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Hong Huang

Publications and source records attributed to Hong Huang.

34 records · Page 2Linked to original sources
PubMed2003

Overexpression of extracellular superoxide dismutase protects mice from radiation-induced lung injury.

PURPOSE: The purpose of this study was to determine if radiation-induced lung injury is associated with prolonged oxidative stress, and whether chronic overexpression of extracellular superoxide dismutase (EC-SOD) in the lung of transgenic mice protects against radiation-induced lung injury. METHODS AND MATERIALS: Whole-lung radiation was delivered to EC-SOD overexpressing B6C3 transgenic (XRT-TG) mice and wild-type littermates (XRT-WT). Pulmonary function was assessed by breathing frequency. Right lung wet weight was used as a gross indicator of lung damage. Histopathology was used to assess collagen deposition and tissue fibrosis according to an established grading system. Immunohistochemistry was used to stain and quantify the number of macrophages. ELISA was used to measure activated TGF-beta1. Oxidative stress was assessed by measuring lipid oxidation products (malondialic acid) by HPLC. RESULTS: Four of six XRT-WT mice required euthanasia at 15-19 weeks postradiation because of respiratory distress, whereas no XRT-TG mouse developed distress. All assessments of lung damage at 15-20 weeks postradiation were higher for XRT-WT mice compared with the XRT-TG mice, including breathing frequency (380 vs. 286 bpm, p <or= 0.0004), right lung weight (228 vs. 113 mg, p <or= 0.06), macrophage count (48 vs. 5 per 40x field, p <or= 0.06), and percent activated TGF-beta1 (37 vs. 11%, p <or= 0.06). Semiquantitative measures, including fibrosis and collagen deposition, were also higher for XRT-WT mice, with an exact Fisher p value of <or=0.03 for both variables. In addition, malondialic acid was elevated in XRT-WT mice 15-20 weeks after radiation delivery, and levels were lower in the XRT-TG mice (624 vs. 323 pmol/mg protein, p <or= 0.06). CONCLUSIONS: After radiation therapy, oxidative stress is present at 15-20 weeks after initial exposure, which correlates with the delayed clinical onset of radiation-induced lung damage. Overexpression of EC-SOD in transgenic mice appears to confer protection against this radiation-induced lung injury, with a corresponding decrease in oxidative stress. EC-SOD may be a potential therapeutic agent for radioprotection in the treatment of thoracic malignancies. Further investigation is needed to confirm and expand on the current results.

Animals↗
PubMed2003

A second-generation 99m technetium single photon emission computed tomography agent that provides in vivo images of the dopamine transporter in primate brain.

The dopamine transporter (DAT), located presynaptically on dopamine neurons, provides a marker for Parkinson's disease (Pd) and attention deficit hyperactivity disorder (ADHD). In ADHD, DAT density levels are elevated, while in Pd these levels are depleted. The depletion of DAT levels also corresponds with the loss of dopamine. We now describe the design, synthesis, biology, and SPECT imaging in nonhuman primates of second-generation (99m)technetium-based tropane ligands that bind potently and selectively to the DAT. We demonstrate that improved selectivity and biological stability allows sufficient agent to enter the brain and label the DAT in vivo to provide a quantitative measure of DAT density in nonhuman primates. We introduce FLUORATEC (N-[(2-((3'-N'-propyl-(1"R)-3"alpha-(4-fluorophenyl)tropane-2"beta-1-propanoyl)(2-mercaptoethyl)amino)acetyl)-2-aminoethanethiolato]technetium(V) oxide), a DAT imaging agent that has emerged from these studies and is now in phase 1 clinical trials in the U.S.

Animals↗
PubMed2003

Risk of long-term complications after TFG-beta1-guided very-high-dose thoracic radiotherapy.

