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mitochondrial fission inhibitor mdivi 1 (MedChemExpress)

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MedChemExpress mitochondrial fission inhibitor mdivi 1
Mitochondrial Fission Inhibitor Mdivi 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 441 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mitochondrial+fission/Mdivi-1/pm42208103-260-15-19
Average 99 stars, based on 441 article reviews

mitochondrial fission inhibitor mdivi 1 - by Bioz Stars, 2026-09

99/100 stars

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Incubation:

Article Title: Deubiquitylases MoUbp12 and MoUbp14 modulated by transcription factor MoMsn2 are critical for mitochondrial fusion/fission balance and infectious growth of the rice blast fungus
Article Snippet: .. To inhibit mitochondrial fission, hyphae of each strain were incubated with 10 μM mitochondrial fission inhibitor Mdivi-1 (MedChem Express, HY-15886, USA) for 16 or 24 hpi (Leesnitzer et al. 2002), and the mitochondrial morphology was observed under a confocal fluorescence microscope (ZEISS LSM980 with airyscan 2). .. Total protein of mycelia from each sample was extracted by RIPA Lysis buffer II (Sangon, C510006), and then assayed by western blot analysis with an anti-Ubiquitin as the primary antibody (1:2000, PTM BIO), and a goat anti rabbit as the secondary antibody (1:10,000, LI-COR).

Fluorescence:

Microscopy:

Blocking Assay:

Article Title: High glucose-induced mitophagy accelerates premature aging of T cells in patients with rheumatoid arthritis.
Article Snippet: Objectives Premature T cell aging, marked by telomere shortening and cell cycle arrest, plays a key role in the pathogenesis of rheumatoid arthritis (RA).. Growing evidence suggests that high glucose-induced metabolic dysfunction critically regulates both cellular aging and RA progression.. This study explores how high glucose exacerbates T cell aging, providing novel insights into the mechanisms underlying RA development.

Activity Assay:

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Rotenone (Rot) 1.325nM treatment does not alter cellular viability, calcium homeostasis or mitochondrial membrane potential, but reduces superoxide production and Nicotinamide (NAM) 10µM pretreatment can recover it. ( A ) MTT viability assay. ( B ) Mitochondrial Calcium uptake obtained by Fluo-4 fluorescence. ( C ) Mitochondrial Membrane Potential (ΔΨm) acquired by TMRE fluorescence. ( D ) Superoxide production rate captured by MitoSOX fluorescence. Results normalized by vehicle group and shown as mean ± standard error ( N = 4 or 5, in duplicate; each dot represent a biological replicate). Statistical analysis performed by ANOVA One-Way with Bonferroni posthoc. It was considered statistically significant p < 0.05; * p < 0.05; ** p < 0.01.

Journal: Scientific Reports

Article Title: Nicotinamide counteracts Rotenone-induced mitochondrial and neuronal dysfunction in a translational early-life model

doi: 10.1038/s41598-026-36651-7

Figure Lengend Snippet: Rotenone (Rot) 1.325nM treatment does not alter cellular viability, calcium homeostasis or mitochondrial membrane potential, but reduces superoxide production and Nicotinamide (NAM) 10µM pretreatment can recover it. ( A ) MTT viability assay. ( B ) Mitochondrial Calcium uptake obtained by Fluo-4 fluorescence. ( C ) Mitochondrial Membrane Potential (ΔΨm) acquired by TMRE fluorescence. ( D ) Superoxide production rate captured by MitoSOX fluorescence. Results normalized by vehicle group and shown as mean ± standard error ( N = 4 or 5, in duplicate; each dot represent a biological replicate). Statistical analysis performed by ANOVA One-Way with Bonferroni posthoc. It was considered statistically significant p < 0.05; * p < 0.05; ** p < 0.01.

Article Snippet: The following proteins were analyzed: (i) Mitochondrial fusion markers: OPA1 (1:750; Cell Signaling 612606), Mitofusin 1 (MFN1; 1:500; Sigma-Aldrich SAB2106161), and Mitofusin 2 (MFN2; 1:750; Sigma M6319); (ii) Mitochondrial fission markers: Phospho-DRP1 (Ser616) (pDRP1; 1:500; Cell Signaling, 3455 S) and DRP1 (1:750; Cell Signaling 14647 S); (iii) Mitochondrial mass markers: TOM40 (1:100; Santa Cruz, SC-365467) and TIM23 (1:500; Abcam ab230253); (iv) Autophagy markers: LC3A/B (1:1000; Cell Signaling 4108 S), p62 (1:500; BD BioScience 610832) and Parkin (1:500; Cell Signaling 2132 S).

