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Bio-Rad rat anti mouse monoclonal f4 80
Rat Anti Mouse Monoclonal F4 80, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 96/100, based on 5700 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse/Rat+anti+Mouse+F4%2F80/10__22203_slash_ecm__v033a11-129-8-16
Average 96 stars, based on 5700 article reviews

rat anti mouse monoclonal f4 80 - by Bioz Stars, 2026-11

96/100 stars

Images

other:

Article Title: Lithium mitigates hippocampal tau pathology in a rodent model of traumatic brain injury
Article Snippet: Vinculin , Mouse , , 1:3000 , Bio-Rad (#MCA465GA).

Article Title: Sympathetic Chain Ganglia in the Female Pig During Prenatal Development: Noradrenergic and Cholinergic Neurons
Article Snippet: Protein gene Product 9.5 , monoclonal , mouse , 1:400 , Biorad (Hercules, CA, USA) , 7863-2004.

Article Title: Tonsil-derived mesenchymal stem cells alleviate skin inflammation by modulating neutrophil extracellular trap formation and T cell migration
Article Snippet: Mouse IgG (H + L) , Mouse , 1706516 , Horseradish Peroxidase , goat , polyclonal , 1:3000 , Bio-Rad.

Transcranial Magnetic Stimulation:

Article Title: Adipocyte Leptin Signaling Regulates Glycemia and Cardiovascular Function via Enhancing Brown Adipose Tissue Thermogenesis in Obese Male Mice
Article Snippet: Immunoblots were probed with antibodies for CD31 (Abcam, ab124432, 1:500), UCP1 (Abcam, ab23841, 1:1000), Anti-β-Actin-Peroxidase antibody (Sigma-Aldrich, A3854, 1:1000), HSL (Cell Signaling, #4107, 1:1000), phospho-HSL (Ser563, Cell Signaling, #4139, 1:1000), ATGL (30A4 ,Cell Signaling, #2439, 1:1000), phospho-ATGL (S406, Abcam, ab317610, 1:1000), TOM20 (Cell Signaling, #42406, 1:1000), LEPR (Abcam, ab104403, 1:1000), vinculin (Cell Signaling, #13901, 1:1000), AKT (Cell Signaling, #9272, 1:1000), and pAKT (Thr308, Cell Signaling, #9275, 1:1000) used with 1% bovine serum albumin (BSA, Millipore Sigma) and TRIS-buffered saline (TBS, 10x) pH 7.4 with MilliQ and 0.05% of tween-20 (Fisher BioReagents) for 1 hour at room temperature. .. Mouse (goat anti-mouse IgG-HRP, Bio-Rad #1706516, 1:1000) and rabbit (goat anti-rabbit IgG-HRP, Bio-Rad #1705046, 1:5000) secondary antibodies diluted by 1% BSA TBS-T were employed. .. Membranes were revealed using the ChemiDoc Imaging System (Bio-Rad) Version 3.0.1.14.

Incubation:

Article Title: Generation of an Induced Pluripotent Stem Cell‐Derived Alveolar Type II In Vitro Model to Study Influenza A Virus Infection and Drug Treatments
Article Snippet: .. Incubation with primary antibodies diluted in BSA (3% in PBS) was done at 4°C overnight: mouse‐anti‐NP (1:300; BioRad, MCA400) and rabbit‐anti‐E‐Cad (1:150; Cell Signaling Technology, #3195). .. Cells were permeabilized with triton X‐100 (0.25%; Sigma‐Aldrich, X100‐100ML) for 30 min at RT.

