ec cell  (Procell Inc)

Journal: Materials Today Bio

Article Title: Procyanidin capsules attenuate PI3K/AKT-mediated mitochondrial dysfunction and accelerate skin wound healing in diabetic mice

doi: 10.1016/j.mtbio.2026.103029

Figure Lengend Snippet: Biocompatibility of PC capsules: (A–B) cell viability of HUVECs (A) and NIH/3T3 cells (B) treated with different concentrations of PC capsules for 24 h detected by MTT assay; (C–D) toxic staining of PC capsules on HUVECs and NIH/3T3 cells detected by living/dead cell staining; (E) photos of the backs of mice after receiving a subcutaneous injection of PC capsules and subcutaneous PC capsules after injection at day 4 and day 7; (F) slices of major organs (heart, liver, spleen, lungs, and kidneys) in mice after 14 days of PC capsule administration; scale bar = 100 μm. Serum liver function indicators were: (G) ALT and (H) AST. Serum renal function indicators were: (I) BUN and (J) CRE. Data are presented as mean ± standard deviation (SD) with n = 3 independent biological replicates per group. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. Significance markers are defined as: ns (p > 0.05).

Article Snippet: Human umbilical vein endothelial cells (HUVECs) (CRL-1730, USA, RRID: CVCL_2959) and NIH/3T3 cells (CRL-1658, USA, RRID: CVCL_0594) used in this study were purchased from American Type Culture Collection.

Techniques: Capsules, MTT Assay, Staining, Injection, Standard Deviation

Journal: Materials Today Bio

Article Title: Procyanidin capsules attenuate PI3K/AKT-mediated mitochondrial dysfunction and accelerate skin wound healing in diabetic mice

doi: 10.1016/j.mtbio.2026.103029

Figure Lengend Snippet: PC capsules increased cell viability under H 2 O 2 stimulation: cell viability of HUVECs (A) and NIH/3T3 (B) cells treated with different concentrations of H 2 O 2 for 6 h detected by MTT assay; viability of H 2 O 2 ‐treated HUVECs (C) and NIH/3T3 cells (D) with different concentrations of PC capsule pretreatment. Data are presented as mean ± standard deviation (SD) with n = 3 independent biological replicates per group. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. Significance markers are defined as: ∗∗∗∗p < 0.0001.

Article Snippet: Human umbilical vein endothelial cells (HUVECs) (CRL-1730, USA, RRID: CVCL_2959) and NIH/3T3 cells (CRL-1658, USA, RRID: CVCL_0594) used in this study were purchased from American Type Culture Collection.

Techniques: Capsules, MTT Assay, Standard Deviation

Journal: Materials Today Bio

Article Title: Procyanidin capsules attenuate PI3K/AKT-mediated mitochondrial dysfunction and accelerate skin wound healing in diabetic mice

doi: 10.1016/j.mtbio.2026.103029

Figure Lengend Snippet: PC capsules restored cell function in H 2 O 2 -treated HUVECs and NIH/3T3 cells. HUVECs and NIH/3T3 cells were treated with PC capsules for 24 h and H 2 O 2 for 6 h. (A) Images of HUVEC migration exposure to H 2 O 2 , NAC, PC capsules after 24 h; (B) quantification of percentage wound area remaining for HUVECs; (C) images of NIH/3T3 cell migration exposure to H 2 O 2 , NAC, PC capsules after 24 h; (D) quantification of percentage wound area remaining for NIH/3T3 cells; (E–F) digital images of endothelial cell microtubule formation after treatment with H 2 O 2 , NAC, and PC capsules. Quantification of (G) number of branch sites, (H) total lengths and (I) numbers of tube nodes. Data are presented as mean ± standard deviation (SD) with n = 3 independent biological replicates per group. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. Significance markers are defined as: ##p < 0.01, ###p < 0.001 (vs. control group); ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 (vs. H 2 O 2 group).

Article Snippet: Human umbilical vein endothelial cells (HUVECs) (CRL-1730, USA, RRID: CVCL_2959) and NIH/3T3 cells (CRL-1658, USA, RRID: CVCL_0594) used in this study were purchased from American Type Culture Collection.

