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Addgene inc pgc1α promoter
Pgc1α Promoter, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgc1%CE%B1+promoter/pm40618856-84-14-16?v=Addgene+inc
Average 93 stars, based on 33 article reviews

pgc1α promoter - by Bioz Stars, 2026-08

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a-b . C57BL/6 WT mice were intravenously injected with AAV-Activin-A low dose and AAV-Activin-A high dose. After 3weeks, the mice were injected intravenously with IB4-A594 and fixable FITC-dextran before harvesting gastrocnemius muscles. a . Representative images of FITC-dextran+ (green) area. b . Intensity of FITC-dextran signal in a (n = 3). Each dot represents one mouse. c-e . The mice were intraperitoneally injected with pimonidazole (100 mg/kg) 1 h before harvesting muscle and the extent of hypoxia in gastrocnemius muscle was determined by the Hypoxyprobe Plus Kit. c . Muscle hypoxia in LLC1-cachexia mice. d . Quantification of surface volume of FITC-pimonidazole in c (n = 3). Each dot represents one mouse. e . Quantification of fluorescence intensity of FITC-pimonidazole in muscles of melanoma cachexia mice (n = 5). Each dot represents one mouse. f . H&E-stained abdominal muscles from control subjects and cancer patients. The yellow boxes were enlarged to show clear vessel structure and the infiltrated immune cells in near blood vessels. R1 and R2 in the upper panel indicate different regions from the same patient muscle. g . Gating strategy for flow cytometry analysis at – . . The proportion (%) of immune cell type relative to total immune cells from control and melanoma 3w mice in the scRNA-Seq data. i . The PGC1α mRNA levels in isolated muscle ECs (n = 4 for control 5 m and n = 6 for KPC 5 m, n = 8 for control and n = 12 for melanoma 3w, n = 3 for control and LLC1 3w). Each dot represents one mouse. j . Expression of PGC1α in control and cancer patient muscle ECs by IF analysis (n = 5). The yellow boxes are enlarged to show the colocalization of CD31 and PGC1α. k-l . HLMVECs were treated with Activin-A (25 ng/mL) for indicated times. k . Immunoblotting to assess phospho-FOXO1/3/4 levels. l . Quantification of p-FOXO1/3/4 immunoblots shown in k (n = 3). Each dot represents one biological replicate. The statistical analysis was performed using a t-test with comparisons versus the 0 min time point. m . HLMVECs were transfected with specific siRNA for control, FOXO-1, −3, or −4. The protein levels of PGC1α, FOXO-1, −3, or −4 were determined by immunoblotting. n . Quantification of PGC1α levels in m (n = 3). Each dot represents one biological replicate. Data are presented as mean ± SEM. Statistical analysis was conducted using an unpaired, two-tailed t-test ( b , d, e, i, l ) or one-way ANOVA with Dunnett’s multiple comparison test ( n ).

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: a-b . C57BL/6 WT mice were intravenously injected with AAV-Activin-A low dose and AAV-Activin-A high dose. After 3weeks, the mice were injected intravenously with IB4-A594 and fixable FITC-dextran before harvesting gastrocnemius muscles. a . Representative images of FITC-dextran+ (green) area. b . Intensity of FITC-dextran signal in a (n = 3). Each dot represents one mouse. c-e . The mice were intraperitoneally injected with pimonidazole (100 mg/kg) 1 h before harvesting muscle and the extent of hypoxia in gastrocnemius muscle was determined by the Hypoxyprobe Plus Kit. c . Muscle hypoxia in LLC1-cachexia mice. d . Quantification of surface volume of FITC-pimonidazole in c (n = 3). Each dot represents one mouse. e . Quantification of fluorescence intensity of FITC-pimonidazole in muscles of melanoma cachexia mice (n = 5). Each dot represents one mouse. f . H&E-stained abdominal muscles from control subjects and cancer patients. The yellow boxes were enlarged to show clear vessel structure and the infiltrated immune cells in near blood vessels. R1 and R2 in the upper panel indicate different regions from the same patient muscle. g . Gating strategy for flow cytometry analysis at – . . The proportion (%) of immune cell type relative to total immune cells from control and melanoma 3w mice in the scRNA-Seq data. i . The PGC1α mRNA levels in isolated muscle ECs (n = 4 for control 5 m and n = 6 for KPC 5 m, n = 8 for control and n = 12 for melanoma 3w, n = 3 for control and LLC1 3w). Each dot represents one mouse. j . Expression of PGC1α in control and cancer patient muscle ECs by IF analysis (n = 5). The yellow boxes are enlarged to show the colocalization of CD31 and PGC1α. k-l . HLMVECs were treated with Activin-A (25 ng/mL) for indicated times. k . Immunoblotting to assess phospho-FOXO1/3/4 levels. l . Quantification of p-FOXO1/3/4 immunoblots shown in k (n = 3). Each dot represents one biological replicate. The statistical analysis was performed using a t-test with comparisons versus the 0 min time point. m . HLMVECs were transfected with specific siRNA for control, FOXO-1, −3, or −4. The protein levels of PGC1α, FOXO-1, −3, or −4 were determined by immunoblotting. n . Quantification of PGC1α levels in m (n = 3). Each dot represents one biological replicate. Data are presented as mean ± SEM. Statistical analysis was conducted using an unpaired, two-tailed t-test ( b , d, e, i, l ) or one-way ANOVA with Dunnett’s multiple comparison test ( n ).

