Review





Similar Products

94
ATCC human microvascular endothelial cells humec
The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human <t>endothelial</t> and epithelial cells. The endogenous IFITMs mRNA levels in <t>HuMEC</t> ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).
Human Microvascular Endothelial Cells Humec, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human microvascular endothelial cells humec/product/ATCC
Average 94 stars, based on 1 article reviews
human microvascular endothelial cells humec - by Bioz Stars, 2026-06
94/100 stars
  Buy from Supplier

95
PromoCell hcmecs
The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human <t>endothelial</t> and epithelial cells. The endogenous IFITMs mRNA levels in <t>HuMEC</t> ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).
Hcmecs, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hcmecs/product/PromoCell
Average 95 stars, based on 1 article reviews
hcmecs - by Bioz Stars, 2026-06
95/100 stars
  Buy from Supplier

mvecs  (ATCC)
95
ATCC mvecs
STDP <t>attenuates</t> <t>vascular</t> endothelial dysfunction by NLRP3 inhibition. A – D The expression levels of NLRP3, pro-IL-1β and cle-IL-1β were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. E , F The expression levels of ICMA-1 were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. G, H Representative fluorescent confocal images of VCAM-1 (green) and DAPI (blue) in <t>MVECs</t> and the summarized data of the immunofluorescence intensity, scale bar = 10 μm. N = 4–6, * P < 0.05, *** P < 0.001 compared to control group, # P < 0.05, ## P < 0.01, ### P < 0.001 compared to LCWE group
Mvecs, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mvecs/product/ATCC
Average 95 stars, based on 1 article reviews
mvecs - by Bioz Stars, 2026-06
95/100 stars
  Buy from Supplier

95
ATCC human microvascular endothelial cells
STDP <t>attenuates</t> <t>vascular</t> endothelial dysfunction by NLRP3 inhibition. A – D The expression levels of NLRP3, pro-IL-1β and cle-IL-1β were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. E , F The expression levels of ICMA-1 were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. G, H Representative fluorescent confocal images of VCAM-1 (green) and DAPI (blue) in <t>MVECs</t> and the summarized data of the immunofluorescence intensity, scale bar = 10 μm. N = 4–6, * P < 0.05, *** P < 0.001 compared to control group, # P < 0.05, ## P < 0.01, ### P < 0.001 compared to LCWE group
Human Microvascular Endothelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human microvascular endothelial cells/product/ATCC
Average 95 stars, based on 1 article reviews
human microvascular endothelial cells - by Bioz Stars, 2026-06
95/100 stars
  Buy from Supplier

95
PromoCell human cardiac capillary endothelial cells
( A ) Predicted impact of in silico inhibition vs. slope of expression change across human aging for genes in cardiac fibroblasts. ( B ) Concordant genes whose inhibition was predicted to be rejuvenating were upregulated across aging, and vice versa. ( C ) Predicted impact of in silico inhibition of genes across the indicated cardiac cell types. ( D ) Beta-gal staining and cell counts quantifying senescence of primary human cardiac capillary <t>endothelial</t> cells in response to predicted pro-aging perturbation of ZBTB16 inhibition. *p<0.05, Wilcoxon rank sums, n=4. ( E ) Predicted impact of in silico perturbation and expression change across human aging and in telomere-shortened mice in each cardiac cell type for top predicted cardiomyocyte age-modulating targets. ( F ) PCA plot and ( G ) differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. p<0.05, Wald test with BH correction, n=4. ( H ) Gene set enrichment of genes differentially expressed in response to all predicted pro-aging perturbations in human iPSC-derived cardiomyocytes (hypergeometric test with g:Set Counts and Sizes (g:SCS) correction). ( I ) Slowed calcium cycle kinetics and ( J ) rhythm irregularities in response to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. *p<0.05, Wilcoxon rank sums with BH correction. Rhythm n=10, time to peak n=180, 111, 139, 37, 237, 150, 191 (bars left to right), decay n=169, 30, 86, 11, 213, 105, 172 (bars left to right). ( K ) Differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes or human primary cardiac fibroblasts where dysregulation of the given gene was statistically significant across all four conditions. Statistical significance of differential expression: p<0.05, Wald test with BH correction, n=4. Statistical significance of overlap of shared dysregulation between the four conditions: p<0.05, one-sided binomial test. RASG.=RASGEF1B. ( L ) Beta-gal staining quantifying senescence of primary human cardiac fibroblasts in response to predicted pro-aging perturbations (AAV overexpression of indicated genes). *p<0.05, Wilcoxon rank sums with BH correction, empty n=6, P4HA1 and RASGEF1B n=4. ( M ) Schematic of in vivo validation experiment. o/e=overexpression. ( N ) In vivo systolic function echocardiographic measurements at 6 weeks post-AAV9 injection. EF: GFP n=8, P4ha1 n=10, Rasgef1b n=10; GLS: GFP n=8, P4ha1 n=9, Rasgef1b n=8. *p<0.05 one-way ANOVA with multiple hypothesis correction.
Human Cardiac Capillary Endothelial Cells, supplied by PromoCell, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human cardiac capillary endothelial cells/product/PromoCell
Average 95 stars, based on 1 article reviews
human cardiac capillary endothelial cells - by Bioz Stars, 2026-06
95/100 stars
  Buy from Supplier

