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Cytek Biosciences annexin v apc

Res-PD-L1@nmEVs Attenuate Inflammation and Oxidative Damage in Lung Epithelial Cells In Vitro . (A-B) Flow cytometric analysis and quantification (B) of DiO-labeled Res-PD-L1@nmEVs uptake by BEAS-2B cells under H/R conditions after pretreatment with different endocytic inhibitors (chlorpromazine, chloroquine, and filipin) or incubation at 4 °C. (C) mRNA expression levels of IL-6, TNF-α, and IL-1β in BEAS-2B cells with or without H/R injury following pretreatment with Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs. (D-E) Representative fluorescence images (D) and quantitative analysis (E) of cell proliferation assessed by BrdU incorporation (red; nuclei stained with DAPI, blue). Scale bar: 50 μm. (F-G) Apoptosis rates detected by flow cytometry (F) and flow cytometric analysis of <t>Annexin</t> V-positive BEAS-2B cells under the indicated conditions (G). (H–K) Fluorescence microscopy images and quantitative analysis of intracellular nitric oxide (NO, green) (H-I) and reactive oxygen species (ROS, red) (J-K). Scale bar: 100 μm. (L) Flow cytometry analysis of intracellular ROS levels. (M − O) Levels of malondialdehyde (MDA) (M), superoxide dismutase 2 (SOD2) activity (N), and glutathione (GSH) content (O) in cells. (P-Q) Cell migration ability evaluated by wound healing assay under different treatments. ∗ vs. Control; # vs. H/R; & vs. H/R + PD-L1@nmEVs, p < 0.05.

Annexin V Apc, supplied by Cytek Biosciences, used in various techniques. Bioz Stars score: 94/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 18 article reviews

annexin v apc - by Bioz Stars, 2026-05

94/100 stars

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1) Product Images from "Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia"

Article Title: Inhalable PD-L1-engineered hybrid cellular vesicles suppress excessive neutrophil activation and restore mitochondrial homeostasis to alleviate ischemia–reperfusion lung injury and pneumonia

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.024

Figure Legend Snippet: Res-PD-L1@nmEVs Attenuate Inflammation and Oxidative Damage in Lung Epithelial Cells In Vitro . (A-B) Flow cytometric analysis and quantification (B) of DiO-labeled Res-PD-L1@nmEVs uptake by BEAS-2B cells under H/R conditions after pretreatment with different endocytic inhibitors (chlorpromazine, chloroquine, and filipin) or incubation at 4 °C. (C) mRNA expression levels of IL-6, TNF-α, and IL-1β in BEAS-2B cells with or without H/R injury following pretreatment with Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs. (D-E) Representative fluorescence images (D) and quantitative analysis (E) of cell proliferation assessed by BrdU incorporation (red; nuclei stained with DAPI, blue). Scale bar: 50 μm. (F-G) Apoptosis rates detected by flow cytometry (F) and flow cytometric analysis of Annexin V-positive BEAS-2B cells under the indicated conditions (G). (H–K) Fluorescence microscopy images and quantitative analysis of intracellular nitric oxide (NO, green) (H-I) and reactive oxygen species (ROS, red) (J-K). Scale bar: 100 μm. (L) Flow cytometry analysis of intracellular ROS levels. (M − O) Levels of malondialdehyde (MDA) (M), superoxide dismutase 2 (SOD2) activity (N), and glutathione (GSH) content (O) in cells. (P-Q) Cell migration ability evaluated by wound healing assay under different treatments. ∗ vs. Control; # vs. H/R; & vs. H/R + PD-L1@nmEVs, p < 0.05.

Techniques Used: In Vitro, Labeling, Incubation, Expressing, Fluorescence, BrdU Incorporation Assay, Staining, Flow Cytometry, Microscopy, Activity Assay, Migration, Wound Healing Assay, Control

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Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.03.024

Figure Lengend Snippet: Res-PD-L1@nmEVs Attenuate Inflammation and Oxidative Damage in Lung Epithelial Cells In Vitro . (A-B) Flow cytometric analysis and quantification (B) of DiO-labeled Res-PD-L1@nmEVs uptake by BEAS-2B cells under H/R conditions after pretreatment with different endocytic inhibitors (chlorpromazine, chloroquine, and filipin) or incubation at 4 °C. (C) mRNA expression levels of IL-6, TNF-α, and IL-1β in BEAS-2B cells with or without H/R injury following pretreatment with Res, nEVs, PD-L1@mEVs, PD-L1@nmEVs, or Res-PD-L1@nmEVs. (D-E) Representative fluorescence images (D) and quantitative analysis (E) of cell proliferation assessed by BrdU incorporation (red; nuclei stained with DAPI, blue). Scale bar: 50 μm. (F-G) Apoptosis rates detected by flow cytometry (F) and flow cytometric analysis of Annexin V-positive BEAS-2B cells under the indicated conditions (G). (H–K) Fluorescence microscopy images and quantitative analysis of intracellular nitric oxide (NO, green) (H-I) and reactive oxygen species (ROS, red) (J-K). Scale bar: 100 μm. (L) Flow cytometry analysis of intracellular ROS levels. (M − O) Levels of malondialdehyde (MDA) (M), superoxide dismutase 2 (SOD2) activity (N), and glutathione (GSH) content (O) in cells. (P-Q) Cell migration ability evaluated by wound healing assay under different treatments. ∗ vs. Control; # vs. H/R; & vs. H/R + PD-L1@nmEVs, p < 0.05.

Article Snippet: Apoptosis was detected using double staining with Annexin V-APC and 7-AAD (35-640-KIT, Tonbo, USA) to distinguish early and late apoptotic cell populations.

