human pulmonary artery microvascular endothelial cells  (ATCC)

Journal: The FASEB Journal

Article Title: SARS ‐ CoV ‐2 Nucleocapsid Protein Does Not Induce Inflammation in Endothelial Cells or Monocytes

doi: 10.1096/fj.202501433R

Figure Lengend Snippet: Effects of recombinant N‐protein (endotoxin nondepleted, NPnon) on inflammatory marker mRNA levels in human microvascular endothelial cells. Cells were treated with vehicle, LPS (1 μg/mL), or NPnon (10 μg/mL, ThermoFisher) for 4 h. The total RNA was isolated, and qPCR analysis was performed to measure the mRNA levels of TNFα, IL‐6, E‐selectin, and ICAM‐1. Data are presented as mean ± SEM and analyzed using one‐way ANOVA followed by Bonferroni's multiple comparisons test. n = 4–5 independent cell cultures per group. **** p < 0.0001 vs. control.

Article Snippet: Human pulmonary artery microvascular endothelial cells (HMEC, American Type Culture Collection (ATCC)) were cultured in endothelial cell media as described above, in an incubator at 37°C with 5% CO 2 .

Techniques: Recombinant, Marker, Isolation, Control

Journal: The FASEB Journal

Article Title: SARS ‐ CoV ‐2 Nucleocapsid Protein Does Not Induce Inflammation in Endothelial Cells or Monocytes

doi: 10.1096/fj.202501433R

Figure Lengend Snippet: Effects of recombinant N‐protein (endotoxin nondepleted, NPnon) on inflammatory marker mRNA levels in mouse microvascular endothelial cells. Cells were treated with vehicle, LPS (1 μg/mL), NPnon (10 μg/mL, ThermoFisher), LPS + polymyxin B (PMB) (1.25 mg/mL), NPnon + PMB (250 μg/mL), or PMB (250 μg/mL) for 4 h. The total RNA was isolated and qPCR analysis was performed to measure the mRNA levels of TNFα, IL‐6, E‐selectin, and ICAM‐1. Data are presented as mean ± SEM and analyzed using one‐way ANOVA followed by Bonferroni's multiple comparisons test. n = 5 independent cell cultures per group. *** p < 0.001, ** p < 0.01 vs. control.

Article Snippet: Human pulmonary artery microvascular endothelial cells (HMEC, American Type Culture Collection (ATCC)) were cultured in endothelial cell media as described above, in an incubator at 37°C with 5% CO 2 .

Techniques: Recombinant, Marker, Isolation, Control

Journal: The FASEB Journal

Article Title: SARS ‐ CoV ‐2 Nucleocapsid Protein Does Not Induce Inflammation in Endothelial Cells or Monocytes

doi: 10.1096/fj.202501433R

Figure Lengend Snippet: Effects of endotoxin‐depleted N‐protein (NPd) on inflammatory marker mRNA levels in mouse microvascular endothelial cells. Cells were treated with vehicle, LPS (1 μg/mL), NPd (50 μg/mL), NPd + PMB (250 μg/mL), or PMB (250 μg/mL) alone (control) for 4 h. Total RNA was isolated and RT‐qPCR analysis was performed to measure mRNA levels of TNFα and E‐selectin. Data are presented as mean ± SEM and analyzed using one‐way ANOVA followed by Bonferroni's multiple comparisons test. n = 3 independent cell cultures per group. *** p < 0.001, ** p < 0.01 vs. control.

Article Snippet: Human pulmonary artery microvascular endothelial cells (HMEC, American Type Culture Collection (ATCC)) were cultured in endothelial cell media as described above, in an incubator at 37°C with 5% CO 2 .

Techniques: Marker, Control, Isolation, Quantitative RT-PCR

Journal: Frontiers in Medicine

Article Title: Serum from patients with cirrhosis undergoing liver transplantation induces permeability in human pulmonary microvascular endothelial cells ex vivo

doi: 10.3389/fmed.2024.1412891

Figure Lengend Snippet: Example plots of transendothelial resistance of human pulmonary microvascular endothelial cells (HPMECs) after stimulation with 5% human serum from healthy subjects (red) or one liver transplant patient (S1–S4, see legend). Measurements were obtained at 4,000 Hz using the ECIS ZΘ system. Resistance was normalized to the plateau value obtained just prior to stimulation at time = 0. (A) HPMECs from a 24-year-old male endothelial cell donor. (B) HPMECs from a 57-year-old female endothelial cell donor. Each plot is obtained from one experiment with all wells measured simultaneously on a 96-well plate. The error bars indicate the SD of three replicate wells. The arrows indicate the peak permeability effect.