97
ATCC human microvascular endothelial cells hmec 1
( A ) Predicted impact of in silico inhibition vs. slope of expression change across human aging for genes in cardiac fibroblasts. ( B ) Concordant genes whose inhibition was predicted to be rejuvenating were upregulated across aging, and vice versa. ( C ) Predicted impact of in silico inhibition of genes across the indicated cardiac cell types. ( D ) Beta-gal staining and cell counts quantifying senescence of primary human cardiac capillary <t>endothelial</t> cells in response to predicted pro-aging perturbation of ZBTB16 inhibition. *p<0.05, Wilcoxon rank sums, n=4. ( E ) Predicted impact of in silico perturbation and expression change across human aging and in telomere-shortened mice in each cardiac cell type for top predicted cardiomyocyte age-modulating targets. ( F ) PCA plot and ( G ) differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. p<0.05, Wald test with BH correction, n=4. ( H ) Gene set enrichment of genes differentially expressed in response to all predicted pro-aging perturbations in human iPSC-derived cardiomyocytes (hypergeometric test with g:Set Counts and Sizes (g:SCS) correction). ( I ) Slowed calcium cycle kinetics and ( J ) rhythm irregularities in response to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. *p<0.05, Wilcoxon rank sums with BH correction. Rhythm n=10, time to peak n=180, 111, 139, 37, 237, 150, 191 (bars left to right), decay n=169, 30, 86, 11, 213, 105, 172 (bars left to right). ( K ) Differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes or human primary cardiac fibroblasts where dysregulation of the given gene was statistically significant across all four conditions. Statistical significance of differential expression: p<0.05, Wald test with BH correction, n=4. Statistical significance of overlap of shared dysregulation between the four conditions: p<0.05, one-sided binomial test. RASG.=RASGEF1B. ( L ) Beta-gal staining quantifying senescence of primary human cardiac fibroblasts in response to predicted pro-aging perturbations (AAV overexpression of indicated genes). *p<0.05, Wilcoxon rank sums with BH correction, empty n=6, P4HA1 and RASGEF1B n=4. ( M ) Schematic of in vivo validation experiment. o/e=overexpression. ( N ) In vivo systolic function echocardiographic measurements at 6 weeks post-AAV9 injection. EF: GFP n=8, P4ha1 n=10, Rasgef1b n=10; GLS: GFP n=8, P4ha1 n=9, Rasgef1b n=8. *p<0.05 one-way ANOVA with multiple hypothesis correction.
Human Microvascular Endothelial Cells Hmec 1, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human microvascular endothelial cells hmec 1/product/ATCC
Average 97 stars, based on 1 article reviews
human microvascular endothelial cells hmec 1 - by Bioz Stars, 2026-06
97/100 stars
  Buy from Supplier

