Journal: Communications Biology

Article Title: Primary cilia prevent activation of the cGAS-STING pathway during mouse decidualization

doi: 10.1038/s42003-025-08030-x

Figure Lengend Snippet: A Cytokine array analysis of the cultured medium from stromal cells treated with DMSO or CBA. B Relative mRNA abundances of Pcsk9 , Prl8a2 , and Prl3c1 after stromal cells were transfected with siScr or siPcsk9 for 24 h and further induced in vitro decidualization for 24 h. C Relative mRNA abundances of Rbp4 , Prl8a2 , and Prl3c1 after stromal cells were transfected with siScr or siRbp4 for 24 h and further induced in vitro decidualization for 24 h. D Relative mRNA abundances of Ccl6 , Prl8a2 , and Prl3c1 after stromal cells were transfected with siScr or siCcl6 for 24 h and further induced in vitro decidualization for 24 h. E Relative mRNA abundances of Prl8a2 and Prl3c1 after stromal cells were treated with recombinant mCCL6 proteins under in vitro decidualization for 24 h. F CCL6 concentrations in cultured medium after stromal cells were treated with DMSO or CBA under in vitro decidualization for 24 h. G CCL6 concentrations after stromal cells were treated DMSO and CalyA under in vitro decidualization for 24 h. H CCL6 concentrations in cultured medium after stromal cells were treated with 2’3’-cGAMP (5 μg/ml) under in vitro decidualization for 24 h. I Schematic model illustrating the working mechanism. TMEM67 is essential for stromal primary cilia formation and mouse decidualization. Primary cilia prevent RhoA-ROCK-MLC2-mediated actomyosin contraction, thereby reducing micronuclei formation and suppressing the cGAS-STING pathway activation. Loss of primary cilia leads to decreased CCL6 secretion and impairs decidualization. All images were representative ones of three biologically independent experiments. All data were presented as means ± SD from three biologically independent experiments. The two-tailed Student’s t- test was used for comparing two groups. One-way ANOVA test was used for comparing more than two groups. * P < 0.05, ** P < 0.01 and *** P < 0.001.

Article Snippet: To analyze the effect of CBA, CalyA, and 2’3’-cGAMP on Chemokine C-C-Motif Ligand 6 (CCL6) secretion from cultured stromal cells, CCL6 in the cultured medium was measured using enzyme-linked immunosorbent assay kits (E-EL-M267, Elabscience, Wuhan, China) according to the manufacturer’s instruction.

Techniques: Cell Culture, Transfection, In Vitro, Recombinant, Activation Assay, Two Tailed Test

Journal: Cells

Article Title: Pharmacological Evidence of the Important Roles of CCR1 and CCR3 and Their Endogenous Ligands CCL2/7/8 in Hypersensitivity Based on a Murine Model of Neuropathic Pain.

doi: 10.3390/cells12010098

Figure Lengend Snippet: Figure 2. Time-dependent changes in CCL2, CCL3, CCL4, CCL5, CCL6, CCL7, CCL8, CCL9, CCL11, CCL24, CCL26 and CCL28 mRNA levels (A–L) in male mice on the 2nd, 7th, 14th and 28th days after chronic constriction injury of the sciatic nerve in the spinal cord. The RT–qPCR data are presented as the fold change of control ± SEMs. Intergroup differences were analyzed using one-way ANOVA with Bonferroni’s post hoc test for multiple comparisons. * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate a significant difference compared with the control group (naive). @ p < 0.05, @@ p < 0.01, and @@@ p < 0.001 indicate differences between the 2nd vs. 7th, 2nd vs. 14th, 2nd vs. 28th, 7th vs. 14th, 7th vs. 28th, and 14th vs. 28th days. The quantity of animals used in the experiment was as follows: RT-qPCR: N (n = 5–7), 2d (n = 8), 7d (n = 8–10), 14d (n = 10), 28d (n = 8–9). Abbreviations: N—naive.