Article Snippet: HLMVECs were transfected with 1 μg of a PGC1α promoter luciferase (Addgene, plasmid 8888) and 35 ng of pRL/TK using PEI transfection reagent.

Techniques: Injection, Muscles, Fluorescence, Staining, Control, Flow Cytometry, Isolation, Expressing, Western Blot, Transfection, Two Tailed Test, Comparison

a , PGC1α protein levels in isolated muscle ECs from control 5-month-old and KPC 5-month-old mice by western blotting. Each lane represents one mouse. b , Quantification of PGC1α in a ( n = 3). Each dot represents one mouse. c , PGC1α mRNA levels in isolated muscle ECs. The mice were evaluated 3 weeks after injecting AAV-control, AAV-activin A low dose or AAV-activin A high dose ( n = 3 for control and n = 5 for AAV-activin A low and high doses). Each dot represents one mouse. d , HLMVECs were transfected with PGC1α promoter luciferase plasmid and Renilla luciferase for 48 h and treated with vehicle (0.1% BSA), TNF (10 ng ml −1 ), activin A (25 ng ml −1 ) or a combination of TNF and activin A for 16 h. The luciferase activity was normalized by Renilla luciferase and is presented as the FC ( n = 11). Each dot represents one independent biological replicate. e – h , HLMVECs were treated with lentiviral shRNA for control and PGC1α for 72 h. e , The apoptotic cells (annexin V–FITC + PI + ) were evaluated by FACS analysis ( n = 6). Each dot represents one independent biological replicate. f , Levels of EndMT marker genes, Cdh5 and Vimentin , by RT–qPCR ( n = 8). Each dot represents one independent biological replicate. g , EC barrier integrity by IF staining with VE-cadherin antibody. Nuclei were stained with DAPI. h , Quantification of the area of VE-cadherin in g ( n = 4). Each dot represents one independent biological replicate. i , j , Muscle vascular barrier integrity of controls and participants with cancer by IF staining with VE-cadherin antibody. i , Representative VE-cadherin images. j , The surface volume of VE-cadherin ( n = 5). Each dot represents one participant. k , Levels of inflammatory genes by RT–qPCR ( n = 4). Each dot represents one independent biological replicate. l , ChIP analysis in control and activin A-treated ECs with PGC1α-specific antibody. Normal mouse IgG antibody was used as a negative control. The enrichment values were normalized with input values and are presented as the FC ( n = 4 for control cells for IgG IP, n = 6 for control cells for anti-PGC1α IP and n = 4 for activin A-treated cells for anti-PGC1α IP). Each dot represents one independent biological replicate. Data are presented as the mean ± s.e.m. Statistical analysis was conducted using either an unpaired two-tailed t-test ( b , e , f , h , j and k ) or a one-way ANOVA with Tukey’s multiple-comparison test ( c , d and l ).

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: a , PGC1α protein levels in isolated muscle ECs from control 5-month-old and KPC 5-month-old mice by western blotting. Each lane represents one mouse. b , Quantification of PGC1α in a ( n = 3). Each dot represents one mouse. c , PGC1α mRNA levels in isolated muscle ECs. The mice were evaluated 3 weeks after injecting AAV-control, AAV-activin A low dose or AAV-activin A high dose ( n = 3 for control and n = 5 for AAV-activin A low and high doses). Each dot represents one mouse. d , HLMVECs were transfected with PGC1α promoter luciferase plasmid and Renilla luciferase for 48 h and treated with vehicle (0.1% BSA), TNF (10 ng ml −1 ), activin A (25 ng ml −1 ) or a combination of TNF and activin A for 16 h. The luciferase activity was normalized by Renilla luciferase and is presented as the FC ( n = 11). Each dot represents one independent biological replicate. e – h , HLMVECs were treated with lentiviral shRNA for control and PGC1α for 72 h. e , The apoptotic cells (annexin V–FITC + PI + ) were evaluated by FACS analysis ( n = 6). Each dot represents one independent biological replicate. f , Levels of EndMT marker genes, Cdh5 and Vimentin , by RT–qPCR ( n = 8). Each dot represents one independent biological replicate. g , EC barrier integrity by IF staining with VE-cadherin antibody. Nuclei were stained with DAPI. h , Quantification of the area of VE-cadherin in g ( n = 4). Each dot represents one independent biological replicate. i , j , Muscle vascular barrier integrity of controls and participants with cancer by IF staining with VE-cadherin antibody. i , Representative VE-cadherin images. j , The surface volume of VE-cadherin ( n = 5). Each dot represents one participant. k , Levels of inflammatory genes by RT–qPCR ( n = 4). Each dot represents one independent biological replicate. l , ChIP analysis in control and activin A-treated ECs with PGC1α-specific antibody. Normal mouse IgG antibody was used as a negative control. The enrichment values were normalized with input values and are presented as the FC ( n = 4 for control cells for IgG IP, n = 6 for control cells for anti-PGC1α IP and n = 4 for activin A-treated cells for anti-PGC1α IP). Each dot represents one independent biological replicate. Data are presented as the mean ± s.e.m. Statistical analysis was conducted using either an unpaired two-tailed t-test ( b , e , f , h , j and k ) or a one-way ANOVA with Tukey’s multiple-comparison test ( c , d and l ).

