Journal: Bioengineered

Article Title: The crystallin alpha B (HSPB5)-tripartite motif containing 33 (TRIM33) axis mediates myocardial fibrosis induced by angiotensinogen II through transforming growth factor-β (TGF-β1)-Smad3/4 signaling

doi: 10.1080/21655979.2022.2054913

Figure Lengend Snippet: qRT-PCR primer sequences

Article Snippet: The TRIM33 and HSPB5 overexpression plasmids were also purchased from Genebay Company (Nanjing, China) (source of genes: TRIM33: NM_053170.3:587–4009 Mus musculus tripartite motif-containing 33 (Trim33), transcript variant 1, mRNA; HSPB5: NM_009964.3:307–834 Mus musculus crystallin, alpha B (Cryab), transcript variant 2, mRNA).

Techniques:

Journal: Bioengineered

Article Title: The crystallin alpha B (HSPB5)-tripartite motif containing 33 (TRIM33) axis mediates myocardial fibrosis induced by angiotensinogen II through transforming growth factor-β (TGF-β1)-Smad3/4 signaling

doi: 10.1080/21655979.2022.2054913

Figure Lengend Snippet: HSPB5-TRIM33 axis suppresses TGF-β1-Smad3/4 signaling in CFs. a-d. Western blot analysis was used to detect the expression of TGF-β1, β-catenin and FOXO3a in CFs after TRIM33 overexpression. e-g. The P-smad3/Smad3 and P-smad4/Smad4 level after TRIM33 overexpression was determined by Western blot. h-j. Western blot analysis was used to detect the expression of HSPB5 and TRIM33 in HSPB5 overexpressed CFs. Each experiment was conducted three times independently. **P < 0.01, ***P < 0.001, ns: No statistical significance.

Article Snippet: The TRIM33 and HSPB5 overexpression plasmids were also purchased from Genebay Company (Nanjing, China) (source of genes: TRIM33: NM_053170.3:587–4009 Mus musculus tripartite motif-containing 33 (Trim33), transcript variant 1, mRNA; HSPB5: NM_009964.3:307–834 Mus musculus crystallin, alpha B (Cryab), transcript variant 2, mRNA).

Techniques: Western Blot, Expressing, Over Expression

Journal: Bioengineered

Article Title: The crystallin alpha B (HSPB5)-tripartite motif containing 33 (TRIM33) axis mediates myocardial fibrosis induced by angiotensinogen II through transforming growth factor-β (TGF-β1)-Smad3/4 signaling

doi: 10.1080/21655979.2022.2054913

Figure Lengend Snippet: TRIM33 attenuates the fibrosis induced by HSPB5. a. The qRT-PCR analysis was used to clarify the expression of HSPB5. b-c. EDU immunofluorescence staining was conducted to detect the proliferation rate of CFs. d-e. The migration assay was used to confirm the migration of CFs in four groups. f-g. The Coll I and a-SMA expression level was determined by Western blot. Each experiment was conducted three times independently. *P < 0.05,**P < 0.01, ***P < 0.001.

Article Snippet: The TRIM33 and HSPB5 overexpression plasmids were also purchased from Genebay Company (Nanjing, China) (source of genes: TRIM33: NM_053170.3:587–4009 Mus musculus tripartite motif-containing 33 (Trim33), transcript variant 1, mRNA; HSPB5: NM_009964.3:307–834 Mus musculus crystallin, alpha B (Cryab), transcript variant 2, mRNA).

Techniques: Quantitative RT-PCR, Expressing, Immunofluorescence, Staining, Migration, Western Blot

