Journal: Cell Death & Disease

Article Title: DJ-1 counteracts Caveolin-1-mediated necroptosis to inhibit epithelial barrier dysfunction in colitis

doi: 10.1038/s41419-025-07989-z

Figure Lengend Snippet: A Representative IHC analysis of DJ-1 expression in colonic tissue samples from healthy controls and patients with UC or CD (magnification ×200; scale bar = 50 µm). B Statistical analysis of DJ-1 expression in the healthy controls ( n = 13), patients with UC ( n = 10) or CD ( n = 11). C Correlation analysis of the CAV1 and DJ-1 IHC staining IOD/area score is shown ( n = 36). D HCT116 cells were infected with a FLAG-tagged CAV1 overexpression plasmid or the empty vector (vehicle), and total FLAG-tagged CAV1 was immunoprecipitated. E Endogenous co-IP: HEK-293 cell lysates were immunoprecipitated with anti–DJ-1 or control IgG antibodies. F Endogenous co-IP: HT29 cell lysates were immunoprecipitated with anti–DJ-1 or control IgG antibodies. G Representative images of immunofluorescence staining of IBD human colon sections (DJ-1: green, CAV1: red, DAPI nuclear: blue, magnification ×600). H Western blot analysis of colonic CAV1 protein levels in the WT and DJ-1 KO mice with DSS-induced colitis. I Quantitative analysis of the above CAV1 protein levels ( n = 4). J HEK293 cells infected with FLAG-tagged CAV1, HA-tagged DJ-1 plasmid and empty vector were stimulated with 100 ng/ml TNF-α and 25 µM zVAD-fmk for 24 h and then treated with MG132 (25 µM, I) for another 6 h. All data are the means ± SD. * p < 0.05, *** p < 0.001, **** p < 0.0001, two-tailed.

Article Snippet: For the necroptosis inhibition experiments, WT and DJ-1 KO mice were treated with 2 mg/mL GSK’872 (MCE, USA) every two days or 1 mg/mL GW806742X (MCE, USA) each day by intraperitoneal injection under a 7-day DSS administration.

Techniques: Expressing, Immunohistochemistry, Infection, Over Expression, Plasmid Preparation, Immunoprecipitation, Co-Immunoprecipitation Assay, Control, Immunofluorescence, Staining, Western Blot, Two Tailed Test

Journal: Cell Death & Disease

Article Title: DJ-1 counteracts Caveolin-1-mediated necroptosis to inhibit epithelial barrier dysfunction in colitis

doi: 10.1038/s41419-025-07989-z

Figure Lengend Snippet: WT, DJ-1 KO, CAV1 KO and DKO mice were treated with DSS for 7 days. WT NC = 5, WT DSS = 12, DJ-1 KO DSS = 12, CAV1 KO DSS = 6, DKO DSS = 5. Body weight change ( A ), survival rates ( B ) and the disease activity index ( C ) were monitored daily. D Mouse colon lengths were measured after sacrifice. E Intestinal permeability was evaluated by measuring the concentration of FITC-dextran in the blood serum. Histological scores ( F ) were determined in a double-blinded manner, and the histological analysis of colon tissue samples is shown ( G ) (upper: magnification ×100; scale bar = 100 µm, lower: magnification ×400; scale bar = 20 µm). H Quantitative PCR analysis was used to assess cytokine and chemokine production in whole-colon homogenates. DAI scores and inflammation scores are expressed as median and IQR. Other All data are the means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns no significant, two-tailed.

Article Snippet: For the necroptosis inhibition experiments, WT and DJ-1 KO mice were treated with 2 mg/mL GSK’872 (MCE, USA) every two days or 1 mg/mL GW806742X (MCE, USA) each day by intraperitoneal injection under a 7-day DSS administration.

Techniques: Activity Assay, Permeability, Concentration Assay, Real-time Polymerase Chain Reaction, Two Tailed Test

Journal: Cell Death & Disease

Article Title: DJ-1 counteracts Caveolin-1-mediated necroptosis to inhibit epithelial barrier dysfunction in colitis

doi: 10.1038/s41419-025-07989-z

Figure Lengend Snippet: A Representative IHC analysis of p-RIPK1 expression in colonic tissue samples (IHC upper: magnification ×100；scale bar = 100 µm, lower: magnification ×400；scale bar = 20 µm). B Quantification of IHC analysis of p-RIPK1 (WT NC = 5, WT DSS = 6, DJ-1 KO DSS = 7, CAV1 KO DSS = 4, DKO DSS = 5) expression. C Western blotting was used to analyze CAV1, DJ-1 and necroptosis signaling pathway molecule protein levels in colon tissue samples from the mice treated as described above. D Intestinal organoids from the WT, DJ-1 KO, CAV1 KO and DKO mice treated as indicated with the combination of TNF-α (100 ng/ml) and zVAD-fmk (25 µM) (TZ), or TZ+ necrostatin-1 (Nec-1, 30 µM) for 12 h and stained with PI (red) for 24 h (magnification ×200；scale bar = 50 µm). E Quantification of PI intensities. n = 12 organoids from 3 mice per group. F DJ-1 and CAV1 expression were knocked down in HCT116 cells, and the cells were stimulated with TZ for 24 h. G Western blot analysis of DJ-1 and CAV1 overexpression in the TZ-stimulated HCT116 cells. All data are the means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, two-tailed.

