Journal: Advanced Science

Article Title: PBRM1 Deficiency in Microglia Leads to Excessive Neurogenesis and Autism‐Like Behaviors via the CCL5‐CCR1/5‐β‐catenin Signaling Axis

doi: 10.1002/advs.78086

Figure Lengend Snippet: Pbrm1 cKO microglia disrupts microglial development and homeostasis. (A) Uniform manifold approximation and projection (UMAP) visualization of 22,201 cells, including 10,727 cells from WT hippocampal samples and 11,474 cells from Pbrm1 cKO hippocampal samples. (B) UMAP visualization of microglia that were divided into 7 subclusters based on the expression of marker genes. (C) Heatmap of normalized expression levels of enriched genes in 7 microglial subclusters. (D) Single‐cell trajectories of microglia by Monocle analysis. Cells are colored by pseudotime trajectories (left panel), clusters (middle panel), or samples (right panel). (E) Bar plot showing relative proportions of each microglial subcluster between WT and cKO samples. (F) Quantitative RT‐PCR analysis showing the relative mRNA levels of P2ry12, Tmem119 , and Tnf in WT and cKO microglia. Compared to WT, cKO microglia displayed significantly lower expression of P2ry12 and Tmem119 , but higher expression of Tnf . Mean ± SEM. * p < 0.05, *** p < 0.001 by Student's t ‐test or Mann–Whitney test. n = 4 mice per group. Males (circles) and females (squares) are indicated. (G) Representative flow cytometry gating strategy for sorting IL‐1α + TNF‐α + microglia from the hippocampus of P15 WT and cKO mice. (H) Quantification of the percentage of IL‐1α + TNF‐α + microglia in the hippocampus of P15 WT and cKO mice. Mean ± SEM. *** p < 0.001 by Student's t ‐test. n = 3 mice per group. (I,J) Representative images (I) and quantifications (J) of GFAP (green) and Tuj1 (red) immunostaining of the differentiation of NSPCs that were indirectly co‐cultured with TNF‐α + , IL‐1α + , TNF‐α + IL1‐α + primary microglia in a Transwell system. In contrast to NSPCs that were indirectly co‐cultured with TNF‐α − IL‐1α − cKO microglia, TNF‐α + , IL‐1α + , TNF‐α + IL‐1α + treated NSPCs differentiated into more Tuj1 + cells and fewer GFAP + cells. Scale bar, 50 µm. Mean ± SEM. * p < 0.05, ** p < 0.01 by Student's t ‐test. n = 3 independent experiments. See also Figure .

Article Snippet: Cells were then stained with anti‐mouse TNFα FITC (130‐124‐212, Miltenyi Biotec, Germany) and anti‐mouse IL‐1α PE (130‐104‐530, Miltenyi Biotec, Germany) antibodies for phenotypic analysis.

Techniques: Expressing, Marker, Single Cell, Analysis, Quantitative RT-PCR, MANN-WHITNEY, Flow Cytometry, Immunostaining, Cell Culture

Journal: Materials Today Bio

Article Title: Toll-like receptor 9-overexpressing red blood cell biomimetic microbubbles adsorb cell-free DNA to relieve steatotic liver ischemia-reperfusion injury