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: NLRC5 is upregulated in microglia within the peri-infarct region following cerebral ischemia. A Schematic diagram of the penumbra area in cerebral ischemic stroke. B Representative western blot images of NLRC5 and GAPDH expression from sham and tMCAO mice penumbra at 1, 3, and 7 days poststroke. C Quantification of NLRC5 levels in the ischemic penumbra of tMCAO mice at different time points, normalized to sham controls. n = 4 per group. One-way ANOVA with Tukey’s post hoc test. D The mRNA levels of Nlrc5 from sham and tMCAO mice penumbra at 1, 3, and 7 days poststroke were detected via RT-qPCR. n = 4–5 per group. One-way ANOVA with Tukey’s post hoc test. E Representative immunofluorescence images showing co-localization of NLRC5 (green) with GFAP, Iba-1 or NeuN (red) in the tMCAO mice penumbra 3 days poststroke. Nucleus were visualized with DAPI (blue). Scale bars: 20 μm. F - H Intensity profiles of indicated proteins along the plotted lines, as analyzed by Image J line scan analysis. I Pearson’s correlation coefficient between NLRC5 intensity and the intensity of GFAP, Iba-1 and NeuN. n = 5 per group. J Immunofluorescence of NLRC5 (green) in microglial cells (Iba-1 + ; red) in the mouse ischemic penumbra 1, 3 and 7 days after stroke. DAPI staining is shown in blue. Scale bars: 20 μm. K Quantification of NLRC5 intensity in Iba-1 + cells in sham and tMCAO mice penumbra at 1, 3, and 7 days poststroke. n = 4 per group. One-way ANOVA with Tukey’s post hoc test. L Representative images of human brain samples in non-stroke and stroke conditions. Stroke-induced NLRC5 (green) expression in human microglia (Iba-1 + , red). DAPI staining is shown in blue. Scale bars: 10 μm. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01 vs. sham control

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: Western Blot, Expressing, Quantitative RT-PCR, Immunofluorescence, Staining, Control

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: Microglia-specific deletion of Nlrc5 attenuates ischemic brain injury. A Timeline of the animal experiments. B , C CBF was measured by LSCI. n = 3 per group. Two-way ANOVA with Sidak’s multiple comparisons test. D The survival curve for the Nlrc5 fl/fl and mCKO mice after tMCAO. n = 28 in Nlrc5 fl/fl group; n = 24 in mCKO group. Kaplan-Meier with Log-rank test. E - H Evaluation of mNSS ( E ), unpaired Student’s t test with Mann-Whitney U test, fault step ratio ( F ), Two-way ANOVA with Sidak’s multiple comparisons test, rotarod test ( G ), Two-way ANOVA with Sidak’s multiple comparisons test, and grip strength (H), Two-way ANOVA with Sidak’s multiple comparisons test, in Nlrc5 fl/fl and mCKO mice at 1, 3 and 7 days after tMCAO. n ≥ 12 per group. I Representative TTC staining of brain sections from Nlrc5 fl/fl and mCKO mice at 1, 3 and 7 days after tMCAO. J Infarct volume. n = 9–10 per group. Two-way ANOVA with Sidak’s multiple comparisons test. K Representative dual- immunofluorescence staining of TUNEL (red)/NeuN (green) at 1 and 3 days after tMCAO. Scale bars: 100 μm. L The percentage of NeuN + TUNEL + cells among all NeuN + cells in the peri-infarct brain regions. n = 4–6 per group, Two-way ANOVA with Sidak’s multiple comparisons test. Modified Neurological Severity Scores ( E ) are shown as median ± ranges, and other values are presented as mean ± SEM. * p < 0.05, ** p < 0.01 vs. Nlrc5 fl/fl group; “ns” indicates no significance ( p > 0.05)

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: MANN-WHITNEY, Staining, Immunofluorescence, TUNEL Assay, Modification

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: Microglial Nlrc5 deletion suppresses post-ischemic neuroinflammation and microglial activation. A Three days after tMCAO, microglia sorted based on the CD45 int and CD11b + strategy were subjected to PCR array analysis. B - I RT-qPCR assessment of pro-inflammatory genes, including Il6 , Il1b , Nos2 , and Tnf , in the ischemic penumbra 1 day and 3 days after tMCAO. n = 4–5 per group. One-way ANOVA with Tukey’s post hoc test. J , K TNF-α and IL-6 protein levels were evaluated by ELISA in mice 3 days poststroke. n = 3–4 per group. One-way ANOVA with Tukey’s post hoc test. L Representative immunofluorescence images for Iba1 (red) and DAPI (blue) and 3D-reconstructed images of Iba1 + microglia 1 day and 3 days after tMCAO. Scale bar: 20 μm. M Quantification of Iba1 MFI. n = 5–7 per group. Two-way ANOVA with Sidak’s multiple comparisons test. N - P Quantification of average branch number, junctions and length of microglia in the peri-infarct region. n = 5–7 per group. Two-way ANOVA with Sidak’s multiple comparisons test. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01 vs. Nlrc5 fl/fl group; “ns” indicates no significance ( p > 0.05)

