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Journal: Frontiers in Endocrinology
Article Title: Mast cell promotes obesity by activating microglia in hypothalamus
doi: 10.3389/fendo.2025.1544213
Figure Lengend Snippet: Pharmacological stabilization of mast cells in brain improves metabolic homeostasis in HFD-fed mice. (A) Body weight and body weight changes (B) in control and cromolyn sodium-injected mice, n = 8 per group. DEXA images (C) and fat mass (D) of control and cromolyn sodium-injected mice. Representative H&E-stained images of adipose tissue (E) and average adipocyte size (F) , n = 8 per group. (G, H) Representative H&E-stained liver images and relative lipid droplet area, n = 8 per group. (I, J) Glucose tolerance test (GTT) and area under the curve (AUC), n = 8 per group. (K-N) Food intake and total energy expenditure in both groups of mice, n = 8 per group. ns, not significant. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, two-tailed Student’s t-test (D, H, J, L, M, N) , two-way ANOVA with Bonferroni’s post hoc test (A, I, K) .
Article Snippet: For
Techniques: Control, Injection, Staining, Two Tailed Test
Journal: Frontiers in Endocrinology
Article Title: Mast cell promotes obesity by activating microglia in hypothalamus
doi: 10.3389/fendo.2025.1544213
Figure Lengend Snippet: Microglia mediates the effects of cromolyn sodium on energy balance. (A, B) Immunostaining and quantification of the microglial marker Iba1 in Kit^W-sh/W-sh mice and control mice. (C, D) Immunostaining and quantification of Iba1 in the control and cromolyn sodium-treated mice. (E, F) Immunostaining and quantification of Iba1 in control and PLX5622 treated mice. (G-I) After intracranial administration of the microglial cell-depleting agent PLX5622, differences in food intake, oxygen consumption, and energy expenditure between the cromolyn-treated group and the control saline group were observed. ns, not significant. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, two-tailed Student’s t-test (B, D, F) , two-way ANOVA with Bonferroni’s post hoc test (G-I) .
Article Snippet: For
Techniques: Immunostaining, Marker, Control, Saline, Two Tailed Test
Journal: Frontiers in Endocrinology
Article Title: Mast cell promotes obesity by activating microglia in hypothalamus
doi: 10.3389/fendo.2025.1544213
Figure Lengend Snippet: Pharmacological inhibition of mast cells activated POMC neurons and ameliorated leptin resistance. (A, B) Immunofluorescence staining of c-Fos in hypothalamus and quantification in control and cromolyn sodium-injected mice. (C, D) Immunofluorescence staining for POMC and c-Fos in the ARC brain region and quantification in control and cromolyn sodium-injected mice. (E, F) Immunofluorescence staining for p-STAT3 in the ARC brain region and quantification in control and cromolyn sodium-injected mice. (G) Food intake after intraperitoneal injection of leptin or saline in control and cromolyn sodium-injected mice. ns, not significant. Data are presented as mean ± SEM. *p < 0.05, ***p < 0.001, two-tailed Student’s t-test (B, D, E, G) , two-way ANOVA with Bonferroni’s post hoc test (H) .
Article Snippet: For
Techniques: Inhibition, Immunofluorescence, Staining, Control, Injection, Saline, Two Tailed Test
Journal: Frontiers in Endocrinology
Article Title: Mast cell promotes obesity by activating microglia in hypothalamus
doi: 10.3389/fendo.2025.1544213
Figure Lengend Snippet: POMC-melanocortin system participated in the effects of cromolyn sodium on energy balance. (A, B) Immunofluorescence staining and quantification of α-MSH in the hypothalamic PVN nucleus in brain slices from control and cromolyn sodium-injected mice. (C, D) Immunofluorescence co-staining and quantification of α-MSH in the hypothalamic DMH nucleus in brain slices from control and cromolyn sodium-injected mice. (E, F) Immunofluorescence staining and quantification of c-Fos in brain slices from control and cromolyn sodium-injected mice, which were i.c.v. saline control and SHU9119. (G, H) Food intake, oxygen consumption, and energy expenditure in control and cromolyn sodium-injected mice, as well as saline and SHU9119. ns, not significant. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, two-tailed Student’s t-test (B, D) , two-way ANOVA with Bonferroni’s post hoc test (F-I) .