Bioprocessing:

Article Title: Leveraging Electron Beam-Inactivated Multi-Strain Staphylococcus Vaccine for Preventing BCO Lameness in Broiler Chickens
Article Snippet: .. Three combinations of mouse-anti-chicken monoclonal antibodies were used: (1) FITC-CD41/61 (Biorad, Hercules, CA, USA), PE-CD3, and SPRD-CD45 to identify leucocytes (CD45 + CD41/61 − ), T cells (CD45 + CD3 + ), and thrombocytes (CD45 low CD41/61 + ), (2) APC-CD45, FITC-CD4, PE- γδTCR, and SPRD-CD8α to identify T cell subsets, and (3) FITC-KUL01, PE-Bu1, and SPRD-CD45 to identify monocytes (CD45 + KUL01 + Bu-1 − ) and B cells (CD45 + KUL01 − Bu-1 + ), respectively. ..

Plasmid Purification:

Article Title: Loss of oligodendrocyte transcription factor 2 protein expression in metabolically stressed oligodendrocytes
Article Snippet: OLIG2 , Mouse , 1:100 , Tris/EDTA , MABN50 , AB_10807410 , Merck Millipore, USA. .. PLP , Mouse , 1:5000 , None , MCA839G , AB_2237198 , BioRAD, USA. .. Phospho-Histone H2A.X (Ser139) , Rabbit , 1:300 , Tris/EDTA , 9718 , AB_2118009 , Cell signaling, UK.

Image Search Results

USP18 expression is induced by cardiac I/R injury. a Gene Ontology (GO) enrichment analysis of the RNA-seq data in I/R and control hearts at 24 h postsurgery ( n =3). b Heatmap displaying differentially expressed ubiquitination-associated genes in I/R and control hearts at 24 h postsurgery ( n =3). c Protein levels of USP18 in donor heart tissue and patients with ischemic heart disease (IHD) ( n =4). d Immunofluorescence staining of USP18 and α-actin in donor heart tissue and patients with IHD ( n =3). Scale bar=35 μm (left) and 50 μm (right). e Protein levels of USP18 in heart tissue post-IR ( n =4). f Immunofluorescence staining of USP18 and WGA in heart tissue 24 h after I/R injury ( n =5). Scale bar=50 μm. g Protein expression of USP18 in primary neonatal rat cardiomyocytes (NRVMs) after H/R challenge ( n =4). h Immunofluorescence staining of USP18 in cardiomyocytes after H/R challenge. Scale bar=50 μm. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WGA. Wheat germ agglutinin; DAPI. 4′,6-diamidino-2-phenylindole; H/R. Hypoxia/reoxygenation; RNA-seq. RNA sequencing; MAPK. Mitogen-activated protein kinase; GABA. γ-aminobutyric acid.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 expression is induced by cardiac I/R injury. a Gene Ontology (GO) enrichment analysis of the RNA-seq data in I/R and control hearts at 24 h postsurgery ( n =3). b Heatmap displaying differentially expressed ubiquitination-associated genes in I/R and control hearts at 24 h postsurgery ( n =3). c Protein levels of USP18 in donor heart tissue and patients with ischemic heart disease (IHD) ( n =4). d Immunofluorescence staining of USP18 and α-actin in donor heart tissue and patients with IHD ( n =3). Scale bar=35 μm (left) and 50 μm (right). e Protein levels of USP18 in heart tissue post-IR ( n =4). f Immunofluorescence staining of USP18 and WGA in heart tissue 24 h after I/R injury ( n =5). Scale bar=50 μm. g Protein expression of USP18 in primary neonatal rat cardiomyocytes (NRVMs) after H/R challenge ( n =4). h Immunofluorescence staining of USP18 in cardiomyocytes after H/R challenge. Scale bar=50 μm. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WGA. Wheat germ agglutinin; DAPI. 4′,6-diamidino-2-phenylindole; H/R. Hypoxia/reoxygenation; RNA-seq. RNA sequencing; MAPK. Mitogen-activated protein kinase; GABA. γ-aminobutyric acid.

Article Snippet: To establish a cardiac-specific USP18 knockout mice model (USP18-cKO), USP18 flox/flox mice (C57BL/6 J; Shanghai Model Organisms, NM-cKO-215042) were bred with α-MHC-MerCreMer mice (C57BL/6 J; Jackson Laboratory, stock No. 024992).