Article Snippet: HLMVECs were transfected with 1 μg of a PGC1α promoter luciferase (Addgene, plasmid 8888) and 35 ng of pRL/TK using PEI transfection reagent.

Techniques: Isolation, Control, Western Blot, Transfection, Luciferase, Plasmid Preparation, Activity Assay, shRNA, Marker, Quantitative RT-PCR, Staining, Negative Control, Two Tailed Test, Comparison

a-e . HLMVECs were transfected with lentiviral shRNA for PGC1α without or with GFP-PGC1α plasmid. a . Representative flow plots of apoptotic cells. b . PGC1α expression levels by IF analysis (n = 3). The red and green colors represent the endogenous PGC1α (red) and exogenous GFP-PGC1α (green), respectively. c . Apoptotic genes (n = 7 for Bcl2 , n = 4 for Mcl1 , n = 3 for Bcl-XL, Bim and Bad, Bax: n = 3 for shControl and shPGC1α, n = 4 for shPGC1α + PGC1α-GFP). Each dot represents one biological replicate. d . The protein levels of VE-cadherin. e . Quantification of VE-cadherin in d (n = 4). Each dot represents one biological replicate. f-h . Abdominal muscles from control subjects and cancer patients. f . Representative images for either CD31+ or VE-cadherin+ ECs by IF analysis. g . Quantification of either CD31+ or VE-cadherin+ ECs in f (n = 3). Each dot represents one patient. h . Percent of VE-cadherin+ ECs to CD31+ ECs (n = 3). Each dot represents one patient. i . VE-cadherin protein levels in TA muscles from control and LLC1-cachexia mice (n = 3). Each lane represents one mouse. j . Quantification of the levels of VE-cadherin in i (n = 6). Each dot represents one mouse. k . PGC1α and Cdh5 mRNA levels in PGC1α depleted HLMVECs with or without GFP-PGC1α overexpression (n = 4). Each dot represents one biological replicate. l-n . Characterization of melanoma 3w-bearing EC WT and ECΔ PGC1α mice. l . Body weight (n = 7). Each dot represents one mouse. m . Grip strength (n = 7). Each dot represents one mouse. n . Muscle weight (n = 7). Each dot represents one mouse. Data are presented as mean ± SEM. Each gene level was evaluated by RTqPCR, normalized by 18 s levels and presented as fold change. Statistical analysis was conducted using unpaired two-tailed t-test ( e, h , j, l-n ), or one-way ANOVA with Tukey’s multiple comparison test ( c , g, k ).

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: a-e . HLMVECs were transfected with lentiviral shRNA for PGC1α without or with GFP-PGC1α plasmid. a . Representative flow plots of apoptotic cells. b . PGC1α expression levels by IF analysis (n = 3). The red and green colors represent the endogenous PGC1α (red) and exogenous GFP-PGC1α (green), respectively. c . Apoptotic genes (n = 7 for Bcl2 , n = 4 for Mcl1 , n = 3 for Bcl-XL, Bim and Bad, Bax: n = 3 for shControl and shPGC1α, n = 4 for shPGC1α + PGC1α-GFP). Each dot represents one biological replicate. d . The protein levels of VE-cadherin. e . Quantification of VE-cadherin in d (n = 4). Each dot represents one biological replicate. f-h . Abdominal muscles from control subjects and cancer patients. f . Representative images for either CD31+ or VE-cadherin+ ECs by IF analysis. g . Quantification of either CD31+ or VE-cadherin+ ECs in f (n = 3). Each dot represents one patient. h . Percent of VE-cadherin+ ECs to CD31+ ECs (n = 3). Each dot represents one patient. i . VE-cadherin protein levels in TA muscles from control and LLC1-cachexia mice (n = 3). Each lane represents one mouse. j . Quantification of the levels of VE-cadherin in i (n = 6). Each dot represents one mouse. k . PGC1α and Cdh5 mRNA levels in PGC1α depleted HLMVECs with or without GFP-PGC1α overexpression (n = 4). Each dot represents one biological replicate. l-n . Characterization of melanoma 3w-bearing EC WT and ECΔ PGC1α mice. l . Body weight (n = 7). Each dot represents one mouse. m . Grip strength (n = 7). Each dot represents one mouse. n . Muscle weight (n = 7). Each dot represents one mouse. Data are presented as mean ± SEM. Each gene level was evaluated by RTqPCR, normalized by 18 s levels and presented as fold change. Statistical analysis was conducted using unpaired two-tailed t-test ( e, h , j, l-n ), or one-way ANOVA with Tukey’s multiple comparison test ( c , g, k ).

Article Snippet: HLMVECs were transfected with 1 μg of a PGC1α promoter luciferase (Addgene, plasmid 8888) and 35 ng of pRL/TK using PEI transfection reagent.