Article Snippet: For
Techniques: Immunofluorescence, Staining, Control, Injection, Saline, Two Tailed Test
Journal: Cell Reports Medicine
Article Title: Mast cell modulation: A novel therapeutic strategy for abdominal pain in irritable bowel syndrome
doi: 10.1016/j.xcrm.2024.101780
Figure Lengend Snippet: Mast cell-targeted therapies as novel treatment strategy for IBS (A) An effective therapeutic strategy is to target the increased degranulation of gut mast cells. This can be achieved using mast cell stabilizing drugs (cromolyn sodium, ketotifen), which block exocytosis and thereby prevent the release of mediators by activated mast cells. An alternative approach is to prevent IgE-dependent or IgE-independent activation of mast cells. For IgE-dependent signaling, this can be achieved by monoclonal anti-IgE antibodies (omalizumab) that target IgE antibodies and thereby prevent the binding of IgE antibodies to FcεRI receptors on gut mast cells. For IgE-independent signaling, this could be achieved by MRGPRX2 receptor antagonists. Alternatively, Siglec-8 is an inhibitory receptor expressed on mast cells which, upon activation by monoclonal anti-Siglec-8 antibodies, initiates intracellular signaling cascades that prevent that IgE-mediated and non-IgE-mediated activation resulting in mast cell degranulation. (B) Targeting mast cell mediator signaling represents a very promising therapeutic strategy in IBS. This therapeutic approach relies on blocking the receptors for pro-nociceptive mast cell mediators such as serotonin (alosetron, ramosetron) or histamine (ebastine), thereby effectively preventing pro-nociceptive signaling on the gut pain innervation. IgE, immunoglobulin E; FceR1, Immunoglobulin E receptor; 5-HT, serotonin; 5-HT3R, serotonin 3 receptor; H1R, histamine 1 receptor.
Article Snippet: The
Techniques: Blocking Assay, Activation Assay, Binding Assay
Journal: JOR Spine
Article Title: Characterization and modulation of the pro‐inflammatory effects of immune cells in the canine intervertebral disk
doi: 10.1002/jsp2.1333
Figure Lengend Snippet: Culture groups.
Article Snippet: In addition to no treatment controls, canine MCs were pre‐treated with 25 μM of
Techniques:
Journal: JOR Spine
Article Title: Characterization and modulation of the pro‐inflammatory effects of immune cells in the canine intervertebral disk
doi: 10.1002/jsp2.1333
Figure Lengend Snippet: (A) Effect of stiffness (1% and 4%) on gene expression of nucleus pulposus (NP) cells at 14 days and 21 days ( N = 3–6). (B) Effect of stiffness (1% and 4%) on gene expression of mast cells (MCs) at 14 days and 21 days ( N = 3–6). (C) Effect of stiffness (1% and 4%) on gene expression in the NP + MC co‐culture at 14 and 21 days ( N = 3–6). (D) Effect of stiffness (1% and 4%) on gene expression in treatment groups NP + MC + protease activated receptor 2 antagonist (PAR2A) and NP + MC + cromolyn sodium (CS) + P at 21 days ( N = 3–6). * p value <0.05, ** p value <0.005. All error bars indicate standard error mean. Statistics = linear mixed model with Benjamini–Hochberg.
Article Snippet: In addition to no treatment controls, canine MCs were pre‐treated with 25 μM of
Techniques: Gene Expression, Co-Culture Assay
Journal: JOR Spine
Article Title: Characterization and modulation of the pro‐inflammatory effects of immune cells in the canine intervertebral disk
doi: 10.1002/jsp2.1333
Figure Lengend Snippet: Effect of treatment (cromolyn sodium [CS] and/or protease activated receptor 2 antagonist [PAR2A]) on gene expression in the 4% stiffness agarose gel at 14 and 21 days ( N = 3–6). * p value <0.05. All error bars indicate standard error mean. Statistics = linear mixed model with Benjamini–Hochberg. MC, mast cell; NP, nucleus pulposus.
Article Snippet: In addition to no treatment controls, canine MCs were pre‐treated with 25 μM of
Techniques: Gene Expression, Agarose Gel Electrophoresis