doi: 10.1016/j.mtbio.2026.103558

Figure Lengend Snippet: c fDNA levels exhibit a significant elevation following hepatic IRI in steatotic liver (A- D) After laparoscopic partial hepatectomy, patients with metabolic dysfunction-associated steatotic liver disease (MASLD) exhibited significantly elevated serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) (A), n = 8/7/7/5; accompanied by pronounced hepatic histopathological alterations (B), n = 3/4/3/4; and increased cfDNA concentrations in both serum (C), n = 8/8/8/7; and liver tissues (D) n = 3/3/3/3. Pre- and post-operative serum and liver tissue specimens were obtained from patients undergoing laparoscopic partial hepatectomy. Liver tissue sections were processed for histological evaluation using hematoxylin and eosin (H&E) staining (B, left panel ), with pathological scores determined according to the Suzuki scoring system (B, right panel ). Additionally, liver tissue sections were immunostained with an anti-DNA antibody (red) and DAPI (blue, nuclei), and then imaged by fluorescence microscopy (D). Scale bar: 200 μm (B); 100 μm (D). The regions of hepatic injury are marked (B, scale bar: 200 μm). (E-F) Serum cfDNA levels positively correlated with serum ALT and AST levels in patients undergoing laparoscopic partial hepatectomy, n = 27. (G-K) MASLD rats exhibited more severe hepatic IRI (G-J), accompanied by a substantial elevation in cfDNA levels (K). Liver tissues and serum samples were obtained from rats maintained on either a normal diet or a high-fat diet at the indicated time points following a 45-min ischemic period and subsequent reperfusion. Liver tissue sections were processed for histological evaluation using H&E staining (G), with pathological scores determined according to the Suzuki scoring system (H), n = 3/4. The regions of hepatic injury are marked (G, scale bar: 100 μm). (L) cfDNA levels were significantly increased in an in vitro hypoxia-reoxygenation (HR) model using steatotic liver cells. BRL-3A cells were treated with 250 μM sodium palmitate and 500 μM sodium oleate for 24 h, followed by hypoxia for 9 h and reoxygenation for 2 h. Cells were then immunostained with an anti-DNA antibody (red) and DAPI (blue, nuclei), and imaged by fluorescence microscopy, n = 5. Scale bar: 50 μm. For (A-C, E, I-M), error bars represent mean ± standard deviation. P values were calculated using the unpaired Student's t-test (A-C, G, I-M) or Pearson's correlation coefficient (E-F). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, not significant.(For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Primary antibodies used included: rabbit polyclonal antibodies against TLR9 (A14642, Abclonal), NF-κB (A2547, Abclonal), MyD88 (A0980, Abclonal), cGAS (A8335, Abclonal), IL-1α (A2170, Abclonal), TNF-α (A0277, Abclonal), IL-6 (A0286, Abclonal), CD206 (A8301, Abclonal), CD86 (A16805, Abclonal), CD47 (A1838, Abclonal), and ATP1A (A0643, Abclonal); rabbit monoclonal antibodies against STING (13647, CST, Beverly, MA, USA), p-NF-κB (3033, CST), p-TBK1 (5483, CST), TBK1 (ab40676, Abcam), p-IκB (2859, CST), IκB (4812, CST), p-IRF3 (4947, CST), and β-actin (AC026, Abclonal).

Techniques: Staining, Fluorescence, Microscopy, In Vitro, Standard Deviation

Journal: Materials Today Bio

Article Title: Toll-like receptor 9-overexpressing red blood cell biomimetic microbubbles adsorb cell-free DNA to relieve steatotic liver ischemia-reperfusion injury

doi: 10.1016/j.mtbio.2026.103558

Figure Lengend Snippet: Synthetic RBC-MBs with high TLR9 expression (A-B) TLR9 protein levels on erythrocyte membranes were significantly decreased in both patients with MASLD (A), n = 9/7, and MASLD rats (B), n = 8/6. Erythrocytes were collected from patients with or without MASLD (A) and from rats fed a normal diet or a high-fat diet (B). Erythrocyte membranes were isolated and subjected to western blotting ( upper panels ). TLR9 levels were normalized to ATP1A levels in each sample, and the normalized values were used for statistical analysis ( lower panels ). (C) Lipopolysaccharide (LPS) treatment significantly increased TLR9 protein levels on erythrocyte membranes. Rats were intravenously injected with 12 mg kg -1 LPS for 6 h. Erythrocytes were collected, and the membranes were isolated and analyzed by western blotting ( upper panel ). TLR9 levels were normalized to ATP1A levels in each sample, and the normalized values were used for statistical analysis ( lower panel ), n = 6. (D) Schematic diagram illustrating the synthesis of RBC-MBs. (E) The ultrasound microbubbles appeared as a milky suspension. (F-G) Size distribution of Con-MBs (F) and RBC-MBs (G) in phosphate-buffered saline. (H-I) Average hydrodynamic diameters (H) and surface charges (ζ-potential) (I) of Con-MBs and RBC-MBs, as determined by dynamic light scattering, n = 6. (J) RBC-MBs were round, uniform, and well-dispersed. Erythrocyte membranes were labeled with DiL (red), and phospholipids were labeled with DiO (green). Scale bar: 30 μm. (K) RBC-MBs contained TLR9, CD47, and ATP1A proteins. Red blood cells, erythrocyte membranes, and RBC-MBs were subjected to western blotting. (L) RBC-MBs effectively adsorbed cfDNA in vitro . BRL-3A cells were treated with 250 μM sodium palmitate and 500 μM sodium oleate for 24 h, followed by hypoxia for 9 h and reoxygenation for 2 h. Subsequently, the cells were co-incubated with DiO-labeled (green) Con-MBs or RBC-MBs for 20 min, then immunostained with an anti-DNA antibody (red) and DAPI (blue, nuclei), and imaged by fluorescence microscopy. Scale bar: 20 μm. For (A-C, H-I), error bars represent mean ± standard deviation. P values were calculated using the unpaired Student's t-test (A, B, C, H, I). *, P < 0.05; ***, P < 0.001; ****, P < 0.0001.(For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Primary antibodies used included: rabbit polyclonal antibodies against TLR9 (A14642, Abclonal), NF-κB (A2547, Abclonal), MyD88 (A0980, Abclonal), cGAS (A8335, Abclonal), IL-1α (A2170, Abclonal), TNF-α (A0277, Abclonal), IL-6 (A0286, Abclonal), CD206 (A8301, Abclonal), CD86 (A16805, Abclonal), CD47 (A1838, Abclonal), and ATP1A (A0643, Abclonal); rabbit monoclonal antibodies against STING (13647, CST, Beverly, MA, USA), p-NF-κB (3033, CST), p-TBK1 (5483, CST), TBK1 (ab40676, Abcam), p-IκB (2859, CST), IκB (4812, CST), p-IRF3 (4947, CST), and β-actin (AC026, Abclonal).