Techniques: Capsules, Cell Function Assay, Migration, Standard Deviation, Control

Journal: Materials Today Bio

Article Title: Procyanidin capsules attenuate PI3K/AKT-mediated mitochondrial dysfunction and accelerate skin wound healing in diabetic mice

doi: 10.1016/j.mtbio.2026.103029

Figure Lengend Snippet: PC capsules improved mitochondrial function in H 2 O 2 -treated HUVECs and NIH/3T3 cells: (A–D) elimination of ROS from HUVECs (A, C) and NIH/3T3 (B, D) cells by PC capsules as determined by MitoSOX; (E–H) assessment of PC-mediated HUVECs (E, G) and NIH/3T3 cells (F, H) MMP using TMRM assays; (I–J) effects of PC capsules on ATP production in HUVECs (I) and NIH/3T3 cells (J). Data are presented as mean ± standard deviation (SD) with n = 3 independent biological replicates per group. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. Significance markers are defined as: ##p < 0.01, ###p < 0.001, ####p < 0.0001 (vs. control group); ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 (vs. H 2 O 2 group).

Article Snippet: Human umbilical vein endothelial cells (HUVECs) (CRL-1730, USA, RRID: CVCL_2959) and NIH/3T3 cells (CRL-1658, USA, RRID: CVCL_0594) used in this study were purchased from American Type Culture Collection.

Techniques: Capsules, Standard Deviation, Control

Journal: Materials Today Bio

Article Title: Procyanidin capsules attenuate PI3K/AKT-mediated mitochondrial dysfunction and accelerate skin wound healing in diabetic mice

doi: 10.1016/j.mtbio.2026.103029

Figure Lengend Snippet: PC capsule–mediated cytoprotection via promoting activation of PI3K/AKT signaling pathway: expression of p-PI3K, PI3K, p-AKT, and AKT in HUVECs treated with PC capsules for 24 h and presence/absence of H 2 O 2 for 6 h (A); and analysis of optical density values of p-PI3K/PI3K (B) and p-AKT/AKT (C); expression of p-PI3K, PI3K, p-AKT, and AKT in NIH/3T3 cells treated with PC capsules for 24 h and presence/absence of H 2 O 2 for 6 h (D); and analysis of optical density values of p-PI3K/PI3K (E) and p-AKT/AKT (F). Data are presented as mean ± standard deviation (SD) with n = 3 independent biological replicates per group. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. Significance markers are defined as: #p < 0.05, ##p < 0.01, ###p < 0.001 (vs control group); ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 (vs PC group or vs H 2 O 2 group).

Article Snippet: Human umbilical vein endothelial cells (HUVECs) (CRL-1730, USA, RRID: CVCL_2959) and NIH/3T3 cells (CRL-1658, USA, RRID: CVCL_0594) used in this study were purchased from American Type Culture Collection.

Techniques: Activation Assay, Expressing, Capsules, Standard Deviation, Control

Journal: Materials Today Bio

Article Title: Procyanidin capsules attenuate PI3K/AKT-mediated mitochondrial dysfunction and accelerate skin wound healing in diabetic mice

doi: 10.1016/j.mtbio.2026.103029

Figure Lengend Snippet: PC capsules improve HUVEC and NIH/3T3 cell dysfunction by regulating PI3K/AKT signaling. HUVECs and NIH/3T3 cells were treated with PC capsules and LY294002 for 24 h and H 2 O 2 for 6 h. (A) Images of HUVEC migration exposure to H 2 O 2 , LY294002, PC capsules after 24 h; (B) quantification of percentage wound area remaining for HUVECs; (C) images of NIH/3T3 cell migration exposure to H 2 O 2 , LY294002, PC capsules after 24 h; (D) quantification of percentage wound area remaining for NIH/3T3 cells; (E–F) digital images of endothelial cell microtubule formation after treatment with H 2 O 2 , LY294002, and PC capsules. Quantification of (G) number of branch sites, (H) total lengths and (I) numbers of tube nodes (J); and analysis of optical density values of p-PI3K/PI3K (K) and p-AKT/AKT (L); expression of p-PI3K, PI3K, p-AKT, and AKT in NIH/3T3 cells treated with PC capsules, and LY294002 for 24 h and presence/absence of H 2 O 2 for 6 h (M); and analysis of optical density values of p-PI3K/PI3K (N) and p-AKT/AKT (O). Data are presented as mean ± standard deviation (SD) with n = 3 independent biological replicates per group. Statistical analysis was performed using one-way ANOVA followed by Tukey's post-hoc test. Significance markers are defined as: ##p < 0.01, ###p < 0.001 (vs. control group); ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 (vs PC group or vs LY294002 group).

Article Snippet: Human umbilical vein endothelial cells (HUVECs) (CRL-1730, USA, RRID: CVCL_2959) and NIH/3T3 cells (CRL-1658, USA, RRID: CVCL_0594) used in this study were purchased from American Type Culture Collection.