86
Procell Inc primary mouse renal microvascular endothelial cells
( A ) Predicted impact of in silico inhibition vs. slope of expression change across human aging for genes in cardiac fibroblasts. ( B ) Concordant genes whose inhibition was predicted to be rejuvenating were upregulated across aging, and vice versa. ( C ) Predicted impact of in silico inhibition of genes across the indicated cardiac cell types. ( D ) Beta-gal staining and cell counts quantifying senescence of primary human cardiac capillary <t>endothelial</t> cells in response to predicted pro-aging perturbation of ZBTB16 inhibition. *p<0.05, Wilcoxon rank sums, n=4. ( E ) Predicted impact of in silico perturbation and expression change across human aging and in telomere-shortened mice in each cardiac cell type for top predicted cardiomyocyte age-modulating targets. ( F ) PCA plot and ( G ) differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. p<0.05, Wald test with BH correction, n=4. ( H ) Gene set enrichment of genes differentially expressed in response to all predicted pro-aging perturbations in human iPSC-derived cardiomyocytes (hypergeometric test with g:Set Counts and Sizes (g:SCS) correction). ( I ) Slowed calcium cycle kinetics and ( J ) rhythm irregularities in response to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. *p<0.05, Wilcoxon rank sums with BH correction. Rhythm n=10, time to peak n=180, 111, 139, 37, 237, 150, 191 (bars left to right), decay n=169, 30, 86, 11, 213, 105, 172 (bars left to right). ( K ) Differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes or human primary cardiac fibroblasts where dysregulation of the given gene was statistically significant across all four conditions. Statistical significance of differential expression: p<0.05, Wald test with BH correction, n=4. Statistical significance of overlap of shared dysregulation between the four conditions: p<0.05, one-sided binomial test. RASG.=RASGEF1B. ( L ) Beta-gal staining quantifying senescence of primary human cardiac fibroblasts in response to predicted pro-aging perturbations (AAV overexpression of indicated genes). *p<0.05, Wilcoxon rank sums with BH correction, empty n=6, P4HA1 and RASGEF1B n=4. ( M ) Schematic of in vivo validation experiment. o/e=overexpression. ( N ) In vivo systolic function echocardiographic measurements at 6 weeks post-AAV9 injection. EF: GFP n=8, P4ha1 n=10, Rasgef1b n=10; GLS: GFP n=8, P4ha1 n=9, Rasgef1b n=8. *p<0.05 one-way ANOVA with multiple hypothesis correction.
Primary Mouse Renal Microvascular Endothelial Cells, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary mouse renal microvascular endothelial cells/product/Procell Inc
Average 86 stars, based on 1 article reviews
primary mouse renal microvascular endothelial cells - by Bioz Stars, 2026-06
86/100 stars
  Buy from Supplier

Image Search Results


The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human endothelial and epithelial cells. The endogenous IFITMs mRNA levels in HuMEC ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).

Journal: bioRxiv

Article Title: IFITM1 inhibits Henipavirus membrane fusion by trapping ephrinB2 receptors in fusion-unfavorable membrane nanodomains

doi: 10.64898/2026.05.06.723334

Figure Lengend Snippet: The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human endothelial and epithelial cells. The endogenous IFITMs mRNA levels in HuMEC ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).

Article Snippet: Human microvascular endothelial cells (HuMEC) (ATCC CRL-4060) were cultured in Vascular cell basal medium (ATCC, PCS-100-030) with Microvascular endothelial cell growth kit – BBE (ATCC, PCS-110-040) and 0.5 ug/ml puromycin (10 mg/ml stock, Gibco A1138-03).

Techniques: Transfection, Expressing, Knockdown, Western Blot, Control, Luciferase, Virus, Labeling

STDP attenuates vascular endothelial dysfunction by NLRP3 inhibition. A – D The expression levels of NLRP3, pro-IL-1β and cle-IL-1β were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. E , F The expression levels of ICMA-1 were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. G, H Representative fluorescent confocal images of VCAM-1 (green) and DAPI (blue) in MVECs and the summarized data of the immunofluorescence intensity, scale bar = 10 μm. N = 4–6, * P < 0.05, *** P < 0.001 compared to control group, # P < 0.05, ## P < 0.01, ### P < 0.001 compared to LCWE group

Journal: Chinese Medicine

Article Title: Shexiang Tongxin Dropping Pills targeting Piezo1/Ca 2+ /NLRP3 axis attenuates vascular endothelial inflammation

doi: 10.1186/s13020-026-01402-3

Figure Lengend Snippet: STDP attenuates vascular endothelial dysfunction by NLRP3 inhibition. A – D The expression levels of NLRP3, pro-IL-1β and cle-IL-1β were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. E , F The expression levels of ICMA-1 were analyzed by western blotting and the relative protein expression level were determined by densitometric analysis. G, H Representative fluorescent confocal images of VCAM-1 (green) and DAPI (blue) in MVECs and the summarized data of the immunofluorescence intensity, scale bar = 10 μm. N = 4–6, * P < 0.05, *** P < 0.001 compared to control group, # P < 0.05, ## P < 0.01, ### P < 0.001 compared to LCWE group

Article Snippet: MVECs (murine vascular endothelial cells) were purchased from ATCC (CRL-2586, Shanghai, China) and cultured in a thermostat incubator at 37 °C with 5% carbon dioxide concentration using high glucose medium containing 10% fetal bovine serum (Gibico, USA).