Techniques: In Vitro, Labeling, Incubation, Expressing, Fluorescence, BrdU Incorporation Assay, Staining, Flow Cytometry, Microscopy, Activity Assay, Migration, Wound Healing Assay, Control

SERPINE1-mediated modulation of the ERK/p38 ratio and anoikis. (A) Upper panel: western blotting showing ERK, p-ERK, p38, and p-p38 levels. Quantitative data showed the p-ERK/ERK and p-p38/p38 ratios in SERPINE1 knockdown cells compared with control cells. Lower panel: western blotting analysis of p-AKT, AKT, p-JNK and JNK (normalized to total protein) levels in the shSE1 and shc groups. The numbers beneath the bands represent the ratios of the expression levels of the indicated proteins. Data represent mean ± SDs of three independent experiments. (B) PLAUR and HSP90AA1 mRNA and protein levels in shSE1 and shc cells analyzed using RNA-seq (left panel) and western blotting (right panel). The numbers beneath the bands represent the ratios of the expression levels of the indicated proteins and represent mean ± SDs of three independent experiments. RNA-seq was performed using one biological replicate per group. (C-D) Upper panel: (C) 231-shSE1 cells were infected with lentivirus containing PLAUR cDNA (ex-PLAUR) or the corresponding empty vector control (vec). (D) H4-shSE1 cells were transfected with siRNA targeting HSP90AA1 (si-HSP90AA1) or siNC. The expression levels of uPAR and HSP90α, as well as the activity of ERK and p38, were detected by western blotting, with GAPDH serving as the loading control. Data represent mean ± SDs of three independent experiments. Lower panel: Cell proliferation was assessed by CCK-8 assay in 231-shSE1 cells infected with ex-PLAUR or vec, and in H4-shSE1 cells transfected with si-HSP90AA1 or siNC. Statistical significance was determined using two-way ANOVA followed by Šídák's multiple comparisons test. The data are presented as the means ± SDs. n=6. (E) Morphology of shSE1 and shc cells cultured under suspension condition. (scale bar, 100 μ m). (F) Apoptotic cells cultured under suspension condition were analyzed by flow cytometry following Annexin V-PE/7AAD staining (72 h of suspension culture). Statistical significance was determined using a two-sided Student's t test. The data are presented as the means ± SDs of three independent experiments. ** P<0.01 *** P<0.001, ns, not significant. SERPINE1, serine protease inhibitor clade e member 1; p-, phosphorylated; shRNA, short hairpin RNA; shSE1, shRNA targeting SERPINE1; shc, shRNA scrambled control; PLAUR, plasminogen activator, urokinase receptor; HSP90AA1, heat shock protein 90 alpha family class a member 1; RNA-seq, RNA sequencing; vec, empty vector control; siRNA, short interfering RNA; siNC, negative control siRNA; uPAR, urokinase-type plasminogen activator receptor; HSP90α, heat shock protein 90-alpha.

Journal: International Journal of Oncology

Article Title: Diverse roles of SERPINE1 in regulating cellular proliferation and invasion

doi: 10.3892/ijo.2026.5871

Figure Lengend Snippet: SERPINE1-mediated modulation of the ERK/p38 ratio and anoikis. (A) Upper panel: western blotting showing ERK, p-ERK, p38, and p-p38 levels. Quantitative data showed the p-ERK/ERK and p-p38/p38 ratios in SERPINE1 knockdown cells compared with control cells. Lower panel: western blotting analysis of p-AKT, AKT, p-JNK and JNK (normalized to total protein) levels in the shSE1 and shc groups. The numbers beneath the bands represent the ratios of the expression levels of the indicated proteins. Data represent mean ± SDs of three independent experiments. (B) PLAUR and HSP90AA1 mRNA and protein levels in shSE1 and shc cells analyzed using RNA-seq (left panel) and western blotting (right panel). The numbers beneath the bands represent the ratios of the expression levels of the indicated proteins and represent mean ± SDs of three independent experiments. RNA-seq was performed using one biological replicate per group. (C-D) Upper panel: (C) 231-shSE1 cells were infected with lentivirus containing PLAUR cDNA (ex-PLAUR) or the corresponding empty vector control (vec). (D) H4-shSE1 cells were transfected with siRNA targeting HSP90AA1 (si-HSP90AA1) or siNC. The expression levels of uPAR and HSP90α, as well as the activity of ERK and p38, were detected by western blotting, with GAPDH serving as the loading control. Data represent mean ± SDs of three independent experiments. Lower panel: Cell proliferation was assessed by CCK-8 assay in 231-shSE1 cells infected with ex-PLAUR or vec, and in H4-shSE1 cells transfected with si-HSP90AA1 or siNC. Statistical significance was determined using two-way ANOVA followed by Šídák's multiple comparisons test. The data are presented as the means ± SDs. n=6. (E) Morphology of shSE1 and shc cells cultured under suspension condition. (scale bar, 100 μ m). (F) Apoptotic cells cultured under suspension condition were analyzed by flow cytometry following Annexin V-PE/7AAD staining (72 h of suspension culture). Statistical significance was determined using a two-sided Student's t test. The data are presented as the means ± SDs of three independent experiments. ** P<0.01 *** P<0.001, ns, not significant. SERPINE1, serine protease inhibitor clade e member 1; p-, phosphorylated; shRNA, short hairpin RNA; shSE1, shRNA targeting SERPINE1; shc, shRNA scrambled control; PLAUR, plasminogen activator, urokinase receptor; HSP90AA1, heat shock protein 90 alpha family class a member 1; RNA-seq, RNA sequencing; vec, empty vector control; siRNA, short interfering RNA; siNC, negative control siRNA; uPAR, urokinase-type plasminogen activator receptor; HSP90α, heat shock protein 90-alpha.

Article Snippet: Subsequently, suspended cells were harvested, and anoikis was quantified using an Annexin V-APC/DAPI apoptosis detection kit (cat. no. E-CK-A258; Elabscience Bionovation Inc.) according to the manufacturer's instructions.