Techniques: Capsules, Migration, Expressing, Standard Deviation, Control

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericyte secretions mediate the inhibition of TNBC cell adhesion to the BBB. (A) Experimental workflow for adhesion assay. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. The astrocyte medium was renewed 24 h before the adhesion experiment with the same ECGMV2 medium. Endothelial cells (ECs) and brain pericytes (hBPs) were co‐cultured for 5 days, and inserts containing brain‐like endothelial cells (hBLECs) were then either maintained with hBPs or transferred to wells without hBPs. After 24 hours, and prior to MDA‐MB‐231 cells seeding, inserts were subjected to the following conditions: maintained without hBPs (hBLEC 24h); transferred to hBPs previously cultured alone for 24 hours (hBLEC 24h then hBP); transferred to wells without hBPs but containing either culture medium (hBLEC) or CM from co‐culture (hBLEC + CM coc ); transferred to wells with astrocytes (hBLEC + A) or maintained in co‐culture with hBPs (hBLEC + hBP). (B–G), Quantification (B, D, F) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E, G) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using one‐way ANOVA followed by Tukey's test (B), Welch's ANOVA followed by Dunnett's T3 test (D) and Kruskal–Wallis test followed by Dunn's test (F). CM coc = conditioned medium from 24 h hBLECs and hBPs coculture, A = astrocytes, hBP mono = 24 h hBPs monoculture. Scale bar = 750 µm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; ECs, endothelial cells; hBLECs, human brain‐like endothelial cells; ns, non‐significant; hBPs, human brain pericytes; TNBC, triple‐negative breast cancer. **** p ≤ 0.0001; * p ≤ 0.05.

Article Snippet: Differentiated ECs were cultured in 100‐mm Petri dishes (Corning) coated with gelatin (Sigma‐Aldrich), in EC growth medium MV 2 (ECGMV2 + Supplement mix C‐39226, PromoCell) and gentamicin (50 μg/ml; Biowest). hBPs (female) were provided by Dr. Fumitaka Shimizu and Pr.

Techniques: Inhibition, Cell Adhesion Assay, Cell Culture, Co-Culture Assay, Incubation

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes limit TNBC cell adhesion to the BBB under hypoxic conditions. (A) Experimental workflow for adhesion assay in hypoxic conditions. All BBB experiments were performed using ECGMV2 medium with supplements for all conditions from day −6 to the end of the experiment. After 5 days of co‐culture with brain pericytes (hBPs), inserts containing brain‐like endothelial cells (hBLECs) were exposed to hypoxia for 24 h in the presence or absence of hBPs. Parallel conditions maintained in normoxia served as controls. (B–E) Quantification (B, D) of MDA‐MB‐231 cell adhesion to hBLECs after 3 h of incubation and representative images (C, E) of adhered MDA‐MB‐231 cells (green) under the different conditions. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test (B) and Kruskal‐Wallis test followed by Dunn's test (D). hBP‐CM mono = conditioned medium from 24 h hBPs monoculture. Scale bar = 750 μm. BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: Differentiated ECs were cultured in 100‐mm Petri dishes (Corning) coated with gelatin (Sigma‐Aldrich), in EC growth medium MV 2 (ECGMV2 + Supplement mix C‐39226, PromoCell) and gentamicin (50 μg/ml; Biowest). hBPs (female) were provided by Dr. Fumitaka Shimizu and Pr.

Techniques: Cell Adhesion Assay, Co-Culture Assay, Incubation

Journal: Journal of Cell Communication and Signaling

Article Title: Human brain pericytes protect the blood–brain barrier from triple‐negative breast cancer cells while promoting tumor aggressiveness

doi: 10.1002/ccs3.70070

Figure Lengend Snippet: Brain pericytes maintain BBB integrity in the presence of TNBC cells under hypoxic conditions and supplement deprivation. (A) After 5 days of co‐culture with brain pericytes (hBPs) in ECGMV2 medium with supplements, inserts containing brain‐like endothelial cells (hBLECs) co‐cultured with hBPs were exposed to hypoxia for 16 h following medium replacement with ECGMV2 basal medium (without supplements). Then, endothelial permeability (Pe) to Lucifer Yellow was assessed after 3 h of incubation with MDA‐MB‐231 cells, in the presence or absence of hBPs, under normoxic and hypoxic conditions. (B) Permeability values (expressed in x10 −3 cm/min ± SD) are summarized in a table. (C) Representative images of endothelial Claudin‐5 (magenta) immunostaining in the absence or presence of hBPs after 3 h of incubation with MDA‐MB‐231 cells (green) under hypoxic conditions in basal medium. Data are obtained from three independent experiments, with three technical replicates per condition. Statistical analyses were performed using Welch's ANOVA followed by Dunnett's T3 test. MDA = MDA‐MB‐231 cells. Scale bars = 300 μm (10X) and 100 μm (40X). BBB, blood–brain barrier; ECGMV2, EC Growth Medium MV 2; hBLECs, human brain‐like endothelial cells; hBPs, human brain pericytes; ns, non‐significant; TNBC, triple‐negative breast cancer. *** p ≤ 0.001; ** p ≤ 0.01; * p ≤ 0.05.