Techniques: Transfection, shRNA, Plasmid Preparation, Expressing, Muscles, Control, Over Expression, Two Tailed Test, Comparison

a – k , EC WT (EC tdTomato,WT ) and EC ΔPGC1α (EC tdTomato,ΔPGC1α ) mice. a , PGC1α knockdown efficiency in isolated muscle ECs. b , Quantification of PGC1α levels in a ( n = 4). Each dot represents one mouse. c , Body weight ( n = 10). Each dot represents one mouse. d , Grip strength ( n = 10). Each dot represents one mouse. e , Muscle weight ( n = 10). Each dot represents one mouse. f , CSA per single fiber ( n = 5 for EC WT and n = 6 for EC ΔPGC1α ). Each dot represents one mouse. g , Expression of MuRF1 mRNA levels in TA muscles ( n = 12 for EC WT and n = 7 for EC ΔPGC1α ). Each dot represents one mouse. h , Representative 3D images of tdTomato + (pseudocolored yellow) vessels in the GC muscles. i , Quantification of GC muscle vascular density ( n = 6 for EC WT and n = 9 for EC ΔPGC1α ). Each dot represents one mouse. j , Representative images of muscle vascular leakage. k , Quantification of FITC–albumin for muscle vascular leakage in j ( n = 5 for EC WT and n = 3 for EC ΔPGC1α ). Each dot represents one mouse. Data are presented as the mean ± s.e.m. Statistical analysis was conducted using an unpaired two-tailed t -test ( b – g , i and k ).

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: a – k , EC WT (EC tdTomato,WT ) and EC ΔPGC1α (EC tdTomato,ΔPGC1α ) mice. a , PGC1α knockdown efficiency in isolated muscle ECs. b , Quantification of PGC1α levels in a ( n = 4). Each dot represents one mouse. c , Body weight ( n = 10). Each dot represents one mouse. d , Grip strength ( n = 10). Each dot represents one mouse. e , Muscle weight ( n = 10). Each dot represents one mouse. f , CSA per single fiber ( n = 5 for EC WT and n = 6 for EC ΔPGC1α ). Each dot represents one mouse. g , Expression of MuRF1 mRNA levels in TA muscles ( n = 12 for EC WT and n = 7 for EC ΔPGC1α ). Each dot represents one mouse. h , Representative 3D images of tdTomato + (pseudocolored yellow) vessels in the GC muscles. i , Quantification of GC muscle vascular density ( n = 6 for EC WT and n = 9 for EC ΔPGC1α ). Each dot represents one mouse. j , Representative images of muscle vascular leakage. k , Quantification of FITC–albumin for muscle vascular leakage in j ( n = 5 for EC WT and n = 3 for EC ΔPGC1α ). Each dot represents one mouse. Data are presented as the mean ± s.e.m. Statistical analysis was conducted using an unpaired two-tailed t -test ( b – g , i and k ).

Article Snippet: HLMVECs were transfected with 1 μg of a PGC1α promoter luciferase (Addgene, plasmid 8888) and 35 ng of pRL/TK using PEI transfection reagent.

Techniques: Knockdown, Isolation, Expressing, Muscles, Two Tailed Test

a-d . Effect of Activin-A neutralizing antibody. a . Timelines for Activin-A neutralizing antibody treatment. b . Expression of EC marker and anti-apoptotic genes in isolated muscle ECs ( CD31 ; n = 8 for PBS, n = 12 for Melanoma + IgG, n = 8 for Melanoma + α-Activin-A ab, Bcl2; n = 8 for PBS, n = 12 for Melanoma + IgG, n = 8 for Melanoma + α-Activin-A ab, Mcl1; n = 8 for PBS, n = 12 for Melanoma + IgG, n = 8 for Melanoma + α-Activin-A ab). Each dot represents one mouse. c . The tumor growth (n = 4 for PBS, n = 5 for Melanoma + IgG and Melanoma + α-Activin-A ab). Each dot represents one mouse. d . The body weight was presented without (Δ) tumor weight (n = 8 for PBS, n = 4 for Melanoma + IgG, n = 5 for Melanoma + α-Activin-A ab). Each dot represents one mouse. e . Timelines for intramuscular injection of lenti-EC-PGC1α-GFP virus. f-i . Efficiency of local vascular overexpression of EC-PGC1α in muscles. f . All mice were perfused with IB4-A594 before harvesting the muscles, and the endothelial-specific expression of lenti-PGC1α-EGFP virus in muscle was determined by IF analysis for IB4. g . Percentage of GFP+ or IB4+ cells per field in f (n = 4). Each dot represents one mouse. h . Percentage of GFP+ cells in IB4+ cells in f (n = 4). Each dot represents one mouse. i . Expression of PGC1α in isolated muscle ECs (n = 7). j-o . Effect of local vascular overexpression of EC-PGC1α in melanoma bearing mice. j . H&E-stained GC muscles (n = 3). The ‘n’ represents the number of mice. k . Quantification of muscle fiber type 2a Fiber (n = 3). Each dot represents one mouse. l . Body weight was presented without (Δ) tumor weight (n = 4 for control, n = 3 for EC-PGC1α im-OE alone, n = 6 for melanoma alone, n = 7 for melanoma with EC-PGC1α im-OE ). Each dot represents one mouse. m . Melanoma growth (n = 4 for control, n = 3 for EC-PGC1α im-OE alone, n = 6 for melanoma alone, n = 6 for melanoma with EC-PGC1α im-OE ). Each dot represents one mouse. n . Melanoma weight (n = 6). Each dot represents one mouse. o . Adipose tissue weight (n = 4 for control, n = 3 for EC-PGC1α im-OE alone, n = 4 for melanoma alone, n = 4 for melanoma with EC-PGC1α im-OE ). Each dot represents one mouse. p-v . Effect of local overexpression of EC-PGC1α in CT26 bearing mice. p . 3D tissue images with IB4+ (green) functional vessels. q . Quantification of functional muscle vascular density (n = 3). Each dot represents one mouse. r . Muscle weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 5 for CT26 alone, n = 5 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. s . Grip strength (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 5 for CT26 alone, n = 5 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. t . Body weight without (Δ) tumor weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 6 for CT26 alone, n = 6 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. u . CT26 tumor weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 6 for CT26 alone, n = 6 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. v . Adipose tissue weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 7 for CT26 alone for sWAT and vWAT, n = 6 for CT26 alone for BAT, n = 6 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. Data are presented as mean ± SEM. Statistical analysis was conducted using unpaired, two-tailed t-test ( i, n ) or one-way ANOVA with Tukey’s multiple comparison test ( b-d, k, l, m , o, q-v ).