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: Activation Assay, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Immunofluorescence

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: NLRC5 exacerbates inflammatory responses and promotes microglia-mediated neuronal death in an in vitro model. A , B Western blot analysis of NLRC5 in primary microglial cells under LPS (0.1 µg/mL, 6 h) or OGD/R (4 h/6 h) stimulation. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. C The mRNA levels of Nlrc5 from primary microglial cells after LPS (0.1 µg/mL, 6 h) or OGD/R (4 h/6 h) stimulation were detected via RT-qPCR. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. D Schematic diagram of extracting primary microglial cells from Nlrc5 global KO ( Nlrc5 KO) mice and their WT littermates for in vitro culture. E - L RT-qPCR assessment of pro-inflammatory genes, including Il6 , Il1b , Nos2 , and Tnf , in primary microglial cells after LPS (0.1 µg/mL, 6 h) or OGD/R (4 h/6 h) stimulation. n = 3–6 per group. One-way ANOVA with Tukey’s post hoc test. M , N TNF-α and IL-6 protein levels were evaluated by ELISA in primary microglial cell culture after OGD/R (4 h/6 h) stimulation. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. O Schematic of primary neuron treatment with microglia-conditioned medium in vitro. CM: conditioned medium. P , Q Immunostaining images of TUNEL (red), MAP2 (green), and DAPI (blue) in WT-O4R6 and Nlrc5 KO-O4R6 groups. Scale bar = 20 μm. The bar graph shows the percentage of TUNEL + cells/DAPI + cells. n = 6 per group. p = 0.0043, unpaired Student’s t test. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01; “ns” indicates no significance ( p > 0.05)

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: In Vitro, Western Blot, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cell Culture, Immunostaining, TUNEL Assay

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: NLRC5-mediated microglial inflammation is associated with lysosomal and autophagic dysfunction. A PCA plot of the 6 samples in WT-O4R6 and Nlrc5 KO-O4R6 groups. B Volcano plot showing the upregulated and downregulated DEPs (∣log 2 FC∣>0.263, p-value<0.05) between primary microglia in WT-O4R6 and Nlrc5 KO-O4R6 groups. C GO analysis of the DEPs, including three categories: cellular components (CC), biological processes (BP), and molecular functions (MF). D KEGG pathway analysis of DEPs. E Heatmap of lysosome pathway related proteins between the WT-O4R6 and Nlrc5 KO-O4R6 groups. F mRNA of lysosome related genes was analyzed by RT-qPCR in primary microglia in WT-O4R6 and Nlrc5 KO-O4R6 groups. n = 3 per group. Two-way ANOVA with Sidak’s multiple comparisons test. G - J RT-qPCR assessment of pro-inflammatory genes, including Il6 , Il1b , Nos2 , and Tnf , in primary microglial cells after OGD/R (4 h/6 h) stimulation with or without BAF addition. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01; “ns” indicates no significance ( p > 0.05)