Techniques: Expressing, RNA Sequencing, Control, Ubiquitin Proteomics, Immunofluorescence, Staining

$USP18 deficiency mitigates mitochondrial dysfunction, acute cardiac I/R injury, and cardiac remodeling in vivo. a 2,3,5-triphenyltetrazolium chloride (TTC) staining of heart tissue 24 h post-I/R in WT and I/R groups ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA ( n =6) and mitochondrial complexes I and II–III activity ( n =5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001. c Representative electron micros c opy images of heart sections 24 h post-I/R; quantitative analysis of the mitochondrial volume density and percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss ⁎⁎⁎ P <0.001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001, ns non-significant. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricle (LV) fibrotic area in WT mice and USP18-cKO mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎ P <0.01. f Representative B-mode and M-mode echocardiographic images of LV from WT mice or USP18-cKO mice 4 weeks after I/R injury. g Cardiac function of WT mice and USP18-cKO mice after I/R injury at the indicated time points ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . WT, ns non-significant. USP18 . Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; USP18-cKO. Ubiquitin-specific protease 18 conditional knockout; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.$

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 deficiency mitigates mitochondrial dysfunction, acute cardiac I/R injury, and cardiac remodeling in vivo. a 2,3,5-triphenyltetrazolium chloride (TTC) staining of heart tissue 24 h post-I/R in WT and I/R groups ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA ( n =6) and mitochondrial complexes I and II–III activity ( n =5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001. c Representative electron micros c opy images of heart sections 24 h post-I/R; quantitative analysis of the mitochondrial volume density and percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss ⁎⁎⁎ P <0.001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎⁎ P <0.01, ⁎⁎⁎⁎ P <0.0001, ns non-significant. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricle (LV) fibrotic area in WT mice and USP18-cKO mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎ P <0.01. f Representative B-mode and M-mode echocardiographic images of LV from WT mice or USP18-cKO mice 4 weeks after I/R injury. g Cardiac function of WT mice and USP18-cKO mice after I/R injury at the indicated time points ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . WT, ns non-significant. USP18 . Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; USP18-cKO. Ubiquitin-specific protease 18 conditional knockout; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.

Techniques: In Vivo, Staining, Activity Assay, Ubiquitin Proteomics, Knock-Out

$Overexpression of USP18 in the heart exacerbates mitochondrial dysfunction, acute cardiac injury, and cardiac remodeling following I/R in mice. a TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA levels ( n= 6) and mitochondrial complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. c Representative electron microscopy images of heart sections 24 h post-I/R. Quantitative analysis of mitochondrial volume density and the percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss. ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎ P <0.05, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricl e (LV) fibrotic area in AAV9-USP18-transfected mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. f Representative B-mode and M-mode echocardiographic images of LV from AAV9-USP18-transfected mice 4 weeks after I/R injury. g Cardiac function of AAV9-USP18-transfected mice after I/R injury at the indicated time points ( n= 6). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . AAV9-NC, ns non-significant. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.$

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Overexpression of USP18 in the heart exacerbates mitochondrial dysfunction, acute cardiac injury, and cardiac remodeling following I/R in mice. a TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. ⁎⁎⁎ P <0.001. b Mitochondrial DNA levels ( n= 6) and mitochondrial complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. c Representative electron microscopy images of heart sections 24 h post-I/R. Quantitative analysis of mitochondrial volume density and the percent of mitochondria with cristae loss in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). Red arrows indicate mitochondria with cristae loss. ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. d Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). ⁎ P <0.05, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. e H&E staining, PSR staining, and quantitative statistical analysis of cell size and left ventricl e (LV) fibrotic area in AAV9-USP18-transfected mice at 4 weeks after I/R injury ( n= 5). Scale bar=1 mm (left), 50 μm (middle), and 100 μm (right). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. f Representative B-mode and M-mode echocardiographic images of LV from AAV9-USP18-transfected mice 4 weeks after I/R injury. g Cardiac function of AAV9-USP18-transfected mice after I/R injury at the indicated time points ( n= 6). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001 vs . AAV9-NC, ns non-significant. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening.