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: a-d . Effect of Activin-A neutralizing antibody. a . Timelines for Activin-A neutralizing antibody treatment. b . Expression of EC marker and anti-apoptotic genes in isolated muscle ECs ( CD31 ; n = 8 for PBS, n = 12 for Melanoma + IgG, n = 8 for Melanoma + α-Activin-A ab, Bcl2; n = 8 for PBS, n = 12 for Melanoma + IgG, n = 8 for Melanoma + α-Activin-A ab, Mcl1; n = 8 for PBS, n = 12 for Melanoma + IgG, n = 8 for Melanoma + α-Activin-A ab). Each dot represents one mouse. c . The tumor growth (n = 4 for PBS, n = 5 for Melanoma + IgG and Melanoma + α-Activin-A ab). Each dot represents one mouse. d . The body weight was presented without (Δ) tumor weight (n = 8 for PBS, n = 4 for Melanoma + IgG, n = 5 for Melanoma + α-Activin-A ab). Each dot represents one mouse. e . Timelines for intramuscular injection of lenti-EC-PGC1α-GFP virus. f-i . Efficiency of local vascular overexpression of EC-PGC1α in muscles. f . All mice were perfused with IB4-A594 before harvesting the muscles, and the endothelial-specific expression of lenti-PGC1α-EGFP virus in muscle was determined by IF analysis for IB4. g . Percentage of GFP+ or IB4+ cells per field in f (n = 4). Each dot represents one mouse. h . Percentage of GFP+ cells in IB4+ cells in f (n = 4). Each dot represents one mouse. i . Expression of PGC1α in isolated muscle ECs (n = 7). j-o . Effect of local vascular overexpression of EC-PGC1α in melanoma bearing mice. j . H&E-stained GC muscles (n = 3). The ‘n’ represents the number of mice. k . Quantification of muscle fiber type 2a Fiber (n = 3). Each dot represents one mouse. l . Body weight was presented without (Δ) tumor weight (n = 4 for control, n = 3 for EC-PGC1α im-OE alone, n = 6 for melanoma alone, n = 7 for melanoma with EC-PGC1α im-OE ). Each dot represents one mouse. m . Melanoma growth (n = 4 for control, n = 3 for EC-PGC1α im-OE alone, n = 6 for melanoma alone, n = 6 for melanoma with EC-PGC1α im-OE ). Each dot represents one mouse. n . Melanoma weight (n = 6). Each dot represents one mouse. o . Adipose tissue weight (n = 4 for control, n = 3 for EC-PGC1α im-OE alone, n = 4 for melanoma alone, n = 4 for melanoma with EC-PGC1α im-OE ). Each dot represents one mouse. p-v . Effect of local overexpression of EC-PGC1α in CT26 bearing mice. p . 3D tissue images with IB4+ (green) functional vessels. q . Quantification of functional muscle vascular density (n = 3). Each dot represents one mouse. r . Muscle weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 5 for CT26 alone, n = 5 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. s . Grip strength (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 5 for CT26 alone, n = 5 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. t . Body weight without (Δ) tumor weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 6 for CT26 alone, n = 6 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. u . CT26 tumor weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 6 for CT26 alone, n = 6 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. v . Adipose tissue weight (n = 4 for control, n = 4 for EC-PGC1α im-OE alone, n = 7 for CT26 alone for sWAT and vWAT, n = 6 for CT26 alone for BAT, n = 6 for CT26 with EC-PGC1α im-OE ). Each dot represents one mouse. Data are presented as mean ± SEM. Statistical analysis was conducted using unpaired, two-tailed t-test ( i, n ) or one-way ANOVA with Tukey’s multiple comparison test ( b-d, k, l, m , o, q-v ).

Article Snippet: HLMVECs were transfected with 1 μg of a PGC1α promoter luciferase (Addgene, plasmid 8888) and 35 ng of pRL/TK using PEI transfection reagent.