Techniques: Western Blot, Knockdown, Control, Expressing, RNA Sequencing, Infection, Plasmid Preparation, Transfection, Activity Assay, CCK-8 Assay, Cell Culture, Suspension, Flow Cytometry, Staining, Protease Inhibitor, shRNA, Small Interfering RNA, Negative Control

The secretion of MMP2 by CAR-M2 activates the transcription factor Rxra in Cxcr2 + ECs (A) Position relationship between CXCR2 + ECs and FAP + fibroblasts was visualized by immunofluorescence staining. Blue: DAPI, green: CD31, red: CXCR2, French gray: FAP. (B) Volcano plot of differentially expressed genes before and after co-culture of CAR-M2 with FAP + fibroblasts. (C) Representative Masson and Sirius red staining images of mice kidney tissue sections following the injection of PBS into the renal subcapsule (Sham and UUO), CAR-M2-loaded HAMA-CS hydrogel injected into the renal subcapsule (CAR-M2), and PBS into the renal subcapsule of MMP2 inhibitor mice (MMP2 inhibitor). Detection at day 7. Scale bars, 100 μm. (D) Average collagen deposition density by Masson staining in (C), n = 5. (E) Average collagen deposition density (the percentage of positively stained area per HPF) by Sirius red staining in (C), n = 5. (F) Re-clustering of endothelial cells from human kidney single-cell sequencing data based on regulon activity, t-SNE (t-distributed stochastic neighbor embedding) displayed by cell type (left), and kidney condition (right). (G) SCENIC analysis of cell stability in clusters derived from regulon activity-based dimensionality reduction. (H) Ranked plot of transcription factor activity in CXCR2 + ECs. (I) Differential expression of the Rxra gene among groups in mouse single-cell transcriptome samples. (J) Changes in the endothelial transcription factor RXRA after CAR-M2 treatment and in MMP2 inhibitor-treated mice. Blue: DAPI, red: CD31, green: Rxra, yellow indicates the co-labeling of CD31 with Rxra, Scale bars, 25 μm. Arrowheads indicate the double positive cells. (K) Statistical analysis of the number of CD31 + Rxra + cells in (J), n = 5. (L) Cell co-culture protocol to verify that CAR-M2 activates the transcription factor Rxra by secreted MMP2. (M) After cell co-culture using protocol in (L), the lentiviral constructs Cxcr2 + ECs were collected to detect the changes in their Rxra and Cxcr2 expression levels. (N) Average collagen deposition density by Masson staining, mice kidney tissue sections following the injection of PBS into the renal subcapsule (Control), CAR-M2-loaded HAMA-CS hydrogel injected into the renal subcapsule (CAR-M2), and PBS into the renal subcapsule of Rxra agonist and inhibitor mice (Rxra agonist and Rxra inhibitor). Detection at day 14. n = 5. (O) Average collagen deposition density by Sirius red staining, mice kidney tissue sections following the injection of PBS into the renal subcapsule (Control), CAR-M2-loaded HAMA-CS hydrogel injected into the renal subcapsule (CAR-M2), and PBS into the renal subcapsule of Rxra agonist and inhibitor mice (Rxra agonist and Rxra inhibitor). Detection at day 14. n = 5. (P) Mitochondrial autophagy-related gene score in human normal and CKD groups. (Q) Apoptotic-related gene score in human normal and CKD groups. (R) Mitochondrial autophagy-related gene score in mice Sham, UUO, and CAR-M2 groups. (S) Apoptotic-related gene score in mice Sham, UUO, and CAR-M2 groups. (T) The changes in the expression levels of autophagy-related protein PINK1 and apoptosis-related protein active caspase-3. (U) The cell apoptosis rate after the aforementioned (T) co-culture was detected by flow cytometry, and the proportion of Annexin-APC positive cells was counted as the cell apoptosis rate. The detection time was 6 h after co-culture. n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; ns, not significant (one-way ANOVA). See also .

Journal: Cell Reports Medicine

Article Title: CAR-M2 immunotherapy resolves renal fibrosis via revascularization and apoptosis of profibrotic Cxcr2 + endothelial cells