PURPOSE: To report the incidence of late complications in long-term survivors of very-high-dose thoracic radiotherapy (RT) treated on a prospective clinical trial. METHODS AND MATERIALS: Patients with locally advanced or medically inoperable non-small-cell lung cancer received three-dimensional conformal RT to the primary tumor and radiographically involved lymph nodes to a dose of 73.6 Gy at 1.6 Gy twice daily. If the plasma transforming growth factor-beta1 (TGF-beta1) level was normal after 73.6 Gy, additional twice-daily RT was delivered to successively higher total doses until the maximal tolerated dose was reached. Patients within a given dose level were followed for 6 months before escalation to the next dose level was permitted. Late complications were defined according to Radiation Therapy Oncology Group/European Organization for Research and Treatment of Cancer criteria. RESULTS: Thirty-eight patients were enrolled between 1996 and 1999. Twenty-four patients were not eligible for radiation dose escalation beyond 73.6 Gy because of persistently abnormal TGF-beta1 levels. Fourteen patients received dose escalation (80 Gy in 8; 86.4 Gy in 6). Grade 3 or greater late complications occurred in 4 of 24, 1 of 8, and 2 of 6 patients treated to 73.6, 80, and 86.4 Gy, respectively. The corresponding patient numbers with late Grade 4-5 toxicity were 3 of 24, 0 of 6, and 0 of 8. Overall, 7 (18%) of the 38 patients developed Grade 3-5 late toxicity. Nonpulmonary complications predominated (4 of 7). Five (71%) of seven serious complications developed within 11 months after RT; however, the remaining two complications (29%) occurred very late (at 43 and 62 months). The 5-year actuarial risk of late Grade 3-5 complications was 33%. CONCLUSION: Long-term survivors of very-high-dose RT for non-small-cell lung cancer have a significant risk of severe treatment-related complications. At these high dose levels, the predominant toxicity may no longer be pulmonary. All Grade 4-5 complications occurred in patients whose dose was limited to 73.6 Gy because of a persistently elevated TGF-beta1. Thus, persistently elevated plasma TGF-beta1 levels toward the end of RT may identify patients at greatest risk of severe complications.

Adult↗
PubMed2003

Expression of P53, P21 in human lung adenocarcinoma A549 cell strains under hypoxia conditions and the effect of TSA on their expression.

This paper was designed to investigate the expression of p53, p21 of A549 cell strains under hypoxic condition and the effect of trichostatin A (TSA), the inhibitor of histone deacetylasel (HDAC1) on their expression. The authors designed 1 normoxia group (control group) and 6 hypoxia groups (experimental group): hypoxia 6 h group (A), TSA+hypoxia 6 h (B), hypoxia 12 h group (C), hypoxia 24 h group (D), TSA+hypoxia 24 h (E), hypoxia 48 h group (F). The expression of HDAC1 in A549 cells was examined by using Western blot and the expression of p53, p21 in A549 cells and the effect of TSA on them were determined by using immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR). The A value expressed by HDAC1 in A549 cell strains was 138+/-11 in the control group, 78+/-4, 86+/-5, 124+/-3, 120+/-9 in experimental groups A, C, D, F, respectively. The A value of the expression of the protein and mRNA of p53 in A549 cell strains were 0.12+/-0.02, 0.62+/-0.02 in the control group, 0.10+/-0.03, 0.32 +/-0.03; 0.11+/-0.01, 0.33+/-0.02; 0.13+/-0.03, 0.58+/-0.01; 0.12+/-0.02, 0.56+/-0.02 in experimental group A, B, D, E, respectively. The A value of the expression of the protein and mRNA of p21 in A549 cell strains were 0.17+/-0.03, 0.62+/-0.03 in the control group, 0.16+/-0.02, 0.50+/-0.02; 0.14+/-0.02, 0.36+/-0.02; 0.15+/-0.03, 0.49+/-0.03; 0.13+/-0.02, 0.33+/-0.02 in experimental groups A, B, D, E, respectively. These results indicate that the expression of HDAC1 is regulated by hypoxia and the effect of TSA is closely related to the expression of P21 under hypoxia condition.