Techniques: Expressing, Marker, Isolation, Injection, Virus, Over Expression, Muscles, Staining, Control, Functional Assay, Two Tailed Test, Comparison

a – e , Mice were intravenously injected with anti-activin A neutralizing antibody or IgG1 isotype every 4 days, 1 week after melanoma implantation. a , Muscle vasculature by IF staining with CD31 antibody. Nuclei were stained with DAPI. b . Muscle vasculature density ( n = 3 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody). Each dot represents one mouse. c , Mouse grip strength ( n = 8 for PBS, n = 4 for melanoma + IgG and n = 5 for melanoma + anti-activin A antibody). Each dot represents one mouse. d , Muscle mass for GC ( n = 6 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody) and TA ( n = 8 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody). Each dot represents one mouse. e , Cachectic marker MuRF1 mRNA in TA muscle ( n = 6 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody). Each dot represents one mouse. f – l , After melanoma implantation, the mice were intramuscularly injected with lentiviral control and lenti-EC PGC1α–GFP. f – h , Mice were retro-orbitally injected with IB4–A594 before isolating muscles. f , Representative 3D vasculature after overlaying with CD31 + (red) and IB4 + (pseudocolored green) vessels in GC muscles. g , Quantification of CD31 + (red) muscle vasculature density in f ( n = 3). Each dot represents one mouse. h , Manders’ colocalization coefficients for CD31 and IB4 in f ( n = 3). Each dot represents one mouse. i , Mouse grip strength ( n = 8 for control, n = 3 for EC PGC1α im-OE alone, n = 8 for melanoma alone and n = 7 for melanoma with EC PGC1α im-OE ). Each dot represents one mouse. j , Muscle mass for GC ( n = 9 for control, n = 4 for EC PGC1α im-OE alone, n = 10 for melanoma alone and n = 10 for melanoma with EC PGC1α im-OE ) and TA ( n = 8 for control, n = 4 for EC PGC1α im-OE alone, n = 9 for melanoma alone and n = 9 for melanoma with EC PGC1α im-OE ). Each dot represents one mouse. k , mRNA levels of MuRF1 ( n = 3 for control and n = 5 for melanoma with or without EC PGC1α im-OE ) and Atrogin1 ( n = 6 for control, n = 5 for melanoma without EC PGC1α im-OE and n = 4 for melanoma with EC PGC1α im-OE ) by RT–qPCR. Each dot represents one mouse. l , Inflammatory genes in GC muscles by RT–qPCR ( TNF , n = 4 for control and n = 8 for melanoma with or without EC PGC1α im-OE ; IL1β , n = 8 for control, n = 12 for melanoma without EC PGC1α im-OE and n = 10 for melanoma with EC PGC1α im-OE ). Each dot represents one mouse. m , Graphical summary. All mice were examined 3 weeks after melanoma implantation. Data are presented as the mean ± s.e.m. Each gene level was normalized by PPIA levels and is presented as the FC. Statistical analysis was conducted using a one-way ANOVA with Tukey’s multiple-comparison tests ( b – e and g – l ).

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: a – e , Mice were intravenously injected with anti-activin A neutralizing antibody or IgG1 isotype every 4 days, 1 week after melanoma implantation. a , Muscle vasculature by IF staining with CD31 antibody. Nuclei were stained with DAPI. b . Muscle vasculature density ( n = 3 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody). Each dot represents one mouse. c , Mouse grip strength ( n = 8 for PBS, n = 4 for melanoma + IgG and n = 5 for melanoma + anti-activin A antibody). Each dot represents one mouse. d , Muscle mass for GC ( n = 6 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody) and TA ( n = 8 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody). Each dot represents one mouse. e , Cachectic marker MuRF1 mRNA in TA muscle ( n = 6 for PBS and n = 5 for melanoma + IgG and melanoma + anti-activin A antibody). Each dot represents one mouse. f – l , After melanoma implantation, the mice were intramuscularly injected with lentiviral control and lenti-EC PGC1α–GFP. f – h , Mice were retro-orbitally injected with IB4–A594 before isolating muscles. f , Representative 3D vasculature after overlaying with CD31 + (red) and IB4 + (pseudocolored green) vessels in GC muscles. g , Quantification of CD31 + (red) muscle vasculature density in f ( n = 3). Each dot represents one mouse. h , Manders’ colocalization coefficients for CD31 and IB4 in f ( n = 3). Each dot represents one mouse. i , Mouse grip strength ( n = 8 for control, n = 3 for EC PGC1α im-OE alone, n = 8 for melanoma alone and n = 7 for melanoma with EC PGC1α im-OE ). Each dot represents one mouse. j , Muscle mass for GC ( n = 9 for control, n = 4 for EC PGC1α im-OE alone, n = 10 for melanoma alone and n = 10 for melanoma with EC PGC1α im-OE ) and TA ( n = 8 for control, n = 4 for EC PGC1α im-OE alone, n = 9 for melanoma alone and n = 9 for melanoma with EC PGC1α im-OE ). Each dot represents one mouse. k , mRNA levels of MuRF1 ( n = 3 for control and n = 5 for melanoma with or without EC PGC1α im-OE ) and Atrogin1 ( n = 6 for control, n = 5 for melanoma without EC PGC1α im-OE and n = 4 for melanoma with EC PGC1α im-OE ) by RT–qPCR. Each dot represents one mouse. l , Inflammatory genes in GC muscles by RT–qPCR ( TNF , n = 4 for control and n = 8 for melanoma with or without EC PGC1α im-OE ; IL1β , n = 8 for control, n = 12 for melanoma without EC PGC1α im-OE and n = 10 for melanoma with EC PGC1α im-OE ). Each dot represents one mouse. m , Graphical summary. All mice were examined 3 weeks after melanoma implantation. Data are presented as the mean ± s.e.m. Each gene level was normalized by PPIA levels and is presented as the FC. Statistical analysis was conducted using a one-way ANOVA with Tukey’s multiple-comparison tests ( b – e and g – l ).

