-mediated and superoxide-mediated enhancing effect of 12(S)-HETE on Ang II constrictions. The role of superoxide was confirmed using aortas from p47 mice where 12(S)-HETE failed to enhance constriction to Ang II. In cultured arterial endothelial cells, 12(S)-HETE increased the production of superoxide, and 12(S)-HETE or Ang II increased the production of an isothromboxane-like metabolite. A TP (thromboxane receptor) antagonist inhibited 12(S)-HETE enhancement of Ang II constriction. Both Ang II-induced hypertension and the enhancing effect of 12(S)-HETE on Ang II contractions were eliminated by a BLT2 (leukotriene B receptor-2) antagonist. These results outline a mechanism where the macrophage 12/15-LO pathway enhances the action of Ang II. 12(S)-HETE, acting on the BLT2, contributes to the hypertensive action of Ang II in part by promoting endothelial synthesis of a superoxide-derived TP agonist.
Tamas Kriska, Anja Herrnreiter, Sandra L Pfister, Adeniyi Adebesin, John R Falck, William B Campbell

2284 related Products with: Macrophage 12(S)-HETE Enhances Angiotensin II-Induced Contraction by a BLT2 (Leukotriene B Type-2 Receptor) and TP (Thromboxane Receptor)-Mediated Mechanism in Murine Arteries.