Journal: Neurotherapeutics

Article Title: Regulatory T cells attenuate astrogliosis via IL-10/STAT3/PKC/vimentin signaling and promote neurological recovery after spinal cord injury

doi: 10.1016/j.neurot.2025.e00827

Figure Lengend Snippet: IL-10 supplementation and PKC phosphorylation inhibition recapitulate Treg-mediated downregulation of vimentin in vitro . A Representative immunofluorescence images of Foxp3 (green) and IL-10 (red) of magnetically sorted Tregs from mouse spleen. B ELISA quantification of IL-10 levels in supernatants of isolated Tregs. Cohen's d = 4.7545. C Experimental timeline of in vitro IL-10 intervention in astrocytes (rIL-10: recombinant IL-10; αIL-10, IL-10 neutralizing antibody). D-H Western blot quantification of p-STAT3/STAT3 (η 2 = 0.8939), SOCS3 (η 2 = 0.9199), p -PKC/PKC (η 2 = 0.9414), and vimentin (η 2 = 0.9252) protein levels in astrocytes following IL-10 intervention. I Representative immunofluorescence images of vimentin in astrocytes following IL-10 intervention. J Experimental timeline of in vitro PKC phosphorylation modulation in astrocytes (Go6976: PKC inhibitor; PMA: PKC activator). K, L Western blot quantification of vimentin protein levels in astrocytes following PKC modulation. η 2 = 0.8597. M, N Immunofluorescence quantification of vimentin levels in astrocytes following PKC modulation. η 2 = 0.6114. Data are mean ± SEM (n = 6 independent cultures). Statistical analyses were performed using two-tailed Student's t -test (B) or one-way ANOVA (E-H, L, N). P values are indicated on the graphs. n.s., not significant.

Article Snippet: For in vitro PKC modulation, we established optimal concentrations through gradient testing: astrocytes were treated with the PKC inhibitor Go6976 (100 nM, Selleck) for 24 h or the PKC activator Phorbol 12-myristate 13-acetate (PMA; 10 nM, Selleck) for 30 min.

Techniques: Phospho-proteomics, Inhibition, In Vitro, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Isolation, Recombinant, Western Blot, Two Tailed Test

Journal: bioRxiv

Article Title: Screening of a kinase inhibitor library in human Huntington’s disease iPSC-derived striatal precursor neurons reveals a neuroprotective effect of PKC-α/β1 inhibition

doi: 10.1101/2025.09.18.677178

Figure Lengend Snippet: Detailed EC50 values for the hits are provided ( A-E ). The top hits were CK1 inhibitor D4476, ATR/CDK inhibitor NU6027, CDK1/GSK3β inhibitor Kenpaullone, GSK3β inhibitor AZD1080, and PKC-α/β1 inhibitor GO6976.

Article Snippet: GO6976, developed by GÖDECKE AG (later acquired by Pfizer) in the early 1990s, is a potent and selective inhibitor of conventional Ca 2+ -dependent PKC isoforms (α and β1) .

Techniques:

Journal: bioRxiv

Article Title: Screening of a kinase inhibitor library in human Huntington’s disease iPSC-derived striatal precursor neurons reveals a neuroprotective effect of PKC-α/β1 inhibition

doi: 10.1101/2025.09.18.677178

Figure Lengend Snippet: A). GO6976 structure formulas. B). ISPNs with 33/18 and 180/18 CAG repeats were stressed by growth factor and nutrients withdrawal (W/O) for 24 hr. 180Q ISPNs were treated with GO6976 at 0.1,0.25,0.5, 1 uM, or Veh (Vehicle control). C). 180Q ISPNs were treated with 1uM GO6976, LY333531, Tetrandrine, GO6983 or Veh upon stress. ATP levels were measured using CellTiter-Glo cell viability assay. The results from B&C are presented as MEAN ± SEM, normalized as % of the value of control (Con) group under normal growth conditions (n=5-10). One-way ANOVA, * p<0.05 vs 33Q W/O+Veh; # p<0.05 vs 180Q Con+Veh; ** p<0.05 vs 180Q W/O+Veh.

Article Snippet: GO6976, developed by GÖDECKE AG (later acquired by Pfizer) in the early 1990s, is a potent and selective inhibitor of conventional Ca 2+ -dependent PKC isoforms (α and β1) .

Techniques: Control, Viability Assay