Article Snippet: Primary human pulmonary artery microvascular endothelial cells from one male (24 years old) and one female (57 years old) cadaver were purchased (PromoCell GmbH, Heidelberg, Germany) and used at passages 3–6.

Techniques: Permeability

Journal: Frontiers in Medicine

Article Title: Serum from patients with cirrhosis undergoing liver transplantation induces permeability in human pulmonary microvascular endothelial cells ex vivo

doi: 10.3389/fmed.2024.1412891

Figure Lengend Snippet: Violin plot of the permeability response (ΔAUC) of human pulmonary microvascular endothelial cells (HPMECs) stimulated with serum from liver transplant patients at the indicated time points. S1, start of surgery; S2, end of the dissection phase; S3, 15 min after portal vein reperfusion; S4, 60 min after portal vein reperfusion; and S5, 120 min after portal vein reperfusion or the end of surgery. Each point represents a different LT serum. The dark-colored bands on the violins indicate the median. The red asterisks indicate the results of the one-sample Wilcoxon signed-rank tests versus zero, the value of ΔAUC that indicates no difference from pooled healthy serum (red dotted line). (A) HPMECs from a 24-year-old male endothelial cell donor. (B) HPMECs from a 57-year-old female endothelial cell donor. The braces indicate the results of Wilcoxon matched-pairs signed-rank tests between S1 and S3. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001.

Article Snippet: Primary human pulmonary artery microvascular endothelial cells from one male (24 years old) and one female (57 years old) cadaver were purchased (PromoCell GmbH, Heidelberg, Germany) and used at passages 3–6.

Techniques: Permeability, Dissection

Journal: Frontiers in Medicine

Article Title: Serum from patients with cirrhosis undergoing liver transplantation induces permeability in human pulmonary microvascular endothelial cells ex vivo

doi: 10.3389/fmed.2024.1412891

Figure Lengend Snippet: Scatter plots of the permeability response (ΔAUC) of human pulmonary microvascular endothelial cells (HPMECs) to liver transplant sera collected at the start of surgery (S1) as a function of the model for end-stage liver disease—sodium (MELD-Na) score. (A) HPMECs from a 24-year-old male endothelial cell donor. There is a negative association between the MELD-Na score and ΔAUC ( F (1, 23) = 17.29, p = 0.0004), with an R 2 of 0.43 and a slope of −0.016 (95% CI -0.023 to −0.008). (B) HPMECs from a 57-year-old female endothelial cell donor. There is no association between the MELD-Na score and ΔAUC ( F (1, 23) = 0.16, p = 0.69), with an R 2 of 0.007 and a slope of 0.007 (95% CI -0.018 to 0.012). Black line, best-fit linear regression; red dotted line, value of ΔAUC for serum pooled from healthy adult men.

Article Snippet: Primary human pulmonary artery microvascular endothelial cells from one male (24 years old) and one female (57 years old) cadaver were purchased (PromoCell GmbH, Heidelberg, Germany) and used at passages 3–6.

Techniques: Permeability

Journal: Frontiers in Medicine

Article Title: Serum from patients with cirrhosis undergoing liver transplantation induces permeability in human pulmonary microvascular endothelial cells ex vivo

doi: 10.3389/fmed.2024.1412891

Figure Lengend Snippet: Association of human pulmonary microvascular endothelial cells (HPMEC) permeability response (ΔAUC) with the type of liver donor and time point during liver transplantation. S1, start of surgery; S3, 15 min after portal vein reperfusion. HPMEC line A is derived from a 24-year-old man and HPMEC line B is derived from a 57-year-old woman. The red dotted line indicates the value of ΔAUC for serum pooled from healthy adult men; gray bars indicate the median of each group. Brackets and p -values indicate the results of Mann–Whitney U -tests.

Article Snippet: Primary human pulmonary artery microvascular endothelial cells from one male (24 years old) and one female (57 years old) cadaver were purchased (PromoCell GmbH, Heidelberg, Germany) and used at passages 3–6.

Techniques: Permeability, Transplantation Assay, Derivative Assay, MANN-WHITNEY

Journal: Frontiers in Medicine

Article Title: Serum from patients with cirrhosis undergoing liver transplantation induces permeability in human pulmonary microvascular endothelial cells ex vivo

doi: 10.3389/fmed.2024.1412891

Figure Lengend Snippet: Transendothelial resistance of human pulmonary microvascular endothelial cells (HPMECs) after stimulation with human serum (5%) in patients with notable clinical courses. (A,B) Treatment of HPMECs from a 57-year-old female endothelial cell donor with serum from two patients on preoperative dialysis. (C) Treatment of HPMECs from a 24-year-old male endothelial cell donor with serum from an LT patient who experienced a 70-min warm ischemia time of the liver graft. The arrows indicate the peak permeability effect.