Techniques: Over Expression, Staining, Activity Assay, Electron Microscopy, Transfection, Ubiquitin Proteomics, Negative Control, Virus

Effects of USP18 on H/R-induced injury to NRVMs. a-d NRVMs were transfected with USP18 siRNA and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( a and b ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( c and d ). e-h NRVMs were infected with Ad-USP18 and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( e and f ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( g and h ). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. US P 18. Ubiquitin-specific protease 18; H/R. Hypoxia/reoxygenation; NC. Negative control; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; NRVMs. Neonatal rat ventricular cardiomyocytes; ATP. Adenosine triphosphate; OCR. Oxygen consumption rate.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Effects of USP18 on H/R-induced injury to NRVMs. a-d NRVMs were transfected with USP18 siRNA and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( a and b ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( c and d ). e-h NRVMs were infected with Ad-USP18 and exposed to H/R. Scale bar=26 μm (top) and 50 μm (bottom). Representative confocal microscopy images showing mitochondrial morphology probed with MitoTracker Red ( n= 6) and quantification of mitochondrial length, mitochondrial fragmentation, and mitochondrial DNA levels ( n= 6) ( e and f ). Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in NRVMs in the indicated groups ( n= 4) ( g and h ). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. US P 18. Ubiquitin-specific protease 18; H/R. Hypoxia/reoxygenation; NC. Negative control; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; NRVMs. Neonatal rat ventricular cardiomyocytes; ATP. Adenosine triphosphate; OCR. Oxygen consumption rate.

Techniques: Transfection, Confocal Microscopy, Infection, Ubiquitin Proteomics, Negative Control

USP18 aggravates cardiac I/R injury through regulation of mitochondria and inhibition of mitophagy. a Electron microscopy image showing mitophagy in USP18-cKO mouse hearts ( n= 5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. b Protein levels of PINK1, Parkin, ubiquitinated proteins (Ub), P62, and LC3II in mitochondria from heart tissue in USP18-cKO and WT mice 24 h after I/R injury ( n =4). c Electron microscopy image showing mitophagy in USP18-overexpres (OV) mouse hearts ( n =5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. d Protein levels of PINK1, Parkin, Ub, P62, and LC3II proteins in mitochondria from the heart tissue of USP18-OV mice 24 h after I/R injury ( n =4). Color shift in mitophagy dye (red) and lysosomal dye (green) in NRVMs showing mitophagy in NRVMs with USP18 siRNA transfection ( e ) or Ad-USP18 infection ( f ) and the quantitative mitophagy index in each group ( n= 5). Scale bar=9 μm. Protein levels of PINK1, Parkin, Ub, P62, and LC3II in mitochondria from NRVMs transfected with USP18 siRNA ( g ) or infected with Ad-USP18 ( h ). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001 ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; KO. Knockout; P62. Sequestosome 1; LC3. Microtubule-associated protein 1 light chain 3; VDAC. Voltage-dependent anion channel.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 aggravates cardiac I/R injury through regulation of mitochondria and inhibition of mitophagy. a Electron microscopy image showing mitophagy in USP18-cKO mouse hearts ( n= 5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. b Protein levels of PINK1, Parkin, ubiquitinated proteins (Ub), P62, and LC3II in mitochondria from heart tissue in USP18-cKO and WT mice 24 h after I/R injury ( n =4). c Electron microscopy image showing mitophagy in USP18-overexpres (OV) mouse hearts ( n =5). Scale bar=3 μm. White arrowheads indicate sites of mitophagy. d Protein levels of PINK1, Parkin, Ub, P62, and LC3II proteins in mitochondria from the heart tissue of USP18-OV mice 24 h after I/R injury ( n =4). Color shift in mitophagy dye (red) and lysosomal dye (green) in NRVMs showing mitophagy in NRVMs with USP18 siRNA transfection ( e ) or Ad-USP18 infection ( f ) and the quantitative mitophagy index in each group ( n= 5). Scale bar=9 μm. Protein levels of PINK1, Parkin, Ub, P62, and LC3II in mitochondria from NRVMs transfected with USP18 siRNA ( g ) or infected with Ad-USP18 ( h ). ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001 ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; WT. Wild-type; KO. Knockout; P62. Sequestosome 1; LC3. Microtubule-associated protein 1 light chain 3; VDAC. Voltage-dependent anion channel.