doi: 10.1016/j.xcrm.2026.102698

Figure Lengend Snippet: The secretion of MMP2 by CAR-M2 activates the transcription factor Rxra in Cxcr2 + ECs (A) Position relationship between CXCR2 + ECs and FAP + fibroblasts was visualized by immunofluorescence staining. Blue: DAPI, green: CD31, red: CXCR2, French gray: FAP. (B) Volcano plot of differentially expressed genes before and after co-culture of CAR-M2 with FAP + fibroblasts. (C) Representative Masson and Sirius red staining images of mice kidney tissue sections following the injection of PBS into the renal subcapsule (Sham and UUO), CAR-M2-loaded HAMA-CS hydrogel injected into the renal subcapsule (CAR-M2), and PBS into the renal subcapsule of MMP2 inhibitor mice (MMP2 inhibitor). Detection at day 7. Scale bars, 100 μm. (D) Average collagen deposition density by Masson staining in (C), n = 5. (E) Average collagen deposition density (the percentage of positively stained area per HPF) by Sirius red staining in (C), n = 5. (F) Re-clustering of endothelial cells from human kidney single-cell sequencing data based on regulon activity, t-SNE (t-distributed stochastic neighbor embedding) displayed by cell type (left), and kidney condition (right). (G) SCENIC analysis of cell stability in clusters derived from regulon activity-based dimensionality reduction. (H) Ranked plot of transcription factor activity in CXCR2 + ECs. (I) Differential expression of the Rxra gene among groups in mouse single-cell transcriptome samples. (J) Changes in the endothelial transcription factor RXRA after CAR-M2 treatment and in MMP2 inhibitor-treated mice. Blue: DAPI, red: CD31, green: Rxra, yellow indicates the co-labeling of CD31 with Rxra, Scale bars, 25 μm. Arrowheads indicate the double positive cells. (K) Statistical analysis of the number of CD31 + Rxra + cells in (J), n = 5. (L) Cell co-culture protocol to verify that CAR-M2 activates the transcription factor Rxra by secreted MMP2. (M) After cell co-culture using protocol in (L), the lentiviral constructs Cxcr2 + ECs were collected to detect the changes in their Rxra and Cxcr2 expression levels. (N) Average collagen deposition density by Masson staining, mice kidney tissue sections following the injection of PBS into the renal subcapsule (Control), CAR-M2-loaded HAMA-CS hydrogel injected into the renal subcapsule (CAR-M2), and PBS into the renal subcapsule of Rxra agonist and inhibitor mice (Rxra agonist and Rxra inhibitor). Detection at day 14. n = 5. (O) Average collagen deposition density by Sirius red staining, mice kidney tissue sections following the injection of PBS into the renal subcapsule (Control), CAR-M2-loaded HAMA-CS hydrogel injected into the renal subcapsule (CAR-M2), and PBS into the renal subcapsule of Rxra agonist and inhibitor mice (Rxra agonist and Rxra inhibitor). Detection at day 14. n = 5. (P) Mitochondrial autophagy-related gene score in human normal and CKD groups. (Q) Apoptotic-related gene score in human normal and CKD groups. (R) Mitochondrial autophagy-related gene score in mice Sham, UUO, and CAR-M2 groups. (S) Apoptotic-related gene score in mice Sham, UUO, and CAR-M2 groups. (T) The changes in the expression levels of autophagy-related protein PINK1 and apoptosis-related protein active caspase-3. (U) The cell apoptosis rate after the aforementioned (T) co-culture was detected by flow cytometry, and the proportion of Annexin-APC positive cells was counted as the cell apoptosis rate. The detection time was 6 h after co-culture. n = 3. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001; ns, not significant (one-way ANOVA). See also .

Article Snippet: Annexin V-APC / PI Apoptosis Detection Kit , Elabscience , Cat#E-CK-A217.

Techniques: Immunofluorescence, Staining, Co-Culture Assay, Injection, Single Cell, Sequencing, Activity Assay, Derivative Assay, Quantitative Proteomics, Labeling, Construct, Expressing, Control, Flow Cytometry

TMC apoptosis is observed in SIG rats (A) IOP of SIG and control rats ( n = 4, n represents the number of mice). (B) Histological analysis of HE-stained tissues. Scale bars, 20 μm. (C) The expression of Bax, Bcl-2, and Caspase-3 in the trabecular meshwork tissues was determined by IHC staining. Scale bars, 20 μm. (D) The apoptosis of trabecular meshwork tissues was determined by Tunel staining ( n = 4, n represents the number of mice). Scale bars, 100 μm. (E) The identification of TMCs by neuron-specific enolase (NSE) and fibronectin (FN). Scale bars, 50 μm. (F) Apoptosis of TMCs after dexamethasone treatment was determined by flow cytometric analysis ( n = 4, n represents the number of mice). (G) Analysis of the data in (F). (H) The apoptosis of TMCs was determined by Tunel staining ( n = 4, n represents the number of mice). Scale bars, 50 μm. (I) The expression of Bax, Bcl-2, Bcl-2/Bax, and Caspase-3 in TMCs was determined by WB staining. (J) Analysis of the data in (I) ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. Data in A, D, G, and J are presented as the mean ± SEM, two-tailed Student’s t test.

Journal: iScience

Article Title: Targeting the PPAR-γ/OPTN axis to inhibit apoptosis in steroid-induced glaucoma

doi: 10.1016/j.isci.2026.115247

Figure Lengend Snippet: TMC apoptosis is observed in SIG rats (A) IOP of SIG and control rats ( n = 4, n represents the number of mice). (B) Histological analysis of HE-stained tissues. Scale bars, 20 μm. (C) The expression of Bax, Bcl-2, and Caspase-3 in the trabecular meshwork tissues was determined by IHC staining. Scale bars, 20 μm. (D) The apoptosis of trabecular meshwork tissues was determined by Tunel staining ( n = 4, n represents the number of mice). Scale bars, 100 μm. (E) The identification of TMCs by neuron-specific enolase (NSE) and fibronectin (FN). Scale bars, 50 μm. (F) Apoptosis of TMCs after dexamethasone treatment was determined by flow cytometric analysis ( n = 4, n represents the number of mice). (G) Analysis of the data in (F). (H) The apoptosis of TMCs was determined by Tunel staining ( n = 4, n represents the number of mice). Scale bars, 50 μm. (I) The expression of Bax, Bcl-2, Bcl-2/Bax, and Caspase-3 in TMCs was determined by WB staining. (J) Analysis of the data in (I) ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. Data in A, D, G, and J are presented as the mean ± SEM, two-tailed Student’s t test.

Article Snippet: Annexin V-APC/PI Apoptosis Kit , CatElabscience , Cat#E-CK-A217.

Techniques: Control, Staining, Expressing, Immunohistochemistry, TUNEL Assay, Two Tailed Test

The apoptosis-related pathway was activated in TMCs after dexamethasone stimulation (A) The heatmap displays the DEGs between TMCs with and without dexamethasone stimulation. (B) The volcano displays the DEGs between TMCs with and without dexamethasone stimulation. (C) KEGG analysis reveals enriched pathways associated with DEGs between TMCs with and without dexamethasone stimulation. (D) The heatmap displays the DEPs between TMCs with and without dexamethasone therapy. (E) The volcano displays the DEPs between TMC with and without dexamethasone therapy. (F) KEGG analysis reveals enriched pathways associated with DEPs between TMCs with and without dexamethasone stimulation.

Journal: iScience

Article Title: Targeting the PPAR-γ/OPTN axis to inhibit apoptosis in steroid-induced glaucoma

doi: 10.1016/j.isci.2026.115247

Figure Lengend Snippet: The apoptosis-related pathway was activated in TMCs after dexamethasone stimulation (A) The heatmap displays the DEGs between TMCs with and without dexamethasone stimulation. (B) The volcano displays the DEGs between TMCs with and without dexamethasone stimulation. (C) KEGG analysis reveals enriched pathways associated with DEGs between TMCs with and without dexamethasone stimulation. (D) The heatmap displays the DEPs between TMCs with and without dexamethasone therapy. (E) The volcano displays the DEPs between TMC with and without dexamethasone therapy. (F) KEGG analysis reveals enriched pathways associated with DEPs between TMCs with and without dexamethasone stimulation.

Article Snippet: Annexin V-APC/PI Apoptosis Kit , CatElabscience , Cat#E-CK-A217.

Techniques:

Activation of PPAR-γ and Optn alleviated SIG in rats (A) Apoptosis of TMCs was determined by flow cytometric analysis ( n = 4, n represents the number of mice). (B) Analysis of the data in (A). (C) The apoptosis of TMCs was determined by Tunel staining ( n = 4, n represents the number of mice). Scale bars, 100 μm. (D) The expression of PPAR-γ, Bcl-2, Bax, Bcl-2/Bax, Caspase-3, and p-NF-κB in the TMCs was determined by WB staining. (E) Analysis of the data in (D) ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. Data in B, C, and E are presented as the mean ± SEM, two-tailed Student’s t test. One-way ANOVA with Tukey’s test.

Journal: iScience

Article Title: Targeting the PPAR-γ/OPTN axis to inhibit apoptosis in steroid-induced glaucoma

doi: 10.1016/j.isci.2026.115247

Figure Lengend Snippet: Activation of PPAR-γ and Optn alleviated SIG in rats (A) Apoptosis of TMCs was determined by flow cytometric analysis ( n = 4, n represents the number of mice). (B) Analysis of the data in (A). (C) The apoptosis of TMCs was determined by Tunel staining ( n = 4, n represents the number of mice). Scale bars, 100 μm. (D) The expression of PPAR-γ, Bcl-2, Bax, Bcl-2/Bax, Caspase-3, and p-NF-κB in the TMCs was determined by WB staining. (E) Analysis of the data in (D) ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. Data in B, C, and E are presented as the mean ± SEM, two-tailed Student’s t test. One-way ANOVA with Tukey’s test.

Article Snippet: Annexin V-APC/PI Apoptosis Kit , CatElabscience , Cat#E-CK-A217.

Techniques: Activation Assay, TUNEL Assay, Staining, Expressing, Two Tailed Test

PPAR-γ inhibited TMCs apoptosis via regulating Optn as a transcriptional factor (A) The expression of Optn in TMCs was determined by WB staining ( n = 3, n represents biological replicates). (B and C) For the dual-luciferase test, a full-length and three potential enhancer segments of the rat promoter region of Optn were created. (D) Luciferase activity was seen in the indicated groups, suggesting that PPAR-γ functioned as a transcriptional enhancer by bidding at the Optn promoter’s 3′–5′ strand’s −1925 to −1898 locations ( n = 3, n represents biological replicates). (E) A UV transilluminator was used to view the PCR products of the TMCs from the ChIP test, and PCR was used to assess the immunoprecipitated DNA ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, not significant. Data in A, D, and E are presented as the mean ± SEM, one-way ANOVA with Tukey’s test and two-way ANOVA with post-hoc tests.

Journal: iScience

Article Title: Targeting the PPAR-γ/OPTN axis to inhibit apoptosis in steroid-induced glaucoma

doi: 10.1016/j.isci.2026.115247

Figure Lengend Snippet: PPAR-γ inhibited TMCs apoptosis via regulating Optn as a transcriptional factor (A) The expression of Optn in TMCs was determined by WB staining ( n = 3, n represents biological replicates). (B and C) For the dual-luciferase test, a full-length and three potential enhancer segments of the rat promoter region of Optn were created. (D) Luciferase activity was seen in the indicated groups, suggesting that PPAR-γ functioned as a transcriptional enhancer by bidding at the Optn promoter’s 3′–5′ strand’s −1925 to −1898 locations ( n = 3, n represents biological replicates). (E) A UV transilluminator was used to view the PCR products of the TMCs from the ChIP test, and PCR was used to assess the immunoprecipitated DNA ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, not significant. Data in A, D, and E are presented as the mean ± SEM, one-way ANOVA with Tukey’s test and two-way ANOVA with post-hoc tests.

Article Snippet: Annexin V-APC/PI Apoptosis Kit , CatElabscience , Cat#E-CK-A217.

Techniques: Expressing, Staining, Luciferase, Activity Assay, Immunoprecipitation

Knockdown of the Optn gene reversed the inhibitory effect of pioglitazone on TMCs apoptosis (A) Apoptosis of TMCs was determined by flow cytometric analysis. (B) Analysis of the data in (A) ( n = 4, n represents the number of cells). (C) The apoptosis of TMCs was determined by Tunel staining. Scale bars, 100 μm. (D) The expression of Bcl-2, Bax, Bcl-2/Bax, Caspase-3, and p-NF-κB in TMCs was determined by WB staining ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, not significant. Data in B and D are presented as the mean ± SEM, two-way ANOVA with post-hoc tests.

Journal: iScience

Article Title: Targeting the PPAR-γ/OPTN axis to inhibit apoptosis in steroid-induced glaucoma

doi: 10.1016/j.isci.2026.115247

Figure Lengend Snippet: Knockdown of the Optn gene reversed the inhibitory effect of pioglitazone on TMCs apoptosis (A) Apoptosis of TMCs was determined by flow cytometric analysis. (B) Analysis of the data in (A) ( n = 4, n represents the number of cells). (C) The apoptosis of TMCs was determined by Tunel staining. Scale bars, 100 μm. (D) The expression of Bcl-2, Bax, Bcl-2/Bax, Caspase-3, and p-NF-κB in TMCs was determined by WB staining ( n = 3, n represents biological replicates). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; ns, not significant. Data in B and D are presented as the mean ± SEM, two-way ANOVA with post-hoc tests.