Techniques: Expressing, Isolation, Western Blot, Injection, Suspension, Saline, Labeling, In Vitro, Incubation, Fluorescence, Microscopy, Standard Deviation

Journal: Materials Today Bio

Article Title: Toll-like receptor 9-overexpressing red blood cell biomimetic microbubbles adsorb cell-free DNA to relieve steatotic liver ischemia-reperfusion injury

doi: 10.1016/j.mtbio.2026.103558

Figure Lengend Snippet: RBC-MBs have excellent biosafety properties (A) RBC-MBs did not induce hemolysis in vitro . Rat erythrocytes were incubated with H 2 O, 1 × PBS, or RBC-MBs at various concentrations, left to stand for 3 h, centrifuged, and then photographed. H 2 O and 1 × PBS were used as positive and negative controls, respectively. (B) RBC-MBs did not activate platelets in vitro . Platelet-rich plasma was incubated with thrombin, 1 × PBS, Con-MBs, or RBC-MBs, and absorbance at 650 nm was recorded at the indicated time points using a microplate reader, n = 6. (C) RBC-MBs had no effect on cell viability in vitro . HUVECs were incubated with Con-MBs or RBC-MBs at various concentrations for 24 h, and cell viability was detected using the CCK-8 assay, n = 5. (D-L) RBC-MBs exhibited no organ toxicity. Rats received daily tail vein injections of Con-MBs or RBC-MBs at a 100-fold therapeutic dose for 7 days. Organs (brain, heart, liver, spleen, lung, kidney) were harvested for hematoxylin and eosin (H&E) staining (D), and serum was analyzed using enzyme-linked immunosorbent assay (ELISA) for biochemical markers (E-J) and inflammatory cytokines (K-L), n = 4. Scale bar: 200 μm (D). For (C, E-K), error bars represent mean ± standard deviation (SD). P values were calculated using two-way ANOVA (B, C) or one-way ANOVA (E-L). ns, not significant.

Article Snippet: Primary antibodies used included: rabbit polyclonal antibodies against TLR9 (A14642, Abclonal), NF-κB (A2547, Abclonal), MyD88 (A0980, Abclonal), cGAS (A8335, Abclonal), IL-1α (A2170, Abclonal), TNF-α (A0277, Abclonal), IL-6 (A0286, Abclonal), CD206 (A8301, Abclonal), CD86 (A16805, Abclonal), CD47 (A1838, Abclonal), and ATP1A (A0643, Abclonal); rabbit monoclonal antibodies against STING (13647, CST, Beverly, MA, USA), p-NF-κB (3033, CST), p-TBK1 (5483, CST), TBK1 (ab40676, Abcam), p-IκB (2859, CST), IκB (4812, CST), p-IRF3 (4947, CST), and β-actin (AC026, Abclonal).