Techniques: Inhibition, Electron Microscopy, Transfection, Infection, Ubiquitin Proteomics, Knock-Out

$Parkin knockdown counteracts the protection of USP18 deficiency in vivo. USP18-cKO mice were infected with AAV9-shParkin and subjected to I/R surgery. a Parkin protein levels in mouse hearts infected with AAV9-shParkin ( n= 4). b TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. c Serum levels of cTnI, CK-MB, and LDH in AAV9-shParkin-infected mice 4 h after I/R surgery ( n= 5). d DNA fragmentation and cleaved caspase-3 activity in heart tissue from AAV9-shParkin-infected mice 24 h after I/R injury ( n= 6). e Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). f Mitochondrial DNA ( n= 6) and complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. g Representative electron microscopy images of heart sections 24 h post-I/R. The mitochondrial volume density and percent of mitochondria with cristae loss were measured in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). h Protein levels of P62, ubiquitinated proteins (Ub), and LC3II in mitochondria from heart tissue 24 h after I/R injury ( n= 4). i H&E staining and quantitative statistical analysis of cell size ( n= 5) in USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. Scale bar=1 μm (top) and 50 μm (bottom). j Heart weight-to-tibia length ratio (HW/TL) ( n= 6) in each group. k Representative B-mode and M-mode echocardiographic images of the left ventricle from USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. l Cardiac function of USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; cTnI. Cardiac Troponin I; CK-MB. Creatine kinase-MB isoenzyme; LDH. Lactate dehydrogenase; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening; HR. Heart rate.$

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Parkin knockdown counteracts the protection of USP18 deficiency in vivo. USP18-cKO mice were infected with AAV9-shParkin and subjected to I/R surgery. a Parkin protein levels in mouse hearts infected with AAV9-shParkin ( n= 4). b TTC staining of heart tissue 24 h post-I/R in each group ( n= 5). Scale bar=0.5 cm. c Serum levels of cTnI, CK-MB, and LDH in AAV9-shParkin-infected mice 4 h after I/R surgery ( n= 5). d DNA fragmentation and cleaved caspase-3 activity in heart tissue from AAV9-shParkin-infected mice 24 h after I/R injury ( n= 6). e Oxygen consumption rate (OCR) and quantitative statistical analysis of basal respiration, ATP-related respiration, maximal respiration, and spare respiratory capacity in mitochondria in the indicated groups ( n= 4). f Mitochondrial DNA ( n= 6) and complexes I and II–III activity ( n= 5) 24 h post-I/R in each group. g Representative electron microscopy images of heart sections 24 h post-I/R. The mitochondrial volume density and percent of mitochondria with cristae loss were measured in each group ( n= 5). Scale bar=10 μm (top) and 6 μm (bottom). h Protein levels of P62, ubiquitinated proteins (Ub), and LC3II in mitochondria from heart tissue 24 h after I/R injury ( n= 4). i H&E staining and quantitative statistical analysis of cell size ( n= 5) in USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. Scale bar=1 μm (top) and 50 μm (bottom). j Heart weight-to-tibia length ratio (HW/TL) ( n= 6) in each group. k Representative B-mode and M-mode echocardiographic images of the left ventricle from USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury. l Cardiac function of USP18-cKO mice and AAV9-shParkin-infected mice 4 weeks after I/R injury ( n= 6). ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; cTnI. Cardiac Troponin I; CK-MB. Creatine kinase-MB isoenzyme; LDH. Lactate dehydrogenase; NC. Negative control; AAV9. Adeno-associated virus serotype 9; AAV9-USP18. Adeno-associated virus serotype 9 encoding USP18; TTC. 2,3,5-triphenyltetrazolium chloride; ATP. Adenosine triphosphate; H&E. Hematoxylin and eosin; PSR. Picrosirius red; FCCP. Carbonyl cyanide p-trifluoromethoxyphenylhydrazone; LVIDd. Left ventricle internal diameter at diastole; LVISd. Left ventricle internal diameter at systole; LVEF. Left ventricle ejection fraction; LVFS. Left ventricle fractional shortening; HR. Heart rate.

