Journal: The Journal of Neuroscience

Article Title: Prolactin Regulates Tuberoinfundibular Dopamine Neuron Discharge Pattern: Novel Feedback Control Mechanisms in the Lactotrophic Axis

doi: 10.1523/JNEUROSCI.0129-12.2012

Figure Lengend Snippet: The LV and HV components of IPrl are activated by distinct signal transduction pathways. A, I–V relationship of IPrl in control (green; n = 14), wortmannin (200 nm; red; n = 8), and AG490 (10 μm; blue; n = 3). Wortmannin, but not AG490, significantly modifies IPrl at VHold = +40 mV. Values expressed as mean ± SEM. ***p < 0.005. B, I–V relationship of IPrl at a concentration of 500 nm Prl (green; n = 14), 40 nm Prl in which both the LV and HV components were present (red; n = 13 of 19), and 40 nm Prl in which only the LV component was present (blue; n = 6 of 19). Values expressed as mean ± SEM. ***p < 0.005.

Article Snippet: TTX was purchased from Alomone Labs. AG490 [( E )-2-cyano-3-(3,4-dihydrophenyl)- N -(phenylmethyl)-2-propenamide], nimodipine, paxilline, {"type":"entrez-protein","attrs":{"text":"SKF96365","term_id":"1156357400","term_text":"SKF96365"}} SKF96365 (1-[2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl-1 H -imidazole hydrochloride), UCL1648 [6,10-diaza-3(1,3)8,(1,4)-dibenzena-1,5(1,4)-diquinolinacy clodecaphane], and wortmannin were purchased from Tocris Bioscience. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 6. caption a7 Prl broadens TIDA APs.

Techniques: Transduction, Concentration Assay

Journal: Journal of Inflammation Research

Article Title: Melatonin Ameliorates Axonal Hypomyelination of Periventricular White Matter by Transforming A1 to A2 Astrocyte via JAK2/STAT3 Pathway in Septic Neonatal Rats

doi: 10.2147/JIR.S337499

Figure Lengend Snippet: Melatonin activated MT1/JAK2/STAT3 pathway in primary astrocytes exposed to IL-1α, C1q and TNF-α in vitro. ( A ) Shows optical density changes of p-JAK2 relative to JAK2, p-STAT3 relative to STAT3 and MT1 relative to GAPDH in each group. IL-1α + C1q + TNF-α treatment for 24h significantly decreased the optical density of MT1, P-JAK2 and P-STAT3 proteins when compared with the corresponding controls. Melatonin reversed the changes, but the effect was prevented by luzindole. Additionally, blockage of JAK2 or STAT3 inhibited the effect of melatonin in modulating the A1/A2 astrocyte polarization. ( B ) Shows A1-marker C3, A2-marker S100A10, p-STAT3, STAT3 and GAPDH immunoreactive bands after IL-1α + C1q + TNF-α, IL-1α + C1q + TNF-α + melatonin, and IL-1α + C1q + TNF-α + AG490 (an inhibitor of JAK2 activity) treatment when compared with the corresponding control in primary astrocyte. ( C ) show immunoreactive bands after IL-1α + C1q + TNF-α, IL-1α + C1q + TNF-α + melatonin, IL-1α + C1q + TNF-α + STAT-IN-3 (an inhibitor of STAT3 activity) treatment when compared with the corresponding control in primary astrocyte. Note melatonin treatment activates MT1/JAK2/STAT3 pathway and then promoted A1 to A2 polarization. RT-qPCR shows mRNA expression changes in neurotrophic factors LIF and FGF2. GAPDH was used as the internal control. IL-1α + C1q + TNF-α treatment for 24h significantly decreased the mRNA expression of LIF and FGF2 when compared with the corresponding controls. Melatonin reversed the changes, but the effect of melatonin was prevented by luzindole ( D ). * P < 0.05, ** P < 0.01, *** P <0.001 (n=3 for each group).

Article Snippet: AG490 (10 μM) (the blocker of JAK2, MCE, CAS No.133550-30-5) and STAT-IN-3 (10 μM) (the blocker of STAT3, MCE, CAS No.2361304-26-7) were used along with melatonin to detect their effects on A1 astrocytes.