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: Quantitative RT-PCR

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: Nlrc5 knockout restores lysosomal function impaired by OGD/R in microglia and promotes autophagic flux. A - C Western blot analysis of NLRC5 (representative blot, not quantified), SQSTM1 and autophagosome marker LC3 in primary microglial cells under OGD/R (4 h/6 h) stimulation with or without BAF addition. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. D Representative TEM images of primary microglia in WT-O4R6 and Nlrc5 KO-O4R6 groups. N, nucleus. Scale bar = 1 μm. E Quantification of autophagosomes in WT-O4R6 and Nlrc5 KO-O4R6 groups. n = 16 per group. p = 0.001, unpaired Student’s t test. F Rationale of the mRFP-GFP-LC3 assay. Under physiological pH LC3 + vesicles fluoresce emit both GFP and RFP fluorescence. Upon fusion with lysosomes and concomitant acidification, GFP fluoresence is rapidly lost, resulting in vesicles with only RFP fluorescence. G Representative images of mRFP-GFP-LC3 staining showing the autophagosome (yellow) and autolysosome (red-only) formation in primary microglial cells, with or without Nlrc5 knockout after OGD/R treatment. Scale bar: 10 μm. H , I Quantification of the number of green and red LC3 puncta. n = 10–14 per group. One-way ANOVA with Tukey’s post hoc test. J Assessment of the autophagic flux rate (RFP: GFP ratio). n = 10–14 per group. One-way ANOVA with Tukey’s post hoc test. K Representative confocal images showing staining of lysosomes with LysoSensor (green) and LysoTracker (red). Scale bar: 20 μm. L Quantification of LysoSensor fluorescence intensity in primary microglial cells. n = 4 per group. One-way ANOVA with Tukey’s post hoc test. M Representative western blot images of LAMP1, mature CTSB (M-CTSB), mature CTSD (M-CTSD) and β-actin in primary microglial cells under OGD/R (4 h/6 h) stimulation. N Quantitative analysis of LAMP1 levels. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. O Quantitative analysis of M-CTSD levels. n = 4 per group. One-way ANOVA with Tukey’s post hoc test. P Quantitative analysis of M-CTSB levels. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01; “ns” indicates no significance ( p > 0.05)

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: Knock-Out, Western Blot, Marker, Fluorescence, Staining

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: NLRC5 binds to ISG15 in microglia and upregulates the protein level of ISG15. A Western blot showing over-expression of NLRC5 in primary microglial cells, representative blot, not quantified. B The whole lysates of primary microglial cells were mixed with anti-HA-coated Protein A/G magnetic beads, and the NLRC5-binding proteins were analyzed by LC-MS/MS. 12 possible binding proteins were identified. C ISG15 was identified as an NLRC5-binding protein. D Heatmap of DEPs in ischemic penumbra between Nllrc5 KO mice and WT mice at 3 days poststroke. E After immunoprecipitation with anti-HA, lysates of primary microglia were immunoblotted with anti-HA and anti-ISG15 antibodies. F After immunoprecipitation with anti-ISG15, lysates of primary microglia were immunoblotted with anti-NLRC5 and anti-ISG15 antibodies. Rabbit IgG served as a control. G Representative images of the Duolink PLA assay showing the PLA signals elicited by the interaction of NLRC5 and ISG15 in primary microglia. Scale bar: 10 μm. H , I Western blot analysis of ISG15 in Nlrc5 fl/fl and mCKO mice penumbra at 3 days poststroke. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. J Representative images of immunofluorescence of ISG15 (green) in microglial cells (Iba-1 + ; red) in Nlrc5 fl/fl and mCKO mice penumbra 3 days poststroke. DAPI staining is shown in blue. Scale bars: 20 μm. K Representative images of intensity profiles of indicated proteins along the plotted lines in Nlrc5 fl/fl mice penumbra 3 days poststroke, as analyzed by Image J line scan analysis. L Representative images of pearson’s correlation coefficient between ISG15 intensity and the intensity of Iba-1 in Nlrc5 fl/fl mice penumbra 3 days poststroke. M Quantification of ISG15 intensity in Iba-1 + cells in sham and tMCAO Nlrc5 fl/fl and mCKO mice penumbra 3 days poststroke. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. N , O Western blot analysis of ISG15 in WT and Nlrc5 KO microglia under OGD/R (4 h/6 h) stimulation. n = 4 per group. One-way ANOVA with Tukey’s post hoc test. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: Western Blot, Over Expression, Magnetic Beads, Binding Assay, Liquid Chromatography with Mass Spectroscopy, Immunoprecipitation, Control, Immunofluorescence, Staining