Techniques: Membrane, MTT Viability Assay, Fluorescence

Oxygen consumption is impaired by Rotenone (Rot) 1.325nM and Nicotinamide (NAM) 10µM pretreatment can improve some parameters. Cellular respiration was obtained using the Seahorse XFe24 Extracellular Flux Analyzer equipment. During the reading of oxygen consumption, solutions of Oligomycin (Oligo) (1µM), Dinitrophenol (DNP) (30mM and 50mM), and Rotenone with Antimycin A (Rot + Aa) (1µM) were injected. ( A ) Representative graph of cellular respiration across time. ( B ) Basal respiration. ( C ) ATP-linked respiration. ( D ) Maximal respiration. ( E ) Spare Capacity. ( F ) Proton leak. ( G ) Non-mitochondrial respiration. Results normalized by vehicle group and shown as mean ± standard error ( N = 4, in duplicate; each dot represent a biological replicate). Statistical analysis performed by ANOVA One-Way with Bonferroni posthoc. It was considered statistically significant p < 0.05; *p < 0.05; * *p < 0.01.

Journal: Scientific Reports

Article Title: Nicotinamide counteracts Rotenone-induced mitochondrial and neuronal dysfunction in a translational early-life model

doi: 10.1038/s41598-026-36651-7

Figure Lengend Snippet: Oxygen consumption is impaired by Rotenone (Rot) 1.325nM and Nicotinamide (NAM) 10µM pretreatment can improve some parameters. Cellular respiration was obtained using the Seahorse XFe24 Extracellular Flux Analyzer equipment. During the reading of oxygen consumption, solutions of Oligomycin (Oligo) (1µM), Dinitrophenol (DNP) (30mM and 50mM), and Rotenone with Antimycin A (Rot + Aa) (1µM) were injected. ( A ) Representative graph of cellular respiration across time. ( B ) Basal respiration. ( C ) ATP-linked respiration. ( D ) Maximal respiration. ( E ) Spare Capacity. ( F ) Proton leak. ( G ) Non-mitochondrial respiration. Results normalized by vehicle group and shown as mean ± standard error ( N = 4, in duplicate; each dot represent a biological replicate). Statistical analysis performed by ANOVA One-Way with Bonferroni posthoc. It was considered statistically significant p < 0.05; *p < 0.05; * *p < 0.01.

Techniques: Injection

Rotenone (Rot) 1.325nM changes mitochondrial dynamics and impairs autophagy, and Nicotinamide (NAM) 10µM pretreatment partially recuperates. Protein levels were obtained by SDS-Page electrophoresis, and each protein’s optical density was calculated using ImageJ. ( A ) Representative image of Opa1 and GAPDH electrophoresis. ( B ) Calculate ratio of protein levels for Opa1/GAPDH. ( C ) Representative image of Mitofusin 1 (Mfn1) and GAPDH electrophoresis. ( D ) Calculate ratio of protein levels for Mfn1/GAPDH. ( E ) Representative image of Mitofusin 2 (Mfn2) and GAPDH electrophoresis. ( F ) Calculate ratio of protein levels for Mfn2/GAPDH. ( G ) Representative image of phosphorylated DRP1 (pDRP1), DRP1 total and GAPDH electrophoresis. ( H ) Calculate ratio of protein levels for pDRP1/DRP1. ( I ) Representative image of TOM40 and GAPDH electrophoresis. ( J ) Calculate ratio of protein levels for TOM40/GAPDH. ( K ) Representative image of TIM23 and GAPDH electrophoresis. ( L ) Calculate ratio of protein levels for TIM23/GAPDH. ( M ) Representative image of LC3 II and GAPDH electrophoresis. ( N ) Representative image of p62 and GAPDH electrophoresis. ( O ) Calculate ratio of protein levels for p62/GAPDH. ( P ) Representative image of Parkin and GAPDH electrophoresis. (Q) Calculate ratio of protein levels for Parkin/GAPDH. Results normalized by vehicle group and shown as mean ± standard error ( N = 6 or 8, each dot represent a biological N). Statistical analysis performed by ANOVA One-Way with Bonferroni posthoc. It was considered statistically significant p < 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Scientific Reports

Article Title: Nicotinamide counteracts Rotenone-induced mitochondrial and neuronal dysfunction in a translational early-life model

doi: 10.1038/s41598-026-36651-7

Figure Lengend Snippet: Rotenone (Rot) 1.325nM changes mitochondrial dynamics and impairs autophagy, and Nicotinamide (NAM) 10µM pretreatment partially recuperates. Protein levels were obtained by SDS-Page electrophoresis, and each protein’s optical density was calculated using ImageJ. ( A ) Representative image of Opa1 and GAPDH electrophoresis. ( B ) Calculate ratio of protein levels for Opa1/GAPDH. ( C ) Representative image of Mitofusin 1 (Mfn1) and GAPDH electrophoresis. ( D ) Calculate ratio of protein levels for Mfn1/GAPDH. ( E ) Representative image of Mitofusin 2 (Mfn2) and GAPDH electrophoresis. ( F ) Calculate ratio of protein levels for Mfn2/GAPDH. ( G ) Representative image of phosphorylated DRP1 (pDRP1), DRP1 total and GAPDH electrophoresis. ( H ) Calculate ratio of protein levels for pDRP1/DRP1. ( I ) Representative image of TOM40 and GAPDH electrophoresis. ( J ) Calculate ratio of protein levels for TOM40/GAPDH. ( K ) Representative image of TIM23 and GAPDH electrophoresis. ( L ) Calculate ratio of protein levels for TIM23/GAPDH. ( M ) Representative image of LC3 II and GAPDH electrophoresis. ( N ) Representative image of p62 and GAPDH electrophoresis. ( O ) Calculate ratio of protein levels for p62/GAPDH. ( P ) Representative image of Parkin and GAPDH electrophoresis. (Q) Calculate ratio of protein levels for Parkin/GAPDH. Results normalized by vehicle group and shown as mean ± standard error ( N = 6 or 8, each dot represent a biological N). Statistical analysis performed by ANOVA One-Way with Bonferroni posthoc. It was considered statistically significant p < 0.05; * p < 0.05; ** p < 0.01; *** p < 0.001.

Techniques: SDS Page, Electrophoresis

Proposed working model of Rotenone and Nicotinamide pretreatment induced mitochondrial and neuronal alterations. Low-dose Rotenone (1.325nM) inhibits mitochondrial Complex I in primary cortical neurons, reducing electron transport chain activity, mitochondrial respiration, ATP production, and superoxide generation. This mitochondrial stress induces SIRT3 upregulation and increased mitochondrial fission but impairs autophagy and mitophagy, leading to the accumulation of dysfunctional mitochondria, synaptic disruption, and reduced dendritic complexity. Nicotinamide (NAM 10µM) pretreatment restores mitochondrial function by supporting NAD⁺-dependent electron transport, enhancing SIRT3 activity, improving autophagic flux, and preserving mitochondrial mass. These effects result in the recovery of ATP and superoxide levels, normalization of dendritic architecture, and reestablishment of synaptic integrity.

Journal: Scientific Reports

Article Title: Nicotinamide counteracts Rotenone-induced mitochondrial and neuronal dysfunction in a translational early-life model

doi: 10.1038/s41598-026-36651-7

Figure Lengend Snippet: Proposed working model of Rotenone and Nicotinamide pretreatment induced mitochondrial and neuronal alterations. Low-dose Rotenone (1.325nM) inhibits mitochondrial Complex I in primary cortical neurons, reducing electron transport chain activity, mitochondrial respiration, ATP production, and superoxide generation. This mitochondrial stress induces SIRT3 upregulation and increased mitochondrial fission but impairs autophagy and mitophagy, leading to the accumulation of dysfunctional mitochondria, synaptic disruption, and reduced dendritic complexity. Nicotinamide (NAM 10µM) pretreatment restores mitochondrial function by supporting NAD⁺-dependent electron transport, enhancing SIRT3 activity, improving autophagic flux, and preserving mitochondrial mass. These effects result in the recovery of ATP and superoxide levels, normalization of dendritic architecture, and reestablishment of synaptic integrity.