Techniques: In Vitro, Marker, Activity Assay, Control, Quantitative RT-PCR, Expressing

Journal: iScience

Article Title: Inhibition of CD44 suppresses the formation of fibrotic scar after spinal cord injury via the JAK2/STAT3 signaling pathway

doi: 10.1016/j.isci.2024.108935

Figure Lengend Snippet: STAT3 was the downstream of JAK2 in CD44-mediated fibrotic effect in the inflammatory microenvironment (A) Western blotting analyzed the expression of p -JAK2, p-STAT3, STAT3, and p -Smad2 in the fibroblasts stimulated with IS after inhibition of AG490. (B‒E) Quantification of western blotting results in A. N = 3 of each group by one-way ANOVA. (F) Western blotting analyzed the expression of CD44, α-SMA, collagen-I, FN, and laminin in the fibroblasts stimulated with IS after inhibition of AG490. (G‒K) Quantification of western blotting results in F. N = 3 of each group by one-way ANOVA. (L and M) Quantification analysis of the rate of proliferation (%) (L) per 10 6 μm 2 (n = 5) and cell numbers of migration (M) per 10 6 μm 2 (n = 5) in different groups by one-way ANOVA. All data were presented as mean ± SEM. (∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001). (See also Figure S3 ).

Article Snippet: AG490 , Targetmol , Cat#T2600;CAS:133550-30-8;Batch:147766.

Techniques: Western Blot, Expressing, Inhibition, Analysis, Migration

Journal: iScience

Article Title: Inhibition of CD44 suppresses the formation of fibrotic scar after spinal cord injury via the JAK2/STAT3 signaling pathway

doi: 10.1016/j.isci.2024.108935

Figure Lengend Snippet: Diagram of molecule mechanism of CD44-JAK2-STAT3 in the fibroblasts following SCI, macrophages are activated and secrete varieties of cytokines and inflammatory factors, and recruit fibroblasts to participate in the subsequent repair process Then CD44 on the fibroblasts would be activated by these proinflammatory factors, which could be inhibited by IM7. The signal is transferred into cells, and activates the JAK2 and STAT3. Activated STAT3 enters into nucleus and regulates the expression of fibrosis-related genes at the transcriptional level by binding specific DNA promoter sequences, which ultimately promotes the proliferation, differentiation, and migration of fibroblasts, leading to the deposition of excessive ECM proteins and finally forms dense fibrotic scar tissue.

Article Snippet: AG490 , Targetmol , Cat#T2600;CAS:133550-30-8;Batch:147766.

Techniques: Expressing, Binding Assay, Migration, Tissue

Journal: iScience

Article Title: Inhibition of CD44 suppresses the formation of fibrotic scar after spinal cord injury via the JAK2/STAT3 signaling pathway

doi: 10.1016/j.isci.2024.108935

Figure Lengend Snippet:

Article Snippet: AG490 , Targetmol , Cat#T2600;CAS:133550-30-8;Batch:147766.

Techniques: Cell-Signaling, Recombinant, In Vivo, Lysis, Acid Assay, Software

Journal: Biochimica et biophysica acta

Article Title: Prolactin and glucocorticoid signaling induces lactation-specific tight junctions concurrent with β-casein expression in mammary epithelial cells.

doi: 10.1016/j.bbamcr.2016.04.023

Figure Lengend Snippet: Fig. 4. Prl and Dex influence the expression patterns of Cldn3 and Cldn4 in MECs (A) Immunostaining images of Cldn3 (green) and Cldn4 (green) with Ocln (red) in MECs cultured with or without Prl (0.5 U/mL) and Dex (1 μM) for 5 days. Nuclei stained with DAPI are blue. The scale bars represent 10 μm. (B–F) The results of western blotting and densitometry analysis of Cldn3 and Cldn4 with β-actin used as an internal control. MECs were cultured for 5 days with or without Prl (0.5 U/mL or 0–2.5 U/mL) and Dex (1 μM). MECs were pretreated with 10 μM AG490 (JAK inhibitor) and 5 μM RU486 (glucocorticoid receptor antagonist) 1 h before Prl (0.5 U/mL) and Dex (100 nM) treatment. The data are presented as the mean (SEM); n = 5; *p b 0.05 and **p b 0.005. (G) The expression of Cldn3 and Cldn4, determined by qRT-PCR. The data are presented as the mean (SEM); n = 6; *p b 0.05 and **p b 0.005.

Article Snippet: AG490 (JAK inhibitor; cat. no. T9969) and RU486 (GR antagonist; cat. no. M3321)were purchased from LKT Laboratories, Inc. (St. Paul, MN).

Techniques: Expressing, Immunostaining, Cell Culture, Staining, Western Blot, Control, Quantitative RT-PCR