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: NLRC5 exacerbates lysosomal dysfunction and microglial inflammation in an ISG15-dependent manner. A Representative western blot images of NLRC5 (representative blot, not quantified), mature CTSD (M-CTSD), LAMP1, mature CTSB (M-CTSB), ISG15 (representative blot, not quantified) and β-actin in primary microglial cells under OGD/R (4 h/6 h) stimulation with Isg15 knockout or NLRC5 overexpression. B - D Western blot analysis of LAMP1, M-CTSD and M-CTSB in primary microglial cells under OGD/R (4 h/6 h) stimulation with Isg15 knockout or NLRC5 overexpression, with β-actin as a loading control. n = 4 per group. One-way ANOVA with Tukey’s post hoc test. E - H RT-qPCR assessment of pro-inflammatory genes, including Il6 , Il1b , Tnf and Nos2 , in primary microglial cells under OGD/R (4 h/6 h) stimulation with Isg15 knockout or NLRC5 overexpression. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. I , J IL-6 and TNF-α protein levels were evaluated by ELISA in primary microglial cell culture under OGD/R (4 h/6 h) stimulation with Isg15 knockout or NLRC5 overexpression. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. K Schematic diagram of different groups. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01 vs. WT-OGD/R group; @ p < 0.05, @@ p < 0.01 vs. WT group; & p < 0.05, && p < 0.01 vs. WT-OGD/R group; % p < 0.05, %% p < 0.01 vs. WT-OENLRC5-OGD/R group; “ns” indicates no significance ( p > 0.05)

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: Western Blot, Knock-Out, Over Expression, Control, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cell Culture

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: The CARD domain of NLRC5 binds ISG15 and specifically inhibits ISG15 degradation via the autophagy-lysosome pathway. A After 18 h of LPS (0.1 µg/mL) stimulation to induce high expression of ISG15 in WT and Nlrc5 KO microglia, CHX (50 µg/mL) was added and harvested at the time points as indicated. The protein levels of NLRC5 (representative blot, not quantified), ISG15 and β-actin were detected by immunoblotting. B Quantification of the levels of ISG15 proteins shown in panel A . The levels of ISG15 proteins in WT and Nlrc5 KO microglia were related to the level of internal control β-actin, respectively, and then the relative level of ISG15 protein at 0 h (starting point) was arbitrarily set as 1. n = 3 per group. Two-way ANOVA with Sidak’s multiple comparisons test. C , D WT and Nlrc5 KO microglia were subjected to OGD/R (4 h/6 h), the cells were treated with MG132 (10 µM), BAF (50 nM), or CQ (40 µM) throughout the OGD/R process. The protein levels of ISG15 and β-actin were detected by immunoblotting. n = 3 per group. One-way ANOVA with Tukey’s post hoc test. E Schematic diagram of NLRC5 protein and its truncations CARD, NOD, and LRR. F 293 T cells were transfected with FLAG-tagged ISG15 lentivirus, and then transfected with individual plasmid of truncated versions of HA-NLRC5 and control plasmid for 36 h. The cells were lysed and used for Co-IP. After immunoprecipitation with anti-FLAG, lysates of 293 T cells were immunoblotted with anti-HA and anti-FLAG antibodies. G Binding pattern analysis of NLRC5 and ISG15. Data are presented as mean ± SEM. ** p < 0.01

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: Expressing, Western Blot, Control, Transfection, Plasmid Preparation, Co-Immunoprecipitation Assay, Immunoprecipitation, Binding Assay

Journal: Journal of Neuroinflammation

Article Title: Microglial NLRC5 drives lysosomal dysfunction to disrupt autophagic flux and promote post-stroke neuroinflammation

doi: 10.1186/s12974-025-03585-2

Figure Lengend Snippet: Schematic diagram illustrating the role of microglial NLRC5 after ischemic stroke

Article Snippet: Autophagic flux monitoring and NLRC5 overexpression were achieved using mRFP-GFP-LC3 adenovirus (GeneChem Co., China) and HA-tagged NLRC5 adenovirus (GeneChem Co., China) respectively.

Techniques: