mitosox red  (MedChemExpress)

Journal: Biology Direct

Article Title: STING‑regulated Ca²⁺–TGF‑β axis drives airway remodeling and lung function decline in asthma: a multi‑omics mechanistic study

doi: 10.1186/s13062-026-00940-y

Figure Lengend Snippet: Mitochondrial stress is associated with the STING-PPM1F-TGF-β axis in vitro. ( A ) MitoSOX staining showing time-dependent mtROS production after OVA treatment (6–24 h), with CCCP as positive control ( p < 0.01). ( B ) JC-1 staining showing time-dependent ΔΨm dissipation after OVA treatment ( p < 0.05, p < 0.001). ( C ) Fura-2 calcium imaging showing STING activation-induced Ca²⁺ mobilization under 2 mM Ca²⁺ or EGTA conditions ( p < 0.001). ( D ) Immunofluorescence co-localization of PPM1F and TGF-β after OVA or CCCP stimulation. ( E - F ) Co-immunoprecipitation confirming PPM1F-TGF-β interaction. ( G ) Cytosolic mtDNA release quantified by qPCR; H-151 did not affect OVA-induced mtDNA release (ns vs. OVA). ( H ) Western blot showing OVA-induced PPM1F and p-Smad2/3 upregulation in WT mice, abolished in STING KO mice. ( I ) PPM1F knockdown blocks TGF‑β1‑induced p‑Smad2 and α‑SMA expression in BEAS‑2B cells. ( J ) p-TBK1 expression in cGAMP/H-151/OVA-treated cells, showing STING-dependent TBK1 activation

Article Snippet: MitoSOX staining: Cells or freshly isolated primary airway epithelial cells were incubated with 5 μM MitoSOX (HY-D1055, MCE, USA) and Hoechst 33,342 (HY-15559, MCE, USA) for 10 min at 37 °C.

Techniques: In Vitro, Staining, Positive Control, Imaging, Activation Assay, Immunofluorescence, Immunoprecipitation, Western Blot, Knockdown, Expressing

Journal: Biology Direct

Article Title: STING‑regulated Ca²⁺–TGF‑β axis drives airway remodeling and lung function decline in asthma: a multi‑omics mechanistic study

doi: 10.1186/s13062-026-00940-y

Figure Lengend Snippet: STING knockout attenuates OVA‑induced airway remodeling and suppresses the PPM1F‑TGF‑β‑mitochondrial axis in vivo. ( A ) H&E and PAS staining of lung and kidney (scale bar: 25 μm); OVA‑induced airway pathology was attenuated in STING KO mice. ( B - C ) MitoSOX staining and quantification in primary airway epithelial cells; OVA increased mtROS in WT mice ( p < 0.001); STING KO partially reduced mtROS ( p < 0.01 vs. WT + OVA). ( D ) BALF TGF‑β levels by ELISA; STING KO abolished OVA‑induced increase ( p < 0.01 vs. WT + OVA). ( E ) PPM1F mRNA by qPCR; STING KO attenuated OVA‑induced upregulation ( p < 0.01 vs. WT + OVA). ( F ) Immunofluorescence co‑localization of SCGB1A1 and SFTPC in airway epithelium. ( G ) Quantification of SCGB1A1⁺SFTPC⁺ double‑positive cells (% of total SFTPC⁺ cells), increased in asthma ( p < 0.001). ( H ) SFTPC⁺ cell density, increased in asthma ( p < 0.05). ( I ) RNA‑seq heatmap of TGF‑β pathway genes (WT + OVA vs. STING KO + OVA). ( J ) KEGG enrichment analysis showing calcium metabolism and ECM‑receptor interaction pathways

Article Snippet: MitoSOX staining: Cells or freshly isolated primary airway epithelial cells were incubated with 5 μM MitoSOX (HY-D1055, MCE, USA) and Hoechst 33,342 (HY-15559, MCE, USA) for 10 min at 37 °C.