Article Snippet: HLMVECs were transfected with 1 μg of a PGC1α promoter luciferase (Addgene, plasmid 8888) and 35 ng of pRL/TK using PEI transfection reagent.

Techniques: Injection, Staining, Marker, Control, Muscles, Quantitative RT-PCR, Comparison

a . Timelines for systemic injection of EC-PGC1α lentivirus. The ‘ sys-OE’ indicates the systematical overexpression. b-i . After tumor implantation, the mice were intravenously injected with lenti-control and lenti-PGC1α-EGFP virus and evaluated 3 weeks later. b . IB4 positive (+) functional vessels in gastrocnemius muscle of control and melanoma 3w mice (n = 4). c . Expression levels of PGC1α in isolated muscle ECs (n = 6). Each dot represents one mouse. d-i . melanoma-bearing mice (n = 4) and CT26-bearing mice (n = 3 for CT26 alone, n = 5 for CT26 with EC-PGC1α sys-OE ). d . Mouse grip strength. e . Tumor growth. f . Body weight without (Δ) tumor weight. g . GC muscle weight. h . TA muscle weight. i . Adipose tissues’ weight. Data are presented as mean ± SEM. Statistical analysis was conducted using an unpaired, two-tailed t-test ( c-i ).

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: a . Timelines for systemic injection of EC-PGC1α lentivirus. The ‘ sys-OE’ indicates the systematical overexpression. b-i . After tumor implantation, the mice were intravenously injected with lenti-control and lenti-PGC1α-EGFP virus and evaluated 3 weeks later. b . IB4 positive (+) functional vessels in gastrocnemius muscle of control and melanoma 3w mice (n = 4). c . Expression levels of PGC1α in isolated muscle ECs (n = 6). Each dot represents one mouse. d-i . melanoma-bearing mice (n = 4) and CT26-bearing mice (n = 3 for CT26 alone, n = 5 for CT26 with EC-PGC1α sys-OE ). d . Mouse grip strength. e . Tumor growth. f . Body weight without (Δ) tumor weight. g . GC muscle weight. h . TA muscle weight. i . Adipose tissues’ weight. Data are presented as mean ± SEM. Statistical analysis was conducted using an unpaired, two-tailed t-test ( c-i ).

Article Snippet: HLMVECs were transfected with 1 μg of a PGC1α promoter luciferase (Addgene, plasmid 8888) and 35 ng of pRL/TK using PEI transfection reagent.

Techniques: Injection, Over Expression, Tumor Implantation, Control, Virus, Functional Assay, Expressing, Isolation, Two Tailed Test

Fig. 6 | Circulating activin A induces vascular dysfunction by suppressing endothelial PGC1α in muscle. a, PGC1α protein levels in isolated muscle ECs from control 5-month-old and KPC 5-month-old mice by western blotting. Each lane represents one mouse. b, Quantification of PGC1α in a (n = 3). Each dot represents one mouse. c, PGC1α mRNA levels in isolated muscle ECs. The mice were evaluated 3 weeks after injecting AAV-control, AAV-activin A low dose or AAV-activin A high dose (n = 3 for control and n = 5 for AAV-activin A low and high doses). Each dot represents one mouse. d, HLMVECs were transfected with PGC1α promoter luciferase plasmid and Renilla luciferase for 48 h and treated with vehicle (0.1% BSA), TNF (10 ng ml−1), activin A (25 ng ml−1) or a combination of TNF and activin A for 16 h. The luciferase activity was normalized by Renilla luciferase and is presented as the FC (n = 11). Each dot represents one independent biological replicate. e–h, HLMVECs were treated with lentiviral shRNA for control and PGC1α for 72 h. e, The apoptotic cells (annexin V–FITC+PI+) were evaluated by FACS analysis (n = 6). Each dot represents one independent biological replicate. f, Levels of EndMT marker genes, Cdh5 and Vimentin, by RT–qPCR

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A-PGC1α axis drives progression of cancer cachexia.

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: Fig. 6 | Circulating activin A induces vascular dysfunction by suppressing endothelial PGC1α in muscle. a, PGC1α protein levels in isolated muscle ECs from control 5-month-old and KPC 5-month-old mice by western blotting. Each lane represents one mouse. b, Quantification of PGC1α in a (n = 3). Each dot represents one mouse. c, PGC1α mRNA levels in isolated muscle ECs. The mice were evaluated 3 weeks after injecting AAV-control, AAV-activin A low dose or AAV-activin A high dose (n = 3 for control and n = 5 for AAV-activin A low and high doses). Each dot represents one mouse. d, HLMVECs were transfected with PGC1α promoter luciferase plasmid and Renilla luciferase for 48 h and treated with vehicle (0.1% BSA), TNF (10 ng ml−1), activin A (25 ng ml−1) or a combination of TNF and activin A for 16 h. The luciferase activity was normalized by Renilla luciferase and is presented as the FC (n = 11). Each dot represents one independent biological replicate. e–h, HLMVECs were treated with lentiviral shRNA for control and PGC1α for 72 h. e, The apoptotic cells (annexin V–FITC+PI+) were evaluated by FACS analysis (n = 6). Each dot represents one independent biological replicate. f, Levels of EndMT marker genes, Cdh5 and Vimentin, by RT–qPCR

Article Snippet: The TRCN0000001166 clone showed the best effect to deplete PGC1α in ECs and we used this clone for experiments. pcDNA4-myc-PGC1α (plasmid 10974) and PGC1α promoter luciferase delta CRE (plasmid 8888) were purchased from Addgene. pRL/TK (Renilla luciferase) was provided by C. Tiruppathi at UIC.