Techniques: Inhibition, Expressing, Western Blot, Immunofluorescence, Control

Piezo1 knockdown abrogates STDP-mediated endothelial protection. A , B Knockdown Piezo1 representative images as well as statistical graphs. C , D The protein expression levels of NLRP3 was analyzed by Western blotting and the relative protein expression level were determined by densitometric analysis. E , F Immunofluorescence double staining to co-localize NLRP3 with Caspase1. G, H The levels of IL-18 and IL-1β in cell culture supernatants were measured by ELISA. I, J The expression levels of pro-Caspase-1, cle-Caspase-1 were analyzed by Western blotting and the relative protein expression level were determined by densitometric analysis. K, L The protein expression levels of ICAM-1 was analyzed by Western blotting and the relative protein expression level were determined by densitometric analysis. M , N Representative fluorescent confocal images of VCAM-1 (green) and DAPI (blue) in MVECs and the summarized data of the immunofluorescence intensity, scale bar = 10 μm. N = 4–6, * P < 0.05, ** P < 0.01, *** P < 0.001 compared to control group, # P < 0.05, ## P < 0.01, ### P < 0.001 compared to LCWE group

Journal: Chinese Medicine

Article Title: Shexiang Tongxin Dropping Pills targeting Piezo1/Ca 2+ /NLRP3 axis attenuates vascular endothelial inflammation

doi: 10.1186/s13020-026-01402-3

Figure Lengend Snippet: Piezo1 knockdown abrogates STDP-mediated endothelial protection. A , B Knockdown Piezo1 representative images as well as statistical graphs. C , D The protein expression levels of NLRP3 was analyzed by Western blotting and the relative protein expression level were determined by densitometric analysis. E , F Immunofluorescence double staining to co-localize NLRP3 with Caspase1. G, H The levels of IL-18 and IL-1β in cell culture supernatants were measured by ELISA. I, J The expression levels of pro-Caspase-1, cle-Caspase-1 were analyzed by Western blotting and the relative protein expression level were determined by densitometric analysis. K, L The protein expression levels of ICAM-1 was analyzed by Western blotting and the relative protein expression level were determined by densitometric analysis. M , N Representative fluorescent confocal images of VCAM-1 (green) and DAPI (blue) in MVECs and the summarized data of the immunofluorescence intensity, scale bar = 10 μm. N = 4–6, * P < 0.05, ** P < 0.01, *** P < 0.001 compared to control group, # P < 0.05, ## P < 0.01, ### P < 0.001 compared to LCWE group

Article Snippet: MVECs (murine vascular endothelial cells) were purchased from ATCC (CRL-2586, Shanghai, China) and cultured in a thermostat incubator at 37 °C with 5% carbon dioxide concentration using high glucose medium containing 10% fetal bovine serum (Gibico, USA).

Techniques: Knockdown, Expressing, Western Blot, Immunofluorescence, Double Staining, Cell Culture, Enzyme-linked Immunosorbent Assay, Control

( A ) Predicted impact of in silico inhibition vs. slope of expression change across human aging for genes in cardiac fibroblasts. ( B ) Concordant genes whose inhibition was predicted to be rejuvenating were upregulated across aging, and vice versa. ( C ) Predicted impact of in silico inhibition of genes across the indicated cardiac cell types. ( D ) Beta-gal staining and cell counts quantifying senescence of primary human cardiac capillary endothelial cells in response to predicted pro-aging perturbation of ZBTB16 inhibition. *p<0.05, Wilcoxon rank sums, n=4. ( E ) Predicted impact of in silico perturbation and expression change across human aging and in telomere-shortened mice in each cardiac cell type for top predicted cardiomyocyte age-modulating targets. ( F ) PCA plot and ( G ) differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. p<0.05, Wald test with BH correction, n=4. ( H ) Gene set enrichment of genes differentially expressed in response to all predicted pro-aging perturbations in human iPSC-derived cardiomyocytes (hypergeometric test with g:Set Counts and Sizes (g:SCS) correction). ( I ) Slowed calcium cycle kinetics and ( J ) rhythm irregularities in response to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. *p<0.05, Wilcoxon rank sums with BH correction. Rhythm n=10, time to peak n=180, 111, 139, 37, 237, 150, 191 (bars left to right), decay n=169, 30, 86, 11, 213, 105, 172 (bars left to right). ( K ) Differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes or human primary cardiac fibroblasts where dysregulation of the given gene was statistically significant across all four conditions. Statistical significance of differential expression: p<0.05, Wald test with BH correction, n=4. Statistical significance of overlap of shared dysregulation between the four conditions: p<0.05, one-sided binomial test. RASG.=RASGEF1B. ( L ) Beta-gal staining quantifying senescence of primary human cardiac fibroblasts in response to predicted pro-aging perturbations (AAV overexpression of indicated genes). *p<0.05, Wilcoxon rank sums with BH correction, empty n=6, P4HA1 and RASGEF1B n=4. ( M ) Schematic of in vivo validation experiment. o/e=overexpression. ( N ) In vivo systolic function echocardiographic measurements at 6 weeks post-AAV9 injection. EF: GFP n=8, P4ha1 n=10, Rasgef1b n=10; GLS: GFP n=8, P4ha1 n=9, Rasgef1b n=8. *p<0.05 one-way ANOVA with multiple hypothesis correction.