Article Snippet: ELISAs for CCL2 (ABclonal, RK00381 Woburn, MA, USA), CCL3 (LSBio, LS–F4952; Seattle, WA, USA), CCL4 (LSBio, LS-F4954), CCL5 (ABclonal, RK00167), CCL6 (Abbexa, abx353305; Cambridge, UK), CCL7 (ABclonal, RK06183), CCL8 (ABclonal, RK00425) and CCL9 (LSBio, LS-F55161) were performed according to the manufacturer’s instructions.

Techniques: Quantitative RT-PCR, Control

Journal: Cells

Article Title: Pharmacological Evidence of the Important Roles of CCR1 and CCR3 and Their Endogenous Ligands CCL2/7/8 in Hypersensitivity Based on a Murine Model of Neuropathic Pain.

doi: 10.3390/cells12010098

Figure Lengend Snippet: Figure 4. Effect of a single (0.3 µg/5 µL) i.t. administration of CCL2, CCL3, CCL5, CCL7, CCL8 and CCL9 on mechanical (A) and thermal hypersensitivity (C) in male mice as measured 1, 3, 5, 10, 24 and 48 h after injection. Moreover, the obtained data were analyzed as areas under the curve (B,D). The data are presented as the means ± SEMs (A,C) or total area under curve ± SEMs. Intergroup differences were analyzed using one-way ANOVA with Bonferroni’s post hoc test for multiple comparisons. * p < 0.05, ** p < 0.01, and *** p < 0.001 indicate a significant difference compared with the control group. @ p < 0.05, @@ p < 0.01, and @@@ p < 0.001 indicate differences between the CCL2 group; % p < 0.05 indicates differences between the CCL3 group; # p < 0.05, and ## p < 0.01 indicate differences between the CCL5 group; ˆˆ p < 0.01 indicates differences between the CCL7 group; $$$ p < 0.001 indicates differences between the CCL8 group. The quantity of animals used in the experiment was as follows: V (n = 8), CCL2 (n = 8), CCL3 (n = 8), CCL5 (n = 7–8), CCL7 (n = 8), CCL8 (n = 8), CCL9 (n = 7–8). Abbreviations: V—control, 2/3/5/7/8/9—CCL2/3/5/7/8/9.

Article Snippet: ELISAs for CCL2 (ABclonal, RK00381 Woburn, MA, USA), CCL3 (LSBio, LS–F4952; Seattle, WA, USA), CCL4 (LSBio, LS-F4954), CCL5 (ABclonal, RK00167), CCL6 (Abbexa, abx353305; Cambridge, UK), CCL7 (ABclonal, RK06183), CCL8 (ABclonal, RK00425) and CCL9 (LSBio, LS-F55161) were performed according to the manufacturer’s instructions.

Techniques: Injection, Control

Journal: Cells

Article Title: Pharmacological Evidence of the Important Roles of CCR1 and CCR3 and Their Endogenous Ligands CCL2/7/8 in Hypersensitivity Based on a Murine Model of Neuropathic Pain.

doi: 10.3390/cells12010098

Figure Lengend Snippet: Scheme 6. Selective inhibition of CCL2/7/8 production by bindarit, as well as blocking of CCR1 and CCR3 by selective (J113863, SB328437) or dual (UCB35625) antagonists, reduced even fully developed mechanical and thermal hypersensitivity in murine model of neuropathic pain.

Article Snippet: ELISAs for CCL2 (ABclonal, RK00381 Woburn, MA, USA), CCL3 (LSBio, LS–F4952; Seattle, WA, USA), CCL4 (LSBio, LS-F4954), CCL5 (ABclonal, RK00167), CCL6 (Abbexa, abx353305; Cambridge, UK), CCL7 (ABclonal, RK06183), CCL8 (ABclonal, RK00425) and CCL9 (LSBio, LS-F55161) were performed according to the manufacturer’s instructions.

Techniques: Inhibition, Blocking Assay