Techniques: Activity Assay, Disruption, Preserving

LPS (lipopolysaccharide) modulates mitochondrial‐ER (endoplasmic reticulum) membrane protein expression and disrupts MAM (mitochondria‐associated endoplasmic reticulum membrane) integrity. (A and B) Protein expression and quantification of MFN2 (mitofusin 2) in mouse mammary epithelial cells (mMEC) detected using Western blot. (C–F) Protein expression and quantification of FIS‐1 (fission protein 1), DRP‐1 (dynamin‐related protein 1), and OPA‐1 (optic atrophy 1) in mMECs detected using Western blot. (G–I) Protein expression and quantification of eIF‐2α (eukaryotic translation initiation factor 2 alpha), p‐eIF‐2α, and PACS2 (phosphofurin acidic cluster sorting protein 2) in mMECs. (J) Protein expression of MFN2 and PACS2 in mMECs after LPS stimulation detected using immunofluorescence. (K) Mitochondrial and ER marker protein PDI (protein disulfide isomerase) expression detected using laser confocal microscopy. Data are presented as mean ± SD (standard deviation).

Journal: Animal Models and Experimental Medicine

Article Title: Overexpression of mitofusin 2 ameliorates inflammation and oxidative stress in lipopolysaccharide‐induced mastitis model by regulating phosphofurin acidic cluster sorting protein 2

doi: 10.1002/ame2.70110

Figure Lengend Snippet: LPS (lipopolysaccharide) modulates mitochondrial‐ER (endoplasmic reticulum) membrane protein expression and disrupts MAM (mitochondria‐associated endoplasmic reticulum membrane) integrity. (A and B) Protein expression and quantification of MFN2 (mitofusin 2) in mouse mammary epithelial cells (mMEC) detected using Western blot. (C–F) Protein expression and quantification of FIS‐1 (fission protein 1), DRP‐1 (dynamin‐related protein 1), and OPA‐1 (optic atrophy 1) in mMECs detected using Western blot. (G–I) Protein expression and quantification of eIF‐2α (eukaryotic translation initiation factor 2 alpha), p‐eIF‐2α, and PACS2 (phosphofurin acidic cluster sorting protein 2) in mMECs. (J) Protein expression of MFN2 and PACS2 in mMECs after LPS stimulation detected using immunofluorescence. (K) Mitochondrial and ER marker protein PDI (protein disulfide isomerase) expression detected using laser confocal microscopy. Data are presented as mean ± SD (standard deviation).

Article Snippet: Mitochondrial fission protein 1 , 10956‐1‐AP , 1:4000 , Proteintech.

Techniques: Membrane, Expressing, Western Blot, Immunofluorescence, Marker, Confocal Microscopy, Standard Deviation

MFN2‐PACS2 (mitofusin 2–phosphofurin acidic cluster sorting protein 2) interaction regulates MAM (mitochondria‐associated endoplasmic reticulum membrane) dynamics and mitigates LPS (lipopolysaccharide)–induced mitochondrial dysfunction. (A) CO‐IP (co‐immunoprecipitation) of MFN2 in mouse mammary epithelial cell (mMEC) lysates. (B) Immunoprecipitation of MFN2 in mMEC lysates. OE‐MFN2 denotes MFN2 overexpression. (C) Immunoprecipitation of MFN2 in mMEC lysates. (D) CO‐IP of PACS2 in mMEC lysates. (E) mRNA (messenger RNA) expression of MFN2 in mammary tissues detected using qRT‐PCR (quantitative reverse transcription polymerase chain reaction). (F) Immunoprecipitation of MFN2 in mMEC lysates. (G) Protein expression and quantification of DRP‐1 (dynamin‐related protein 1), OPA‐1 (optic atrophy 1), FIS‐1 (fission protein 1), and MFN1 in mMECs detected using Western blot. (H and I) Mitochondrial and ER marker protein PDI (protein disulfide isomerase) expression detected using laser confocal microscopy.

Journal: Animal Models and Experimental Medicine

doi: 10.1002/ame2.70110

Figure Lengend Snippet: MFN2‐PACS2 (mitofusin 2–phosphofurin acidic cluster sorting protein 2) interaction regulates MAM (mitochondria‐associated endoplasmic reticulum membrane) dynamics and mitigates LPS (lipopolysaccharide)–induced mitochondrial dysfunction. (A) CO‐IP (co‐immunoprecipitation) of MFN2 in mouse mammary epithelial cell (mMEC) lysates. (B) Immunoprecipitation of MFN2 in mMEC lysates. OE‐MFN2 denotes MFN2 overexpression. (C) Immunoprecipitation of MFN2 in mMEC lysates. (D) CO‐IP of PACS2 in mMEC lysates. (E) mRNA (messenger RNA) expression of MFN2 in mammary tissues detected using qRT‐PCR (quantitative reverse transcription polymerase chain reaction). (F) Immunoprecipitation of MFN2 in mMEC lysates. (G) Protein expression and quantification of DRP‐1 (dynamin‐related protein 1), OPA‐1 (optic atrophy 1), FIS‐1 (fission protein 1), and MFN1 in mMECs detected using Western blot. (H and I) Mitochondrial and ER marker protein PDI (protein disulfide isomerase) expression detected using laser confocal microscopy.

Article Snippet: Mitochondrial fission protein 1 , 10956‐1‐AP , 1:4000 , Proteintech.

Techniques: Membrane, Co-Immunoprecipitation Assay, Immunoprecipitation, Over Expression, RNA Expression, Quantitative RT-PCR, Reverse Transcription, Polymerase Chain Reaction, Expressing, Western Blot, Marker, Confocal Microscopy

A Images of representative liver dissected from 34-week-old mice (top) with a corresponding hematoxylin and eosin (H&E) stain (bottom). The inset H&E image is illustrating normal blood vessels (circular or oval areas that do not stain with H&E) in liver sections from LFD mice, or areas of HCC in WD + DEN/TAA treated mice, which also do not stain with H&E but are larger, irregularly shaped, and surrounded by nuclei (blue staining) ( n = 6 mice per group). B Serum ALT activity was elevated in WD + DEN/TAA groups. The male and female LFD groups and female WD + DEN/TAA group had an n = 3. The male WD + DEN/TAA group had an n = 4. C Serum AST activity was elevated in WD + DEN/TAA groups ( n = 3 per group). D Nuclei (Hoechst) and Ki-67 (proliferation marker, upregulated in HCC) fluorescent images of liver sections. Ki-67 staining was higher in WD + DEN/TAA treated liver sections ( n = 6 per group). E Relative fluorescent intensity of Ki-67 staining from images shown in D ( n = 6 per group). F PCA plot of mitochondrial lipids between non-tumor and tumor mitochondria ( n = 6 per group). G Heatmap of select lipids that were differentially altered between non-tumor and tumor mitochondria ( n = 6 per group). H The abundance of mitochondrial phospholipids was not different between non-tumor and tumor mitochondria ( n = 6 per group). The data are presented as means ± S.D.

Journal: Oncogenesis

Article Title: Targeting mitochondrial phosphatidylethanolamine alters mitochondrial metabolism and proliferation in hepatocellular carcinoma

doi: 10.1038/s41389-025-00593-y

Figure Lengend Snippet: A Images of representative liver dissected from 34-week-old mice (top) with a corresponding hematoxylin and eosin (H&E) stain (bottom). The inset H&E image is illustrating normal blood vessels (circular or oval areas that do not stain with H&E) in liver sections from LFD mice, or areas of HCC in WD + DEN/TAA treated mice, which also do not stain with H&E but are larger, irregularly shaped, and surrounded by nuclei (blue staining) ( n = 6 mice per group). B Serum ALT activity was elevated in WD + DEN/TAA groups. The male and female LFD groups and female WD + DEN/TAA group had an n = 3. The male WD + DEN/TAA group had an n = 4. C Serum AST activity was elevated in WD + DEN/TAA groups ( n = 3 per group). D Nuclei (Hoechst) and Ki-67 (proliferation marker, upregulated in HCC) fluorescent images of liver sections. Ki-67 staining was higher in WD + DEN/TAA treated liver sections ( n = 6 per group). E Relative fluorescent intensity of Ki-67 staining from images shown in D ( n = 6 per group). F PCA plot of mitochondrial lipids between non-tumor and tumor mitochondria ( n = 6 per group). G Heatmap of select lipids that were differentially altered between non-tumor and tumor mitochondria ( n = 6 per group). H The abundance of mitochondrial phospholipids was not different between non-tumor and tumor mitochondria ( n = 6 per group). The data are presented as means ± S.D.

Article Snippet: Between 12 and 20 μg of protein was resolved by SDS-PAGE (Bio-Rad Laboratories, Hercules, CA, USA), transferred onto nitrocellulose membrane or methanol-activated polyvinylidene fluoride (PVDF), normalized using Ponceau S staining solution (40000279, Thermo Fisher Scientific), cut to appropriate size, and blocked in 5% non-fat milk for 75 min. Blots were incubated overnight at 4 °C with total OXPHOS rodent WB antibody cocktail (ab110413, Abcam), voltage-dependent anion channel (VDAC, 4866, Cell Signaling Technology, Danvers, MA, USA), peroxin-5 (PEX5, 83020, Cell Signaling Technology), glucose transporter 1 (Glut 1, 12939, Cell Signaling Technology), transketolase (TKT, 64414, Cell Signaling Technology), phosphoenolpyruvate carboxykinase 1 (PCK1, 12940, Cell Signaling Technology), enolase 1 (ENO1, 3810, Cell Signaling Technology), aldolase a (ALDOA, 8060, Cell Signaling Technology), glyceraldehyde-3-phosphate dehydrogenase (GAPDH, 2118S, Cell Signaling Technology), phosphoglycerate mutase (PGAM1, Cell Signaling Technology), superoxide dismutase 2 (SOD2, 13194, Cell Signaling Technology), dynamin-related protein 1 (DRP1, 8570, Cell Signaling Technology), mitochondrial fission factor (MFF, 84580, Cell Signaling Technology), optic atrophy 1 (OPA1, 80471, Cell Signaling Technology), mitofusin 1 (MFN1, 14739, Cell Signaling Technology), mitofusin 2 (MFN2, 9482, Cell Signaling Technology), Parkin (4211, Cell Signaling Technology), liver kinase B1 (LKB1, 3047, Cell Signaling Technology), phosphorylated LKB1 S428 (3482, Cell Signaling Technology), adenosine monophosphate activated protein kinase (AMPK, 2532, Cell Signaling Technology), phosphorylated AMPK (2535, Cell Signaling Technology), mammalian target of rapamycin (mTOR, 2983, Cell Signaling Technology), phosphorylated mTOR S2448 (2971, Cell Signaling Technology), eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1, 9452, Cell Signaling Technology), or phosphorylated 4E-BP1 S65 (9451, Cell Signaling Technology).

Techniques: Staining, Activity Assay, Marker

A Schematic created using BioRender illustrating PISD enzyme reaction with phosphatidylserine (PS) to form CO 2 and phosphatidylethanolamine (PE). B Schematic created using BioRender showing generation of shScrambled (shSCR) and shPISD lentivirus in 293T cells and subsequent infection and gene silencing in HEPA1-6 cells. C The shPISD lentivirus reduced PISD mRNA abundance ( n = 2 per group) and altered the abundance of various genes involved in phospholipid metabolism ( n = 5 per group). D PISD activity was reduced in shPISD treated cells ( n = 3 per group). E , F Thin layer chromatography images indicating shPISD treated cells had reduced mitochondrial PE content ( E ) and densitometry quantification of thin layer chromatography images presented in E ( n = 3 per group) ( F ). G A Seahorse mitochondrial stress test reveals shPISD treated cells have reduced FCCP stimulated respiration rates ( n = 10 per group). H shPISD treated cells have elevated proton leak, calculated by subtracting oxygen consumption rates (OCR) during basal conditions from OCR during oligomycin (oligo) treated conditions ( n = 10 per group). I , J Western blot image indicating shPISD treated cells have reduced complex I and IV protein abundance ( I ) and densitometry quantification of Western blot images shown in I ( n = 6 per group) ( J ). K 1- 14 C oleate oxidation is reduced in shPISD treated cells ( n = 6 per group). L 1- 14 C lignoceric acid oxidation is increased in shPISD treated cells ( n = 6 per group). M PCA plot of untargeted metabolomics data illustrating that shPISD treated cells have an altered metabolome compared to shSCR treated cells ( n = 3 per group). N Volcano plot of untargeted metabolomics data illustrating differences in metabolites between shSCR and shPISD treated cells ( n = 3 per group). O Heatmap of select lipid metabolism related metabolites that were differentially expressed between shSCR and shPISD treated cells ( n = 3 per group). The data are presented as means ± S.D.