Article Snippet: For the necroptosis inhibition experiments, WT and DJ-1 KO mice were treated with 2 mg/mL GSK’872 (MCE, USA) every two days or 1 mg/mL GW806742X (MCE, USA) each day by intraperitoneal injection under a 7-day DSS administration.

Techniques: Paraffin-embedded Immunohistochemistry, Expressing, Western Blot, Staining, Over Expression, Two Tailed Test

Journal: Cell Death & Disease

Article Title: DJ-1 counteracts Caveolin-1-mediated necroptosis to inhibit epithelial barrier dysfunction in colitis

doi: 10.1038/s41419-025-07989-z

Figure Lengend Snippet: WT and DJ-1 KO mice were treated with 2 mg/ml GSK’872 every two days by intraperitoneal injection after 7 days of DSS administration. WT DSS = 7, WT DSS + GSK’872 = 9, DJ-1 KO DSS = 7, DJ-1 KO DSS + GSK’872 = 6. Body weight change ( A ), survival rates ( B ) and the DAI scores ( C ) were scored daily. Mice were sacrificed on Day 7, and colon lengths ( D ) were measured. E HE staining in colon tissue samples from the WT and DJ-1 KO mice is shown (magnification ×100; scale bar=100 µm). F Semiquantitative histopathological scoring was performed. G Quantitative PCR analysis of cytokines and chemokines in colons from the WT and DJ-1 KO DSS-treated mice. The WT and DJ-1 KO mice were treated with 1 mg/ml GW806742X (GW) for each day by intraperitoneal injection under a 7-day DSS administration. WT DSS = 5; WT DSS + GW = 7; DJ-1 KO + GW = 7. Body weight change ( H ), survival rates ( I ) and DAI scores ( J ) were scored daily. Colon lengths ( K ) were measured. H&E staining ( L ) in colon tissue samples is shown, and semiquantitative scoring of histopathology ( M ) was performed (upper: magnification ×40; scale bar = 500 µm, lower: magnification ×100; scale bar=200 µm). N Quantitative PCR analysis of cytokines and chemokines in colons. DAI scores and inflammation scores are expressed as median and IQR. Other All data are the means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, two-tailed.

Article Snippet: For the necroptosis inhibition experiments, WT and DJ-1 KO mice were treated with 2 mg/mL GSK’872 (MCE, USA) every two days or 1 mg/mL GW806742X (MCE, USA) each day by intraperitoneal injection under a 7-day DSS administration.

Techniques: Injection, Staining, Real-time Polymerase Chain Reaction, Histopathology, Two Tailed Test

Journal: Science Advances

Article Title: CHCHD2 mutant mice link mitochondrial deficits to PD pathophysiology

doi: 10.1126/sciadv.adu0726

Figure Lengend Snippet: ( A ) Activity of complex I isolated from brain was slightly increased in T61I HOM mice at 5 months but unchanged from WT at 11 months. ( B ) ROS (H 2 O 2 ) levels from brain showed progressive increase in T61I HOM mice from 5 to 11 months. In (A) and (B), n = 3 WT and 4 HOM mice at 5 months and 4 WT and 5 HOM mice at 11 months. Data represent mean ± SEM. * P < 0.05 by two-way ANOVA with Sidak’s post hoc test. ( C ) Circos plot showed PPIs with ROS-associated proteins present in the mitochondrial fraction in WT but lost (below threshold) in T61I mutants. Each line represents a PPI between two proteins. Interactions with Prdx2 in blue, Park7 in red, Sod2 in orange, Prdx3 in green, and Prdx4 in purple. ( D ) Proposed pathological model. The T61I mutation leads to CHCHD2 insolubility, likely due to a toxic gain of function, resulting in protein aggregation primarily within mitochondria in SN DA neurons. This mutation also elevates both the total level and phosphorylation of α-synuclein, potentially as a direct consequence or secondary effect of the T61I mutation. Energy failure caused by mitochondrial dysfunction and ROS is proposed to be a key contributor to DA neuron dysfunction and degeneration.

Article Snippet: PARK7 antibody , Proteintech 82913-2-RR , AB_3670647.

Techniques: Activity Assay, Isolation, Mutagenesis, Phospho-proteomics