Article Snippet: Annexin V-APC/PI Apoptosis Kit , CatElabscience , Cat#E-CK-A217.

Techniques: Knockdown, TUNEL Assay, Staining, Expressing

In Vivo validation: PPAR-γ/OPTN pathway protects against SIG (A) IOP of SIG, SIG+Piog, and control rats ( n = 4, n represents the number of mice). (B) Histological analysis of HE-stained tissues. Scale bars, 20 μm. (C) The apoptosis of trabecular meshwork tissues was determined by Tunel staining. Scale bars, 100 μm. (D) Analysis of the data in (C) ( n = 4, n represents the number of mice). (E) The expression of PPAR-γ, OPTN, Bcl-2, Bax, Caspase-3, and p-NF-κB in the trabecular meshwork tissues was determined by IHC staining. Scale bars, 20 μm. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. Data in A and D are presented as the mean ± SEM, one-way ANOVA with Tukey’s test.

Journal: iScience

Article Title: Targeting the PPAR-γ/OPTN axis to inhibit apoptosis in steroid-induced glaucoma

doi: 10.1016/j.isci.2026.115247

Figure Lengend Snippet: In Vivo validation: PPAR-γ/OPTN pathway protects against SIG (A) IOP of SIG, SIG+Piog, and control rats ( n = 4, n represents the number of mice). (B) Histological analysis of HE-stained tissues. Scale bars, 20 μm. (C) The apoptosis of trabecular meshwork tissues was determined by Tunel staining. Scale bars, 100 μm. (D) Analysis of the data in (C) ( n = 4, n represents the number of mice). (E) The expression of PPAR-γ, OPTN, Bcl-2, Bax, Caspase-3, and p-NF-κB in the trabecular meshwork tissues was determined by IHC staining. Scale bars, 20 μm. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001. Data in A and D are presented as the mean ± SEM, one-way ANOVA with Tukey’s test.

Article Snippet: Annexin V-APC/PI Apoptosis Kit , CatElabscience , Cat#E-CK-A217.

Techniques: In Vivo, Biomarker Discovery, Control, Staining, TUNEL Assay, Expressing, Immunohistochemistry

A schematic model proposes the targeting of the PPAR-γ/OPTN axis, a key mechanism regulating TMCS apoptosis, as a potential strategy for intervening in SIG

Journal: iScience

Article Title: Targeting the PPAR-γ/OPTN axis to inhibit apoptosis in steroid-induced glaucoma

doi: 10.1016/j.isci.2026.115247

Figure Lengend Snippet: A schematic model proposes the targeting of the PPAR-γ/OPTN axis, a key mechanism regulating TMCS apoptosis, as a potential strategy for intervening in SIG

Article Snippet: Annexin V-APC/PI Apoptosis Kit , CatElabscience , Cat#E-CK-A217.

Techniques:

Identification of a PANoptotic DPC cluster in human clinical pulpitis samples (A) Gene sets associated with PANoptosis were constructed on the basis of previous studies. (B–D) The expression scores for pyroptosis-related (B, also see ), necroptosis-related (C, also see ), and apoptosis-related (D, also see ) genes were calculated using the AddModuleScore function in Seurat. NCs: neural cells, unknown: cells expressed mitochondrial genes as markers, RBCs: red blood cells, DPSCs: dental pulp stem cells, ECs: endothelial cells, GCs: glial cells, Ms: macrophages, TCs: T cells, DPCs: dental pulp cells, BCs: B cells, DCs: dendritic cells, PCs: plasma cells. (E) Multiple immunofluorescence staining of biomarkers of apoptosis, pyroptosis, and necroptosis in healthy and inflamed human dental pulp tissues. Vimentin-positive cells indicate DPCs. Scale bars, 10 μm. (F) Quantification of the staining results in E ( n = 4 samples in each group). Data are represented as mean ± SEM. ∗ p < 0.05 by Mann-Whitney U test (F).

Journal: iScience

Article Title: FOXE1 promotes the progression of pulp inflammation by activating PANoptosis in dental pulp cells

doi: 10.1016/j.isci.2026.115204

Figure Lengend Snippet: Identification of a PANoptotic DPC cluster in human clinical pulpitis samples (A) Gene sets associated with PANoptosis were constructed on the basis of previous studies. (B–D) The expression scores for pyroptosis-related (B, also see ), necroptosis-related (C, also see ), and apoptosis-related (D, also see ) genes were calculated using the AddModuleScore function in Seurat. NCs: neural cells, unknown: cells expressed mitochondrial genes as markers, RBCs: red blood cells, DPSCs: dental pulp stem cells, ECs: endothelial cells, GCs: glial cells, Ms: macrophages, TCs: T cells, DPCs: dental pulp cells, BCs: B cells, DCs: dendritic cells, PCs: plasma cells. (E) Multiple immunofluorescence staining of biomarkers of apoptosis, pyroptosis, and necroptosis in healthy and inflamed human dental pulp tissues. Vimentin-positive cells indicate DPCs. Scale bars, 10 μm. (F) Quantification of the staining results in E ( n = 4 samples in each group). Data are represented as mean ± SEM. ∗ p < 0.05 by Mann-Whitney U test (F).

Article Snippet: Annexin V-FITC/PI Apoptosis Kit , Multi Sciences , Cat#AP101.