Journal: Oncogenesis

Article Title: Targeting mitochondrial phosphatidylethanolamine alters mitochondrial metabolism and proliferation in hepatocellular carcinoma

doi: 10.1038/s41389-025-00593-y

Figure Lengend Snippet: A Schematic created using BioRender illustrating PISD enzyme reaction with phosphatidylserine (PS) to form CO 2 and phosphatidylethanolamine (PE). B Schematic created using BioRender showing generation of shScrambled (shSCR) and shPISD lentivirus in 293T cells and subsequent infection and gene silencing in HEPA1-6 cells. C The shPISD lentivirus reduced PISD mRNA abundance ( n = 2 per group) and altered the abundance of various genes involved in phospholipid metabolism ( n = 5 per group). D PISD activity was reduced in shPISD treated cells ( n = 3 per group). E , F Thin layer chromatography images indicating shPISD treated cells had reduced mitochondrial PE content ( E ) and densitometry quantification of thin layer chromatography images presented in E ( n = 3 per group) ( F ). G A Seahorse mitochondrial stress test reveals shPISD treated cells have reduced FCCP stimulated respiration rates ( n = 10 per group). H shPISD treated cells have elevated proton leak, calculated by subtracting oxygen consumption rates (OCR) during basal conditions from OCR during oligomycin (oligo) treated conditions ( n = 10 per group). I , J Western blot image indicating shPISD treated cells have reduced complex I and IV protein abundance ( I ) and densitometry quantification of Western blot images shown in I ( n = 6 per group) ( J ). K 1- 14 C oleate oxidation is reduced in shPISD treated cells ( n = 6 per group). L 1- 14 C lignoceric acid oxidation is increased in shPISD treated cells ( n = 6 per group). M PCA plot of untargeted metabolomics data illustrating that shPISD treated cells have an altered metabolome compared to shSCR treated cells ( n = 3 per group). N Volcano plot of untargeted metabolomics data illustrating differences in metabolites between shSCR and shPISD treated cells ( n = 3 per group). O Heatmap of select lipid metabolism related metabolites that were differentially expressed between shSCR and shPISD treated cells ( n = 3 per group). The data are presented as means ± S.D.

Techniques: Infection, Activity Assay, Thin Layer Chromatography, Western Blot, Quantitative Proteomics

A Extracellular acidification rates (ECAR) during a Seahorse mitochondrial stress test were elevated in shPISD treated cells after the injection of glucose and oligomycin into the media ( n = 10 per group). B Percentage change in media lactate over a 24-h period revealed shPISD treated cells generate more lactate ( n = 6 per group). C 1- 14 C glucose oxidation was reduced in shPISD treated cells ( n = 12 per group). D 6- 14 C glucose oxidation was reduced in shPISD treated cells ( n = 12 per group). E Percentage decrease in media glucose concentration was greater in shPISD treated cells, indicating an increase in glucose uptake ( n = 6 per group). F 1- 14 C 2-deoxy-d-glucose uptake was greater in shPISD treated cells ( n = 12 for shSCR, n = 11 for shPISD). G, H Representative fluorescent images illustrating greater glucose uptake in shPISD treated cells ( G ) and quantification of fluorescent intensity of images presented in G ( n = 25 per group) ( H ). I, J Western blot images illustrating shPISD treated cells have increased GLUT 1 protein abundance, while other markers of glucose metabolism were unaltered ( I ) and densitometry quantification of Western blot images presented in I ( n = 6 per group) ( J ). K Heatmap of carbohydrate related metabolites that were significantly different between shSCR and shPISD treated cells ( n = 3 per group). L Number of metabolites in each KEGG classification that were significantly different between shSCR and shPISD treated cells. M Percentage of significantly different metabolites within each class. N Heatmap of significantly different glycerophospholipids between shSCR and shPISD treated cells ( n = 3 per group). The data are presented as means ± S.D.