Techniques: Knockdown, In Vivo, Infection, Staining, Activity Assay, Electron Microscopy, Ubiquitin Proteomics, Negative Control, Virus

USP18 inhibits mitophagy degradation and facilitates cardiac I/R injury through deubiquitinating and upregulating PTEN-L. a The protein levels of PTEN-L and PTEN in USP18-cKO mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎⁎ P <0.0001, ns non-significant. b The protein levels of PTEN-L and PTEN in AAV9-USP18-infected mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. c Co-IP of USP18 and PTEN-L in NRVMs (left); NRVMs were transfected with HA-PTEN-L and Flag-USP18 (middle); Co-IP of Flag-USP18 and HA-PTEN-L in NRVMs (right). d Endogenous Co-IP of USP18 and PTEN-L in NRVMs subjected to H/R injury. e Endogenous Co-IP of USP18 and PTEN-L in hearts subjected to I/R injury. f PTEN-L ubiquitination (Ub) levels assessed by CO-IP in NRVMs subjected to H/R injury (top) and hearts subjected to I/R injury (bottom). g NRVMs were transfected with Ad-USP18 or USP18 siRNA or HA-PTEN-L and Myc-Ub and treated with MG132. Co-IP of Myc-Ub and HA-PTEN-L. h Schematic representations of t h e domains of PTEN-L involved in binding to USP18. Full-length PTEN-L or truncated PTEN-L was coexpressed with USP18 in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. i Schematic representations of USP18 residues involved in binding to PTEN-L. Full-length USP18 or USP18 truncations were coexpressed with PTEN-L in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. j Ub assay of PTEN-L in HEK293T cells cotransfected with Myc-USP18, Myc-USP18-mut, and Flag-PTEN-L and treated with 10 μmol/L MG132. k, l NRVMs were transfected with scRNA or USP18 siRNA ( k ), infected with Ad-NC or Ad-USP18 ( l ), and then treated with cycloheximide (CHX, 10 μmol/L) for the indicated time periods. Representative immunoblot analysis of PTEN-L protein levels in each group. ⁎⁎⁎⁎ P <0.0001 vs . scRNA or Ad-NC. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; H/R. Hypoxia-reoxygenation; PTEN. Phosphatase and tensin homolog; PTEN-L. Phosphatase and tensin homolog-long; AAV9. Adeno-associated virus serotype 9; NC. Negative control.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: USP18 inhibits mitophagy degradation and facilitates cardiac I/R injury through deubiquitinating and upregulating PTEN-L. a The protein levels of PTEN-L and PTEN in USP18-cKO mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎⁎ P <0.0001, ns non-significant. b The protein levels of PTEN-L and PTEN in AAV9-USP18-infected mouse hearts 24 h after I/R injury ( n= 4). ⁎⁎⁎ P <0.001, ⁎⁎⁎⁎ P <0.0001, ns non-significant. c Co-IP of USP18 and PTEN-L in NRVMs (left); NRVMs were transfected with HA-PTEN-L and Flag-USP18 (middle); Co-IP of Flag-USP18 and HA-PTEN-L in NRVMs (right). d Endogenous Co-IP of USP18 and PTEN-L in NRVMs subjected to H/R injury. e Endogenous Co-IP of USP18 and PTEN-L in hearts subjected to I/R injury. f PTEN-L ubiquitination (Ub) levels assessed by CO-IP in NRVMs subjected to H/R injury (top) and hearts subjected to I/R injury (bottom). g NRVMs were transfected with Ad-USP18 or USP18 siRNA or HA-PTEN-L and Myc-Ub and treated with MG132. Co-IP of Myc-Ub and HA-PTEN-L. h Schematic representations of t h e domains of PTEN-L involved in binding to USP18. Full-length PTEN-L or truncated PTEN-L was coexpressed with USP18 in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. i Schematic representations of USP18 residues involved in binding to PTEN-L. Full-length USP18 or USP18 truncations were coexpressed with PTEN-L in HEK293T cells. Cells were subjected to immunoprecipitation with an anti-Myc antibody or an anti-HA antibody, followed by immunoblotting with the indicated antibodies. j Ub assay of PTEN-L in HEK293T cells cotransfected with Myc-USP18, Myc-USP18-mut, and Flag-PTEN-L and treated with 10 μmol/L MG132. k, l NRVMs were transfected with scRNA or USP18 siRNA ( k ), infected with Ad-NC or Ad-USP18 ( l ), and then treated with cycloheximide (CHX, 10 μmol/L) for the indicated time periods. Representative immunoblot analysis of PTEN-L protein levels in each group. ⁎⁎⁎⁎ P <0.0001 vs . scRNA or Ad-NC. USP18. Ubiquitin-specific protease 18; I/R. Ischemia/reperfusion; H/R. Hypoxia-reoxygenation; PTEN. Phosphatase and tensin homolog; PTEN-L. Phosphatase and tensin homolog-long; AAV9. Adeno-associated virus serotype 9; NC. Negative control.

