mProX™ Human S1PR5 Stable Cell Line

Zeng MN, et al. "[Platycladi Semen oil ameliorates Abeta_(25-35)-induced brain injury in mice based ." Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese , 2023.
The current study aimed to investigate the protective effect and underlying mechanism of Platycladi Semen oil (SP) on Abeta_(25-35)-induced brain injury in male Kunming (KM) mice. The control, model (injected with Abeta_(25-35)), positive drug (donepezil), and low and high dose SP groups were analyzed for learning and memory ability, neuronal damage, levels of Abeta_(1-42)/Abeta_(1-40), p-Tau, indicators of apoptosis and oxidative stress, immune cells, and expression of the sphingosine kinase 1 (SPHK1)/sphingosine-1-phosphate (S1P)/sphingosine-1-phosphate receptor 5 (S1PR5) signaling pathway. Gas chromatography-mass spectrometry (GC-MS) and network pharmacology were used to determine the compounds and mechanism of action of SP. The study found that SP improved learning and memory function, reduced neuronal damage and levels of Abeta_(1-42)/Abeta_(1-40), p-Tau, and indicators of apoptosis and oxidative stress in the brain, and maintained immune cell and gut microbiota (GM) homeostasis. Network pharmacology and GM sequencing analysis suggested that SP's therapeutic effect against Alzheimer's disease (AD) is linked to the sphingolipid signaling pathway. The components (Z,Z,Z)-9,12,15-octadecatrienoic acid and (Z,Z)-9,12-octadecadienoic acid in SP showed good binding activity to SPHK1 and S1PR5, indicating their potential as material basis for SP's anti-AD effects. These findings suggest that SP may exert anti-apoptosis and antioxidant effects by regulating GM and inhibiting the SPHK1/S1P/S1PR5 pathway, thereby protecting against Abeta_(25-35)-induced brain injury in mice.
Pubmed: 37802772   DOI: 10.19540/j.cnki.cjcmm.20230306.701

Sozio F, et al. "CCRL2 Expression by Specialized Lung Capillary Endothelial Cells Controls NK-cell ." Cancer immunology research, 2023.
The homing of leukocytes to tissues is regulated by patterns of receptors for chemotactic factors. A new study has revealed that the CCRL2/chemerin/CMKLR1 axis is a specialized pathway for the homing of natural killer (NK) cells to the lungs. Based on a lung cancer cell model, it was found that C-C motif chemokine receptor-like 2 (CCRL2) plays a crucial role in controlling lung tumor growth. Deletion or ablation of CCRL2 in endothelial cells, as well as the absence of its ligand chemerin, resulted in increased tumor progression. This was attributed to a decrease in the recruitment of mature NK cells to the lungs. While other chemotactic receptors (Cxcr3, Cx3cr1, and S1pr5) were identified in lung-infiltrating NK cells, they were found to be dispensable for the regulation of NK cell infiltration and tumor growth. The study also identified CCRL2 as a key marker of general alveolar lung capillary endothelial cells. Further investigations revealed that CCRL2's expression is regulated by epigenetic factors and can be upregulated by the demethylating drug 5-aza-2'-deoxycytidine (5-Aza). In vivo experiments demonstrated that low doses of 5-Aza induced CCRL2 expression, increased the recruitment of NK cells, and reduced lung tumor growth. These findings highlight the potential of CCRL2 as a key molecule in NK cell-mediated lung immune surveillance and suggest its potential use in immune-based therapies for lung cancer.
Pubmed: 37343073   DOI: 10.1158/2326-6066.CIR-22-0951