Article Snippet: Primary human pulmonary artery microvascular endothelial cells from one male (24 years old) and one female (57 years old) cadaver were purchased (PromoCell GmbH, Heidelberg, Germany) and used at passages 3–6.

Techniques: Permeability

Journal: Cells

Article Title: PTPN1 Deficiency Modulates BMPR2 Signaling and Induces Endothelial Dysfunction in Pulmonary Arterial Hypertension.

doi: 10.3390/cells12020316

Figure Lengend Snippet: Figure 2. PTPN1 deficiency induced endothelial dysfunction in PAECs. (A) siRNA-mediated knockdown of PTPN1 showed decreased PAEC viability, as assessed by MTT assay and hemocytome- ter countings. (B) PTPN1 silencing induced apoptosis, as evidenced by increased caspase 3/7 levels in PAECs. (C) PTPN1 silencing decreased ability of PAEC tube formation in a Matrigel tube formation assay. Angiogenesis was quantified in the images using ImageJ software. Total tube lengths were presented in µm. The number of nodes were counted in the analyzed area. Scale bar = 1000 µm. Data represented as mean ± SEM (n = 3–6), student t-test. * p < 0.05, *** p < 0.001.

Article Snippet: Human healthy primary pulmonary arterial endothelial cells (PAECs) were purchased from PromoCell GmbH, Heidelberg, Germany (Cat # C12281).

Techniques: Knockdown, MTT Assay, Tube Formation Assay, Software

Journal: Cells

Article Title: PTPN1 Deficiency Modulates BMPR2 Signaling and Induces Endothelial Dysfunction in Pulmonary Arterial Hypertension.

doi: 10.3390/cells12020316

Figure Lengend Snippet: Figure 3. PTPN1 is downregulated in healthy human PAECs exposed to hypoxia and in the lung sugen5416/hypoxia-induced PH rats. (A) 150,000 PAECs were seeded onto 6-well plates and exposed to 72 h of hypoxia. After that, PTPN1 expression was measured by qRT-PCR. Induction of hypoxia was verified by measuring VEGF expression by qRT-PCR [20]. (B,C) PTPN1 mRNA and protein expression was also measured in the lung of sugen5416/hypoxia rate models by qRT-PCR and western blotting (please see the PH model description and phenotypes data in [8]). Data are represented as mean ± standard error mean, n = 3–5; student t-test was performed to compare data between two samples. **** p < 0.0001. ns, not significant.

Article Snippet: Human healthy primary pulmonary arterial endothelial cells (PAECs) were purchased from PromoCell GmbH, Heidelberg, Germany (Cat # C12281).

Techniques: Expressing, Quantitative RT-PCR, Western Blot

Journal: Cells

Article Title: PTPN1 Deficiency Modulates BMPR2 Signaling and Induces Endothelial Dysfunction in Pulmonary Arterial Hypertension.

doi: 10.3390/cells12020316

Figure Lengend Snippet: Figure 4. PTPN1 is downregulated in the blood but not in the PAECs of PAH patients. We ana- lyzed RNA-seq data of PTPN1 expression in the whole blood ((n = 72 healthy and n = 359 PAH), for subject characteristics, please see [22]) (A) and in PAECs (n = 9/group, (GSE0126262, [23])) of PAH patients (B). TPM values for PTPN1 expression is shown in the graphs. PTPN1 was correlated with expression of BMPR2, SMAD5, and SMAD9 in healthy and PAH PAECs (GSE0126262) (C–E).

Article Snippet: Human healthy primary pulmonary arterial endothelial cells (PAECs) were purchased from PromoCell GmbH, Heidelberg, Germany (Cat # C12281).

Techniques: RNA Sequencing, Expressing

Journal: Cells

Article Title: PTPN1 Deficiency Modulates BMPR2 Signaling and Induces Endothelial Dysfunction in Pulmonary Arterial Hypertension.

doi: 10.3390/cells12020316

Figure Lengend Snippet: Figure 5. Correlation of PTPN1 expression with SMAD1 and ID1 in PAECs collected from healthy and PAH patients (GSE0126262). PTPN1 expression was not significantly correlated with SMAD1 (A) and ID1 (B) in the PAECs of PAH patients and healthy controls.

Article Snippet: Human healthy primary pulmonary arterial endothelial cells (PAECs) were purchased from PromoCell GmbH, Heidelberg, Germany (Cat # C12281).

Techniques: Expressing