Article Snippet: Differentiated ECs were cultured in 100‐mm Petri dishes (Corning) coated with gelatin (Sigma‐Aldrich), in EC growth medium MV 2 (ECGMV2 + Supplement mix C‐39226, PromoCell) and gentamicin (50 μg/ml; Biowest). hBPs (female) were provided by Dr. Fumitaka Shimizu and Pr.

Techniques: Co-Culture Assay, Cell Culture, Permeability, Incubation, Immunostaining

Journal: bioRxiv

Article Title: Chlamydia trachomatis infection upregulates MicroRNA21 to deplete tumor suppressor PTEN

doi: 10.64898/2026.05.11.723860

Figure Lengend Snippet: Chlamydia trachomatis infection leads to up regulation of oncomiR, miR21 to deplete PTEN level. A. Hela229 cells were infected with heat killed or infectious Ct for different (early) time points and miR21 levels were detected by northern blotting. U6 was detected as loading control. B. Hela229 cells were left uninfected (UI) or infected with infectious Ct for different time points. The total RNA was used to perform northern blotting to detect levels of miR21. U6 serves as loading control and Ct R5 is the infection control. n=3. C. Human Fimb and Huvec cells were infected with infectious Ct for 30 h and the total RNA was used for Northern blot analysis to detect the levels of miR21; UI-uninfected, Ct R5-infection control and U6 is the loading control. D. HeLa229 cells were either left uninfected or infected with Ct for different time points. The total RNA was isolated and quantitative RT-PCR was used to quantify the levels of miR21. Three independent experiments were performed with the mean values (±SEM) compared to levels of uninfected HeLa229 cells. Statistical analysis was performed using Student t test (**p ≤ 0.01). E. HeLa229 cells were treated with scrambled RNA or antagomiR against miR21 or F over expressed with scramble RNA or miR21 RNA. The cells were left uninfected or infected with Ct for 36h and lysed for western blot analysis. The data provided is the representative of three independent experiments. n=3. G. The cells (uninfected and infected) from E (primary infection) were lysed to re-infect freshly plated HeLa229 cells to analyze the progeny, secondary infection. For the above experiments F . and G . Beta actin serves as the loading control and cHSP60, Chlamydial HSP60, detects the rate of infection. Fc shows the fold change in the levels of protein compared to UI, normalized to levels of beta actin. The data provided is the representative of three independent experiments. n=3.

Article Snippet: HeLa229 (ATCC ® CCL-2.1 TM ), human Fimb: epithelial cells isolated from fimbriae of healthy donors after hysterectomy and Huvec cells (ATCC ® CRL-1730 TM ) were used in the experiments.

Techniques: Infection, Northern Blot, Control, Isolation, Quantitative RT-PCR, Western Blot