Techniques: Infection, Co-Immunoprecipitation Assay, Transfection, Ubiquitin Proteomics, Binding Assay, Immunoprecipitation, Western Blot, Virus, Negative Control

Summary of the key findings in this paper. Cardiac I/R injury upregulates USP18 in both mouse and human hearts. USP18 interacts with PTEN-L, inhibiting Parkin phosphorylation and mitochondrial translocation, thereby suppressing mitophagy and exacerbating mitochondrial dysfunction and myocardial injury. PTEN-L additionally promotes cardiac damage via a paracrine mechanism. Genetic or pharmacological targeting of the USP18-PTEN-L axis restores mitophagy and protects against I/R-induced cardiac injury, representing a potential therapeutic strategy. I/R. Ischemia/reperfusion; PTEN-L. Phosphatase and tensin homolog-long; USP18. Ubiquitin-specific protease 18; Ub. Ubiquitination.

Journal: Military Medical Research

Article Title: USP18 exacerbates myocardial I/R injury by inhibiting Parkin mitophagy through the deubiquitinase PTEN-L

doi: 10.1016/j.mmr.2026.100004

Figure Lengend Snippet: Summary of the key findings in this paper. Cardiac I/R injury upregulates USP18 in both mouse and human hearts. USP18 interacts with PTEN-L, inhibiting Parkin phosphorylation and mitochondrial translocation, thereby suppressing mitophagy and exacerbating mitochondrial dysfunction and myocardial injury. PTEN-L additionally promotes cardiac damage via a paracrine mechanism. Genetic or pharmacological targeting of the USP18-PTEN-L axis restores mitophagy and protects against I/R-induced cardiac injury, representing a potential therapeutic strategy. I/R. Ischemia/reperfusion; PTEN-L. Phosphatase and tensin homolog-long; USP18. Ubiquitin-specific protease 18; Ub. Ubiquitination.

Techniques: Phospho-proteomics, Translocation Assay, Ubiquitin Proteomics

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