Techniques: Isolation, Control, Western Blot, Transfection, Luciferase, Plasmid Preparation, Activity Assay, shRNA, Marker, Quantitative RT-PCR

Fig. 7 | Endothelial-specific PGC1α depleted mice manifest elements of cachexia phenotypes. a–k, ECWT (ECtdTomato, WT) and EC∆PGC1α (ECtdTomato, ∆PGC1α) mice. a, PGC1α knockdown efficiency in isolated muscle ECs. b, Quantification of PGC1α levels in a (n = 4). Each dot represents one mouse. c, Body weight (n = 10). Each dot represents one mouse. d, Grip strength (n = 10). Each dot represents one mouse. e, Muscle weight (n = 10). Each dot represents one mouse. f, CSA per single fiber (n = 5 for ECWT and n = 6 for EC∆PGC1α). Each dot represents one mouse. g, Expression of MuRF1 mRNA levels in TA muscles (n = 12 for ECWT and

Journal: Nature cancer

Article Title: Skeletal muscle endothelial dysfunction through the activin A-PGC1α axis drives progression of cancer cachexia.

doi: 10.1038/s43018-025-00975-6

Figure Lengend Snippet: Fig. 7 | Endothelial-specific PGC1α depleted mice manifest elements of cachexia phenotypes. a–k, ECWT (ECtdTomato, WT) and EC∆PGC1α (ECtdTomato, ∆PGC1α) mice. a, PGC1α knockdown efficiency in isolated muscle ECs. b, Quantification of PGC1α levels in a (n = 4). Each dot represents one mouse. c, Body weight (n = 10). Each dot represents one mouse. d, Grip strength (n = 10). Each dot represents one mouse. e, Muscle weight (n = 10). Each dot represents one mouse. f, CSA per single fiber (n = 5 for ECWT and n = 6 for EC∆PGC1α). Each dot represents one mouse. g, Expression of MuRF1 mRNA levels in TA muscles (n = 12 for ECWT and

Techniques: Knockdown, Isolation, Expressing, Muscles

FIGURE 6 Restoration of neurite outgrowth in ZIP12 deficient cells by genetic or chemical means. A-D, Cells were transfected with (A,C) PGC1α or PGC1β or (B,D) superoxide dismutases SOD1 and SOD2 in (A,B) ZIP12 shRNA or (C,D) ZIP12 KO cells. Neurite length was measured after differentiation with retinoic acid for 48 hours. Significant differences were determined using two-way ANOVA (n ≥ 100), followed by Dunn’s post hoc test. *P < .05, ***P < .001 versus ZIP12 shRNA or KO (ZIP12KO1) cells transfected with empty expression plasmid. E-G, Co- incubation with 2.5 µM of alpha-tocopherol, 0.5 µM of MitoTEMPO, or 50 nM of MitoQ (mitoquinone) during retinoic acid differentiation over 48 hours. Significant differences were determined using two-way ANOVA (n ≥ 50), followed by Dunn's post hoc test. *P < .05, **P < .01 versus KO (ZIP12KO1) cells incubated without antioxidant (and with DMSO in media as control where applicable). For all graphs, columns and error bars indicate means ± SEM

Journal: The FASEB Journal

Article Title: Role of zinc transporter ZIP12 in susceptibility‐weighted brain magnetic resonance imaging (MRI) phenotypes and mitochondrial function

doi: 10.1096/fj.202000772r

Figure Lengend Snippet: FIGURE 6 Restoration of neurite outgrowth in ZIP12 deficient cells by genetic or chemical means. A-D, Cells were transfected with (A,C) PGC1α or PGC1β or (B,D) superoxide dismutases SOD1 and SOD2 in (A,B) ZIP12 shRNA or (C,D) ZIP12 KO cells. Neurite length was measured after differentiation with retinoic acid for 48 hours. Significant differences were determined using two-way ANOVA (n ≥ 100), followed by Dunn’s post hoc test. *P < .05, ***P < .001 versus ZIP12 shRNA or KO (ZIP12KO1) cells transfected with empty expression plasmid. E-G, Co- incubation with 2.5 µM of alpha-tocopherol, 0.5 µM of MitoTEMPO, or 50 nM of MitoQ (mitoquinone) during retinoic acid differentiation over 48 hours. Significant differences were determined using two-way ANOVA (n ≥ 50), followed by Dunn's post hoc test. *P < .05, **P < .01 versus KO (ZIP12KO1) cells incubated without antioxidant (and with DMSO in media as control where applicable). For all graphs, columns and error bars indicate means ± SEM

Article Snippet: Mouse PGC1α promoter regions, from −2,533 to +78 relative to the transcriptional start site, was obtained as inserted in pGL3 (PGC-1 alpha promoter 2 kb luciferase (Addgene plasmid 888729) and mouse PGC1α promoter luciferase delta CRE (Addgene plasmid 888829) from Addgene, and the promoter regions were digested with KpnI and XhoI and ligated into pGL4 (Promega) for better signal to noise responses during reporter assays.

Techniques: Transfection, shRNA, Expressing, Plasmid Preparation, Incubation, Control

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