Techniques: In Vitro, Incubation, Clinical Proteomics, CCK-8 Assay, Staining, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: Materials Today Bio

Article Title: Toll-like receptor 9-overexpressing red blood cell biomimetic microbubbles adsorb cell-free DNA to relieve steatotic liver ischemia-reperfusion injury

doi: 10.1016/j.mtbio.2026.103558

Figure Lengend Snippet: cfDNA promotes the polarization of macrophages towards the M1 phenotype by activating the TLR9-MyD88 and cGAS-STING pathways (A- D) CpG DNA treatment increased the protein levels of IL-1α, TNF-α, and IL-6. RAW264.7 cells were treated with 1 μg mL -1 CpG DNA for 24 h and then subjected to western blotting (A). IL-1α (B), TNF-α (C), and IL-6 (D) levels were normalized to the β-actin level in each sample, and the normalized values were used for statistical analysis, n = 4. (E-F) CpG DNA treatment significantly enhanced CD86 expression in macrophages. RAW264.7 cells were treated with 1 μg mL -1 CpG DNA for 24 h, then immunostained with an anti-CD86 antibody (green) and DAPI (blue, nuclei), and imaged by fluorescence microscopy. Representative images (E) and quantitative fluorescence graph (F) are shown, n = 6. Scale bar: 50 μm. (G-J) CpG DNA treatment significantly upregulated the expression of key proteins associated with the TLR9-MyD88 and cGAS-STING pathways. RAW264.7 cells were treated with 1 μg mL -1 CpG DNA for 24 h and then subjected to western blotting, n = 8/4(G, I). STING, cGAS, TLR9, and MyD88 levels were normalized to the β-actin level in each sample. p-NF-κB, p-IκB, p-TBK1, and p-IRF3 levels were normalized to their respective total protein levels (NF-κB, IκB, TBK1, and IRF3) in each sample. These normalized values were then used for statistical analysis, n = 8/4(H, J). For (B-D, F, H, J), error bars represent mean ± standard deviation. P values were calculated using one-way analysis of variance (ANOVA) (B-D, F, H, J). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not significant.(For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Primary antibodies used included: rabbit polyclonal antibodies against TLR9 (A14642, Abclonal), NF-κB (A2547, Abclonal), MyD88 (A0980, Abclonal), cGAS (A8335, Abclonal), IL-1α (A2170, Abclonal), TNF-α (A0277, Abclonal), IL-6 (A0286, Abclonal), CD206 (A8301, Abclonal), CD86 (A16805, Abclonal), CD47 (A1838, Abclonal), and ATP1A (A0643, Abclonal); rabbit monoclonal antibodies against STING (13647, CST, Beverly, MA, USA), p-NF-κB (3033, CST), p-TBK1 (5483, CST), TBK1 (ab40676, Abcam), p-IκB (2859, CST), IκB (4812, CST), p-IRF3 (4947, CST), and β-actin (AC026, Abclonal).

Techniques: Western Blot, Expressing, Fluorescence, Microscopy, Standard Deviation

Journal: Materials Today Bio

Article Title: Toll-like receptor 9-overexpressing red blood cell biomimetic microbubbles adsorb cell-free DNA to relieve steatotic liver ischemia-reperfusion injury

doi: 10.1016/j.mtbio.2026.103558

Figure Lengend Snippet: RBC-MBs promotes the polarization of macrophages towards the M2 phenotype by inhibiting the TLR9-MyD88 and cGAS-STING pathways (A-F) RBC-MB treatment significantly attenuated CpG DNA-induced upregulation of pro-inflammatory cytokines (A-B), key proteins in the TLR9-MyD88 (C-D) and cGAS-STING (E-F) pathways. RAW264.7 cells were treated with 1 μg mL -1 CpG DNA for 24 h, followed by incubation with 0.5 mL RBC-MBs (concentration: 1 × 10 8 particles mL -1 ) for 24 h, and then subjected to western blot analysis (A, C, E). IL-1α, TNF-α, IL-6, TLR9, MyD88, STING, and cGAS levels were normalized to the β-actin level in each sample. p-NF-κB, p-TBK1, and p-IRF3 levels were normalized to their respective total protein levels (NF-κB, TBK1, and IRF3) in each sample. These normalized values were then used for statistical analysis (B, D, F), n = 6. (G) RBC-MB treatment significantly attenuated CpG DNA-induced upregulation of CD86 in macrophages. RAW264.7 cells were treated with 1 μg mL -1 CpG DNA for 24 h, followed by incubation with 0.5 mL RBC-MBs (concentration: 1 × 10 8 particles mL -1 ) for 24 h, then immunostained with an anti-CD86 antibody (green) and DAPI (blue, nuclei), and imaged by fluorescence microscopy. Representative images (left panel) and quantitative fluorescence graph (right panel) are shown. Scale bar: 50 μm, n = 6. (H-J) RBC-MB treatment significantly inhibited hepatic IRI-induced polarization of macrophages toward the M1 phenotype (H) and activation of the TLR9-MyD88 and cGAS-STING pathways (I-J). MASLD rats underwent 45 min of hepatic ischemia followed by reperfusion. At 0, 6, 12, 18, and 24 h post-reperfusion, the rats were treated with either Con-MBs or RBC-MBs. Primary macrophages were isolated from rat livers, then co-stained with CD68 and CD163 followed by flow cytometric analysis (H), n = 3/4, or subjected to western blotting (I-J). CD206, iNOS, TLR9, MyD88, STING, and cGAS levels were normalized to the β-actin level in each sample, and these normalized values were used for statistical analysis (J), n = 3. For (B, D, F, G right panel , H right panel , J), error bars represent mean ± standard deviation. P values were calculated using the unpaired Student's t-test (B, D, F, G right panel ) or one-way analysis of variance (ANOVA) (H right panel , J). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001; ns, not significant.(For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Primary antibodies used included: rabbit polyclonal antibodies against TLR9 (A14642, Abclonal), NF-κB (A2547, Abclonal), MyD88 (A0980, Abclonal), cGAS (A8335, Abclonal), IL-1α (A2170, Abclonal), TNF-α (A0277, Abclonal), IL-6 (A0286, Abclonal), CD206 (A8301, Abclonal), CD86 (A16805, Abclonal), CD47 (A1838, Abclonal), and ATP1A (A0643, Abclonal); rabbit monoclonal antibodies against STING (13647, CST, Beverly, MA, USA), p-NF-κB (3033, CST), p-TBK1 (5483, CST), TBK1 (ab40676, Abcam), p-IκB (2859, CST), IκB (4812, CST), p-IRF3 (4947, CST), and β-actin (AC026, Abclonal).