Journal: Oncogenesis

Article Title: Targeting mitochondrial phosphatidylethanolamine alters mitochondrial metabolism and proliferation in hepatocellular carcinoma

doi: 10.1038/s41389-025-00593-y

Figure Lengend Snippet: A Extracellular acidification rates (ECAR) during a Seahorse mitochondrial stress test were elevated in shPISD treated cells after the injection of glucose and oligomycin into the media ( n = 10 per group). B Percentage change in media lactate over a 24-h period revealed shPISD treated cells generate more lactate ( n = 6 per group). C 1- 14 C glucose oxidation was reduced in shPISD treated cells ( n = 12 per group). D 6- 14 C glucose oxidation was reduced in shPISD treated cells ( n = 12 per group). E Percentage decrease in media glucose concentration was greater in shPISD treated cells, indicating an increase in glucose uptake ( n = 6 per group). F 1- 14 C 2-deoxy-d-glucose uptake was greater in shPISD treated cells ( n = 12 for shSCR, n = 11 for shPISD). G, H Representative fluorescent images illustrating greater glucose uptake in shPISD treated cells ( G ) and quantification of fluorescent intensity of images presented in G ( n = 25 per group) ( H ). I, J Western blot images illustrating shPISD treated cells have increased GLUT 1 protein abundance, while other markers of glucose metabolism were unaltered ( I ) and densitometry quantification of Western blot images presented in I ( n = 6 per group) ( J ). K Heatmap of carbohydrate related metabolites that were significantly different between shSCR and shPISD treated cells ( n = 3 per group). L Number of metabolites in each KEGG classification that were significantly different between shSCR and shPISD treated cells. M Percentage of significantly different metabolites within each class. N Heatmap of significantly different glycerophospholipids between shSCR and shPISD treated cells ( n = 3 per group). The data are presented as means ± S.D.

Techniques: Injection, Concentration Assay, Western Blot, Quantitative Proteomics

A Representative images of MitoSOX staining illustrating greater mitochondrial superoxide content in shPISD treated cells. B Quantification of MitoSOX fluorescent intensity from images presented in A ( n = 30 per group). C Relative abundance (measured using metabolomics) of reduced glutathione (GSH) and glutathione disulfide (GSSG) in shSCR and shPISD treated cells ( n = 3 per group). D The relative protein abundance of superoxide dismutase 2 (SOD2) was reduced in shPISD treated cells ( n = 6 per group). E Western blot image of SOD2 protein abundance. F Western blot image showing protein abundances of markers of mitochondrial fission (DRP, MFF), fusion (OPA1, MFN1, MFN2), or mitophagy (Parkin) ( n = 3 per group). G Densitometry quantification of images shown in F ( n = 3 per group). H , I Representative fluorescent images of MitoTracker and LysoTracker colocalization. The white arrows are pointing to extracellular mitochondria stained green with MitoTracker. J Greater Manders colocalization coefficient of MitoTracker and LysoTracker indicates more mitophagy in shPISD treated cells ( n = 5 per group). K Number of extracellular mitochondria puncta was greater around shPISD treated cells ( n = 3 per group). The data are presented as means ± S.D.

Journal: Oncogenesis

Article Title: Targeting mitochondrial phosphatidylethanolamine alters mitochondrial metabolism and proliferation in hepatocellular carcinoma

doi: 10.1038/s41389-025-00593-y

Figure Lengend Snippet: A Representative images of MitoSOX staining illustrating greater mitochondrial superoxide content in shPISD treated cells. B Quantification of MitoSOX fluorescent intensity from images presented in A ( n = 30 per group). C Relative abundance (measured using metabolomics) of reduced glutathione (GSH) and glutathione disulfide (GSSG) in shSCR and shPISD treated cells ( n = 3 per group). D The relative protein abundance of superoxide dismutase 2 (SOD2) was reduced in shPISD treated cells ( n = 6 per group). E Western blot image of SOD2 protein abundance. F Western blot image showing protein abundances of markers of mitochondrial fission (DRP, MFF), fusion (OPA1, MFN1, MFN2), or mitophagy (Parkin) ( n = 3 per group). G Densitometry quantification of images shown in F ( n = 3 per group). H , I Representative fluorescent images of MitoTracker and LysoTracker colocalization. The white arrows are pointing to extracellular mitochondria stained green with MitoTracker. J Greater Manders colocalization coefficient of MitoTracker and LysoTracker indicates more mitophagy in shPISD treated cells ( n = 5 per group). K Number of extracellular mitochondria puncta was greater around shPISD treated cells ( n = 3 per group). The data are presented as means ± S.D.

Techniques: Staining, Quantitative Proteomics, Western Blot

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mitochondrial fission inhibitor mdivi 1 (MedChemExpress)

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