Journal: bioRxiv

Article Title: Temporal AI model predicts drivers of cell state trajectories across human aging

doi: 10.64898/2026.03.30.715396

Figure Lengend Snippet: ( A ) Predicted impact of in silico inhibition vs. slope of expression change across human aging for genes in cardiac fibroblasts. ( B ) Concordant genes whose inhibition was predicted to be rejuvenating were upregulated across aging, and vice versa. ( C ) Predicted impact of in silico inhibition of genes across the indicated cardiac cell types. ( D ) Beta-gal staining and cell counts quantifying senescence of primary human cardiac capillary endothelial cells in response to predicted pro-aging perturbation of ZBTB16 inhibition. *p<0.05, Wilcoxon rank sums, n=4. ( E ) Predicted impact of in silico perturbation and expression change across human aging and in telomere-shortened mice in each cardiac cell type for top predicted cardiomyocyte age-modulating targets. ( F ) PCA plot and ( G ) differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. p<0.05, Wald test with BH correction, n=4. ( H ) Gene set enrichment of genes differentially expressed in response to all predicted pro-aging perturbations in human iPSC-derived cardiomyocytes (hypergeometric test with g:Set Counts and Sizes (g:SCS) correction). ( I ) Slowed calcium cycle kinetics and ( J ) rhythm irregularities in response to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes. *p<0.05, Wilcoxon rank sums with BH correction. Rhythm n=10, time to peak n=180, 111, 139, 37, 237, 150, 191 (bars left to right), decay n=169, 30, 86, 11, 213, 105, 172 (bars left to right). ( K ) Differential gene expression heatmap of transcriptional response (measured by bulk RNA sequencing) to predicted pro-aging perturbations (AAV overexpression of indicated genes vs. GFP) in human iPSC-derived cardiomyocytes or human primary cardiac fibroblasts where dysregulation of the given gene was statistically significant across all four conditions. Statistical significance of differential expression: p<0.05, Wald test with BH correction, n=4. Statistical significance of overlap of shared dysregulation between the four conditions: p<0.05, one-sided binomial test. RASG.=RASGEF1B. ( L ) Beta-gal staining quantifying senescence of primary human cardiac fibroblasts in response to predicted pro-aging perturbations (AAV overexpression of indicated genes). *p<0.05, Wilcoxon rank sums with BH correction, empty n=6, P4HA1 and RASGEF1B n=4. ( M ) Schematic of in vivo validation experiment. o/e=overexpression. ( N ) In vivo systolic function echocardiographic measurements at 6 weeks post-AAV9 injection. EF: GFP n=8, P4ha1 n=10, Rasgef1b n=10; GLS: GFP n=8, P4ha1 n=9, Rasgef1b n=8. *p<0.05 one-way ANOVA with multiple hypothesis correction.

Article Snippet: Human cardiac capillary endothelial cells were purchased from PromoCell (C-12285) and cultured in endothelial basal medium (EBM, CC-3121, Lonza) supplemented with 10% fetal bovine serum (10100147, Gibco).

Techniques: In Silico, Inhibition, Expressing, Staining, Gene Expression, RNA Sequencing, Over Expression, Derivative Assay, Quantitative Proteomics, In Vivo, Biomarker Discovery, Injection