Techniques: Knock-Out, In Vivo, Staining, Enzyme-linked Immunosorbent Assay, Immunofluorescence

Journal: Aging Cell

Article Title: HNRNPC Succinylation Influences the Neurodegeneration of Alzheimer's Disease Through YME1L1 ‐Mediated Mitochondrial Metabolism

doi: 10.1111/acel.70646

Figure Lengend Snippet: YME1L1 promotes neuronal mitochondrial damage after AD. (A) CCK8 assay for cell viability. (B) Flow cytometry for apoptosis detection. (C) TEM for mitochondrial assessment (The green arrow indicates normal mitochondria, and the red arrow indicates damaged mitochondria). (D) ATP level measurement. (E) JC‐1 staining for cellular mitochondrial membrane potential measurement. (F) MitoSOX fluorescence staining for cellular mitochondrial ROS analysis. n = 3. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Intracellular superoxide levels were measured using the MitoSOX Red fluorescent probe (HY‐D1055; MCE, USA).

Techniques: CCK-8 Assay, Flow Cytometry, Staining, Membrane, Fluorescence

Journal: Aging Cell

Article Title: HNRNPC Succinylation Influences the Neurodegeneration of Alzheimer's Disease Through YME1L1 ‐Mediated Mitochondrial Metabolism

doi: 10.1111/acel.70646

Figure Lengend Snippet: YME1L1 induces neuronal mitochondrial damage and neuronal death following AD through OPA1 hydrolysis. (A) WB detection of OPA1 expression in hippocampal tissue ( n = 6). (B) WB detection of OPA1 expression. (C) CCK8 assay for cell viability. (D) Flow cytometry for apoptosis detection. (E) TEM for mitochondrial detection (The red arrow indicates damaged mitochondria). (F) ATP level detection. (G) JC‐1 staining for measuring mitochondrial membrane potential. (H) MitoSOX fluorescence staining for analyzing mitochondrial ROS. n = 3. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Intracellular superoxide levels were measured using the MitoSOX Red fluorescent probe (HY‐D1055; MCE, USA).

Techniques: Expressing, CCK-8 Assay, Flow Cytometry, Staining, Membrane, Fluorescence

Journal: Aging Cell

Article Title: HNRNPC Succinylation Influences the Neurodegeneration of Alzheimer's Disease Through YME1L1 ‐Mediated Mitochondrial Metabolism

doi: 10.1111/acel.70646

Figure Lengend Snippet: HNRNPC succinylation modifies neuronal mitochondrial damage and neuronal death following AD via YME1L1. (A) PCR and WB detection of YME1L1, WB detection of OPA1. (B) CCK8 analysis of cell activity. (C) Flow cytometry to detect cell apoptosis. (D) TEM detection of mitochondria (The green arrow points to normal mitochondria, and the red arrow points to damaged mitochondria). (E) ATP level detection. (F) JC‐1 staining was used to measure the mitochondrial membrane potential of cells. (G) MitoSOX fluorescent staining analysis of mitochondrial ROS in cells. n = 3. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Intracellular superoxide levels were measured using the MitoSOX Red fluorescent probe (HY‐D1055; MCE, USA).

Techniques: Activity Assay, Flow Cytometry, Staining, Membrane

Journal: Aging Cell

Article Title: HNRNPC Succinylation Influences the Neurodegeneration of Alzheimer's Disease Through YME1L1 ‐Mediated Mitochondrial Metabolism

doi: 10.1111/acel.70646

Figure Lengend Snippet: SIRT5 affects neuronal mitochondrial function by desuccinylating HNRNPC. (A) WB detection of YME1L1 and OPA1 expression. (B) CCK8 analysis of cell activity. (C) Flow cytometry detection of cell apoptosis. (D) TEM detection of mitochondrial morphology (The green arrow points to normal mitochondria, and the red arrow points to damaged mitochondria). (E) ATP level detection. (F) JC‐1 staining to measure cell mitochondrial membrane potential. (G) MitoSOX fluorescent staining analysis of mitochondrial ROS in cells. n = 3. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001; ns stands for no significant difference.

Article Snippet: Intracellular superoxide levels were measured using the MitoSOX Red fluorescent probe (HY‐D1055; MCE, USA).

Techniques: Expressing, Activity Assay, Flow Cytometry, Staining, Membrane