Journal: bioRxiv

Article Title: A Long-lived Avatar for Modeling Age-Related Vascular Disease

doi: 10.64898/2026.04.29.721776

Figure Lengend Snippet: A , Representative images of iPSC-ECs in low serum (3%) and treated with VEGF, SB, or VEGF+SB (VSL) at the indicated time points reveals that VSL further improves EC morphology. The above treatments were performed using EC medium (Lonza, EGM-2MV) with 3% FBS. Ctrl* = EC medium with 3% FBS; VEGF = VEGF (10 ng/mL) added to EC medium with 3% FBS; SB = SB (SB 431542, 10 µM) added to EC medium with 3% FBS; VEGF + SB = VEGF (10 ng/mL) and SB (SB 431542, 10 µM) added to EC medium with 3% FBS, referred to as VSL. (scale bar: 100 µm) B , Quantification of cell circularity from ( A ) reveals that VSL reduces cell circularity. C , Quantification of cell area from ( A ) reveals that VSL reduces cell area. D , UMAP analysis of iPSC-ECs treated with different viability factors or combinatorial treatments of viability factors at day 40 shows that VSL restores the transcriptional profile of HAECs at day 40 to that at day 0 (n=3). The prophylactic antibiotic (Lonza Walkersville MycoZap, 0.2%; AB) was used to prevent mycoplasma contamination. D0_Ctrl = iPSC-ECs at day 0; D40_Ctrl = iPSC-ECs treated with 3%FBS EC medium (Lonza, EGM-2MV) for 40 days; D40_VEGF = iPSC-ECs treated with the 3%FBS EC medium with the addition of VEGF (10 ng/mL) for 40 days; D40_AB = iPSC-ECs treated with 3%FBS EC medium + prophylactic antibiotic (Lonza Walkersville MycoZap, 0.2%; AB) for 40 days; D40_VSL = iPSC-ECs treated with VSL for 40 days; D40_VSL+cAMP = iPSC-ECs treated with VSL and cAMP (10 µM) for 40 days; D40_VSL+cGMP = iPSC-ECs treated with VSL and cGMP (10 µM) for 40 days; D40_VSL+Camp + cGMP = iPSC-ECs treated with VSL, cAMP (10 µM), and cGMP (10 µM) for 40 days; D40_VSL + cAMP + cGMP + AB = iPSC-ECs treated with VSL, cAMP (10 µM), cGMP (10 µM) and AB (Lonza Walkersville MycoZap, 0.2%;) for 40 days. E , Representative images of β-gal staining for iPSC-ECs treated with or without VSL at day 40 are shown (scale bar: 200 µm). F , Quantification of (E) shows that VSL reduces the percentage of β-gal positive cells (n-=3). Each dot represents one single field. G , The expression of sICAM-1 and sVCAM-1 in culture media from iPSC-ECs treated with VEGF alone or VSL at day 0 or day 20 detected by ELISA assay shows that VSL effectively suppresses inflammatory cytokines (n=3). D0_Ctrl = iPSC-ECs at day 0; D20_ Ctrl = iPSC-ECs treated with standard EC medium (Lonza, EGM-2MV) for 20 days; D20_VEGF = iPSC-ECs treated with standard EC medium and addition of VEGF (10 ng/mL) for 20 days; D20_VSL = iPSC-ECs treated with VSL for 20 days. Each dot represents one technical repeat. H , Heatmap analysis of EC marker genes and fibroblast marker genes expressed in iPSC-ECs treated with or without VSL at day 60 reveals that VSL preserves EC identity during long-term culture. Each group includes triplicate in this analysis. Ctrl_D60 = iPSC-ECs treated with 3%FBS EC medium (Lonza, EGM-2MV) for 60 days. VSL_D60 = iPSC-ECs treated with VSL. Data between two groups were analyzed by Student’s t-test. Data between multiple groups are analyzed by one-way ANOVA. Results are considered statistically significant with P<0.05(*), P<0.01(**), P<0.001(***), and P<0.0001(****).

Article Snippet: HAECs were purchased from ATCC (Cat# PCS-100-011). iPSC-ECs were generated using established methods in our laboratory .

Techniques: Staining, Expressing, Enzyme-linked Immunosorbent Assay, Marker

Journal: bioRxiv

Article Title: A Long-lived Avatar for Modeling Age-Related Vascular Disease

doi: 10.64898/2026.04.29.721776

Figure Lengend Snippet: A , mVSL+ maintains co-culture of human iPSC-ECs and iPSC-VSMCs for over 180 days, with endothelial cells aligning with the lumen direction throughout the 180-day culture (scale bar: 40 µm). B , Quantification of ( A ) shows that mVSL+ preserves lumen surface integrity throughout 180-day culture. C, Immunofluorescence staining of VE-Cadherin and α-SMA in the avatars at the indicated time points (scale bar: 40 µm). D , mVSL+ maintains the expression of sICAM-1 and sVCAM-1 in the vascular avatars at a relatively low level compared to day 5 throughout the 180-day culture. (n=3). E , Bio-plex analysis shows that mVSL+ maintains the vascular avatars at a low inflammatory state compared to day 5 throughout the 180-day culture . F , The duration of prior 3D models of vascular lumens using monoculture (in red) or co-culture (in blue). Each dot represents the duration noted in one paper. 17 papers are cited in total. The large red dot indicates our monoculture duration, and the large blue dot indicates our co-culture duration.

Article Snippet: HAECs were purchased from ATCC (Cat# PCS-100-011). iPSC-ECs were generated using established methods in our laboratory .

Techniques: Co-Culture Assay, Immunofluorescence, Staining, Expressing