Techniques: Construct, Expressing, Clinical Proteomics, Immunofluorescence, Staining, MANN-WHITNEY

Mixed infection with S.m. and F.n. induced PANoptosis in DPCs (A–H) Dental pulp cells were infected with S.m. (MOI = 100), F.n. (MOI = 100), or a combination of S.m. (MOI = 100) and F.n. (MOI = 100) or treated with PBS (negative control, NC) for 8 h. (A) Dental pulp cells were treated with PBS, S.m. , F.n. , or a combination of S.m. and F.n. ( n = 5 experiments in each group), and cell death was quantified by measuring LDH release. (B) Dental pulp cells were treated with PBS, S.m. , F.n. , or a combination of S.m. and F.n . Treated DPCs were stained with PI, fixed, counterstained with DAPI, and visualized under a microscope. Scale bars, 100 μm. (C) Quantification of the proportions of PI-positive cells in B ( n = 6 experiments in each group). (D) Dental pulp cells were treated as indicated and analyzed by flow cytometry. (E) PANoptotic DPCs were quantified by determining the percentages of PI + /annexin V + cells ( n = 3 experiments in each group). (F) The protein levels of cleaved caspase-3 p17, cleaved GSDMD NT, and p -MLKL were assessed by Western blot. (G) Immunofluorescence staining of PANoptotic markers in infected DPCs, as visualized using a confocal microscope. Scale bars, 10 μm. (H) Quantification of PANoptotic cell proportions in DPCs treated with PBS, S.m. , F.n. , or a combination of S.m. and F.n. ( n = 8 samples in each group), corresponding to (G). Data are represented as mean ± SEM. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by one-way ANOVA (A, C, and E) or by Kruskal-Wallis test (H).

Journal: iScience

Article Title: FOXE1 promotes the progression of pulp inflammation by activating PANoptosis in dental pulp cells

doi: 10.1016/j.isci.2026.115204

Figure Lengend Snippet: Mixed infection with S.m. and F.n. induced PANoptosis in DPCs (A–H) Dental pulp cells were infected with S.m. (MOI = 100), F.n. (MOI = 100), or a combination of S.m. (MOI = 100) and F.n. (MOI = 100) or treated with PBS (negative control, NC) for 8 h. (A) Dental pulp cells were treated with PBS, S.m. , F.n. , or a combination of S.m. and F.n. ( n = 5 experiments in each group), and cell death was quantified by measuring LDH release. (B) Dental pulp cells were treated with PBS, S.m. , F.n. , or a combination of S.m. and F.n . Treated DPCs were stained with PI, fixed, counterstained with DAPI, and visualized under a microscope. Scale bars, 100 μm. (C) Quantification of the proportions of PI-positive cells in B ( n = 6 experiments in each group). (D) Dental pulp cells were treated as indicated and analyzed by flow cytometry. (E) PANoptotic DPCs were quantified by determining the percentages of PI + /annexin V + cells ( n = 3 experiments in each group). (F) The protein levels of cleaved caspase-3 p17, cleaved GSDMD NT, and p -MLKL were assessed by Western blot. (G) Immunofluorescence staining of PANoptotic markers in infected DPCs, as visualized using a confocal microscope. Scale bars, 10 μm. (H) Quantification of PANoptotic cell proportions in DPCs treated with PBS, S.m. , F.n. , or a combination of S.m. and F.n. ( n = 8 samples in each group), corresponding to (G). Data are represented as mean ± SEM. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by one-way ANOVA (A, C, and E) or by Kruskal-Wallis test (H).

Article Snippet: Annexin V-FITC/PI Apoptosis Kit , Multi Sciences , Cat#AP101.

Techniques: Infection, Negative Control, Staining, Microscopy, Flow Cytometry, Western Blot, Immunofluorescence

Identification and validation of FOXE1 as a key transcription factor that regulates PANoptosis in DPCs (A) Differentially expressed gene analysis was performed between the PANoptotic DPC cluster (cluster 1) and other DPC clusters (clusters 0, 2, 4, 5, and 6) and between cluster 1 and all remaining clusters. The candidate regulators were selected from the overlapping DEGs between these comparisons. (B) The top five candidate regulators were identified after comparison. (C) siRNA targeting FOXE1 (20 μM) was transfected into DPCs with Lipofectamine 2000 for 24 h. The knockdown efficiency was validated by qRT-PCR ( n = 3 experiments in each group) and Western blot. (D–H) Dental pulp cells were pretreated with siRNAs (20 μM) targeting candidate regulators for 24 h, followed by infection with S.m. (MOI = 100) and F.n. (MOI = 100) for 8 h. (D) Cell death was quantified by the LDH release assays ( n = 5 experiments in each group). (E, also see in ) Cell death was assessed by PI staining ( n = 4 experiments in each group). (F) Treated cells were analyzed by flow cytometry. (G) PANoptotic DPCs were quantified by determining the percentages of PI + /annexin V + cells ( n = 3 experiments in each group). (H) Western blot analysis was used to assess the expression of cleaved caspase-3 p17, cleaved GSDMD NT and p -MLKL. (I) Immunofluorescence staining of PANoptotic markers in si FOXE1 -and siCON-transfected DPCs. Scale bars, 10 μm. (J) Quantification of PANoptotic DPCs in I ( n = 5 samples in each group). Data are represented as mean ± SEM. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by Student’s t test (C, G, and J) or by one-way ANOVA (D and E).