Techniques: Incubation, Concentration Assay, Western Blot, Fluorescence, Microscopy, Activation Assay, Isolation, Staining, Standard Deviation

Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Topical calcitriol application ameliorates IMQ‐induced psoriasis in mice. (A) Schematic illustration of the unilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the right ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of right ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

Techniques: Staining, Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Topical calcitriol treatment ameliorates distant psoriatic skin lesions in the bilateral ear model. (A) Schematic illustration of the bilateral ear model experimental design. (B) Serum calcium levels. (C) Body weight changes. (D) Clinical severity scores (erythema, scaling and thickness) of the right ear, assessed on indicated days using a 0–4 scale. Cumulative scores are presented as mean ± SD. (E) Representative photographs of the left ear at endpoint. (F) Haematoxylin and eosin (H&E) staining of left ear sections. Scale bar = 100 μm. (G) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. ** p < 0.01, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

Techniques: Staining, Expressing

Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Calcitriol ameliorates M5‐induced abnormal proliferation, migration and inflammatory responses in HaCaT cells. (A) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (B) Cell viability was assessed in different treatment groups. (C) Colony formation assay was performed to evaluate the proliferative capacity of cells in each group. (D) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (E) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

Techniques: Migration, Expressing, Western Blot, Control, Colony Assay, Wound Healing Assay

Journal: Journal of Cellular and Molecular Medicine

Article Title: Downregulating CHI3L2 via the STAT3 Pathway: The Mechanism of Calcitriol in Suppressing Psoriatic Inflammation and Keratinocyte Hyperproliferation

doi: 10.1111/jcmm.71367

Figure Lengend Snippet: Calcitriol ameliorates M5‐induced psoriasis‐like phenotypes through CHI3L2 downregulation. (A) The mRNA expression of RPL36A, PPBP, UBE2F, MGC32805, IL4I1, LINC00519, CHI3L2, ABHD14A and PCDHGB7 , validated by RT‐qPCR assay. (B) Efficacy of shRNA‐mediated CHI3L2 knockdown confirmed by RT‐qPCR. (C) Protein expression levels of KRT1 and KRT6 were determined by Western blot analysis, with β‐Actin serving as the internal loading control. (D) Cell viability was assessed in different treatment groups. (E) Representative images of wound healing assay at 0 and 24 h post‐treatment. Scale bar = 400 μm. (F) Relative mRNA expression levels of IL‐1α, IL‐6, IL‐17A and IL‐23A . Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: To mimic psoriatic keratinocyte dysfunction, HaCaT cells were incubated with 10 ng/mL M5 (IL‐17A, IL‐22, IL‐1α, oncostatin M and TNF‐α) (ABclonal Technology Co. Ltd., Wuhan, China) for 24 h as reported previously [ , , , ].

Techniques: Expressing, Quantitative RT-PCR, shRNA, Knockdown, Western Blot, Control, Wound Healing Assay