Journal: iScience

Article Title: FOXE1 promotes the progression of pulp inflammation by activating PANoptosis in dental pulp cells

doi: 10.1016/j.isci.2026.115204

Figure Lengend Snippet: Identification and validation of FOXE1 as a key transcription factor that regulates PANoptosis in DPCs (A) Differentially expressed gene analysis was performed between the PANoptotic DPC cluster (cluster 1) and other DPC clusters (clusters 0, 2, 4, 5, and 6) and between cluster 1 and all remaining clusters. The candidate regulators were selected from the overlapping DEGs between these comparisons. (B) The top five candidate regulators were identified after comparison. (C) siRNA targeting FOXE1 (20 μM) was transfected into DPCs with Lipofectamine 2000 for 24 h. The knockdown efficiency was validated by qRT-PCR ( n = 3 experiments in each group) and Western blot. (D–H) Dental pulp cells were pretreated with siRNAs (20 μM) targeting candidate regulators for 24 h, followed by infection with S.m. (MOI = 100) and F.n. (MOI = 100) for 8 h. (D) Cell death was quantified by the LDH release assays ( n = 5 experiments in each group). (E, also see in ) Cell death was assessed by PI staining ( n = 4 experiments in each group). (F) Treated cells were analyzed by flow cytometry. (G) PANoptotic DPCs were quantified by determining the percentages of PI + /annexin V + cells ( n = 3 experiments in each group). (H) Western blot analysis was used to assess the expression of cleaved caspase-3 p17, cleaved GSDMD NT and p -MLKL. (I) Immunofluorescence staining of PANoptotic markers in si FOXE1 -and siCON-transfected DPCs. Scale bars, 10 μm. (J) Quantification of PANoptotic DPCs in I ( n = 5 samples in each group). Data are represented as mean ± SEM. ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001 by Student’s t test (C, G, and J) or by one-way ANOVA (D and E).

Article Snippet: Annexin V-FITC/PI Apoptosis Kit , Multi Sciences , Cat#AP101.

Techniques: Biomarker Discovery, Comparison, Transfection, Knockdown, Quantitative RT-PCR, Western Blot, Infection, Staining, Flow Cytometry, Expressing, Immunofluorescence

BCAT1 regulates T-ALL cell fate decisions. ( A ) Representative flow cytometry plots of leukemia cells (GFP + ) in the peripheral blood of recipient mice 3 weeks after secondary transplantation. ( B ) Quantification of leukemia cells (GFP + ) in peripheral blood after secondary transplantation ( n = 6). ( C ) Representative images of the size of the liver, spleen and thymus from recipient mice post-secondary transplantation. ( D ) Quantification of the data shown in ( C ) ( n = 6). ( E ) Overall survival was determined for the leukemic mice shown in ( B ) ( n = 6). ( F ) Representative flow cytometry plots of leukemia cells (GFP + ) in the peripheral blood of recipient mice 3 weeks after tertiary transplantation. ( G ) Quantification of leukemia cells (GFP + ) in peripheral blood after tertiary transplantation ( n = 6). ( H ) Organ weight quantification of the liver, spleen and thymus from transplanted mice ( n = 4). ( I ) Overall survival was determined for the leukemic mice shown in ( G ) ( n = 10). ( J ) Representative flow cytometry plots showing early and late apoptosis of WT and KO T-ALL cells in peripheral blood after secondary transplantation. ( K ) Quantification of apoptotic populations from Panel ( J ) ( n = 3). ( L ) Flow cytometric analysis of the homing efficiency of WT and KO T-ALL cells to bone marrow 16 h post-injection. ( M ) Quantification of homing efficiency, shown in ( L ) ( n = 5). ( N ) Cell cycle status was determined in WT and KO T-ALL cells of the recipients. ( O )Quantification data of the phases of the cell cycle in Panel ( N ) ( n = 3). The data are presented as the means ± SDs. Student’s two-tailed unpaired t test (B, G, M) , log-rank test ( E , I ) and two-way ANOVA with Sidak’s multiple comparison test ( D , H , K , O ) were used for the comparison of statistical significance (*, P < 0.05; **, P < 0.01; and ***, P < 0.001)

Journal: Cellular Oncology

Article Title: BCAA catabolism mediates POU2AF1 propionylation to enhance T-ALL development

doi: 10.1007/s13402-026-01201-w

Figure Lengend Snippet: BCAT1 regulates T-ALL cell fate decisions. ( A ) Representative flow cytometry plots of leukemia cells (GFP + ) in the peripheral blood of recipient mice 3 weeks after secondary transplantation. ( B ) Quantification of leukemia cells (GFP + ) in peripheral blood after secondary transplantation ( n = 6). ( C ) Representative images of the size of the liver, spleen and thymus from recipient mice post-secondary transplantation. ( D ) Quantification of the data shown in ( C ) ( n = 6). ( E ) Overall survival was determined for the leukemic mice shown in ( B ) ( n = 6). ( F ) Representative flow cytometry plots of leukemia cells (GFP + ) in the peripheral blood of recipient mice 3 weeks after tertiary transplantation. ( G ) Quantification of leukemia cells (GFP + ) in peripheral blood after tertiary transplantation ( n = 6). ( H ) Organ weight quantification of the liver, spleen and thymus from transplanted mice ( n = 4). ( I ) Overall survival was determined for the leukemic mice shown in ( G ) ( n = 10). ( J ) Representative flow cytometry plots showing early and late apoptosis of WT and KO T-ALL cells in peripheral blood after secondary transplantation. ( K ) Quantification of apoptotic populations from Panel ( J ) ( n = 3). ( L ) Flow cytometric analysis of the homing efficiency of WT and KO T-ALL cells to bone marrow 16 h post-injection. ( M ) Quantification of homing efficiency, shown in ( L ) ( n = 5). ( N ) Cell cycle status was determined in WT and KO T-ALL cells of the recipients. ( O )Quantification data of the phases of the cell cycle in Panel ( N ) ( n = 3). The data are presented as the means ± SDs. Student’s two-tailed unpaired t test (B, G, M) , log-rank test ( E , I ) and two-way ANOVA with Sidak’s multiple comparison test ( D , H , K , O ) were used for the comparison of statistical significance (*, P < 0.05; **, P < 0.01; and ***, P < 0.001)

Article Snippet: Apoptosis was assessed using an Annexin V-APC Apoptosis Detection Kit (MULTI SCIENCE, AP105) according to the manufacturer’s protocol.

Techniques: Flow Cytometry, Transplantation Assay, Injection, Two Tailed Test, Comparison

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