Adenocarcinoma↗
PubMed2003

Acute toxicity of benzene derivatives to the tadpoles (Rana japonica) and QSAR analyses.

Acute lethal toxicity (the negative logarithm of molar concentrations of 12 h acute median lethal, expressed as 12 h-log1/LC50) of 46 benzene derivatives to Rana japonica tadpoles was determined. 1-octanol/water partition coefficient (logKow)-dependent models were developed to study the toxicity of different categories chemicals. In an effort to model all chemicals, response surface analyses and stepwise multiple regression analyses were performed and successful models were obtained. A general and robust QSAR model was achieved with the combined application of variables reflecting hydrophobicity, electric property, and molecular size respectively (12h-log1/LC50 = 0.393logKow - 0.428Elumo + 0.0110Vol. + 1.362 n = 51, r2 = 0.834) using stepwise multiple regression analyses. Because of strong dissociation of carboxyl group greatly decreasing their observed toxicity, using logDow in instead of logKow the quality of the models is greatly improved. The conventional r2 and cross-validation r2(CV) were 0.914 and 0.785, respectively, indicating that QSAR was both internally consistent and highly predictive.

Animals↗
PubMed2003

Involvement of the mitochondrial pathway in cold storage and rewarming-associated apoptosis of human renal proximal tubular cells.

The cellular and molecular mechanisms of cold storage-ATN are not well characterized. In our earlier studies, cold storage caused necrosis of human proximal tubular epithelial (RPTE) cells, whereas apoptosis was prominent during rewarming. An intriguing finding was the pronounced swelling of the mitochondria in the cold, which promoted us to further characterize its role in rewarming-associated apoptosis. Human proximal tubular epithelial cells were cold stored in University of Wisconsin (UW) solution for 48 h followed by 24 h of rewarming in regular cell culture medium. During the cold storage, there was no significant change in the Bcl-2 to Bax protein ratio, mitochondrial location of cytochrome C or caspse-3 activity. However, during rewarming, the Bcl-2 to Bax ratio increased, cytochrome C was translocated to cytosol, and caspase-3 was activated: events and timing were consistent with the occurrence of apoptosis during rewarming. In a time-course experiment, mitochondrial swelling was discernable by electron microscopy as early as at 2 h. Cold storage of isolated-mitochondria for 2 h was attended by an increase in the opening of the permeability transition pores (PTP), suggesting PTP opening as an early mechanism for mitochondrial swelling. Addition of antioxidants (deferoxamine or 2-methyaminochroman) to the storage solution suppressed mitochondrial pore opening and swelling, Bcl-2 to Bax ratio increase, cytochrome C translocation, caspase-3 activation as well as rewarming-induced apoptosis. Our data demonstrate for the first time that apoptosis following cold storage and rewarming of human renal tubular cells is accompanied by specific mitochondrial events, and that these events and apoptosis can be suppressed by adding antioxidants to the cold storage solution.

Apoptosis↗
PubMed2003

Deferoxamine reduces cold-ischemic renal injury in a syngeneic kidney transplant model.

In cell-culture models, addition of deferoxamine (DFO) to University of Wisconsin Solution (UW solution) reduces cold-storage injury. The efficacy of DFO was therefore tested in a kidney transplantation model employing inbred Wistar Furth rats. Donor left kidneys, cold stored for 18 h in UW solution with or without 0.125 mM or 0.625 mM DFO were transplanted to the recipients' left renal fosse. Deferoxamine dose-dependently and significantly increased glomerular filtration rate (GFR) and renal blood flow (RBF), and suppressed renal F2-isoprostanes (vasoactive lipid peroxidation products) and apoptotic and necrotic injury 3 days post-transplantation. In a second set of similar experiments, the remaining native kidneys of the recipient rats were removed on day 7 of transplantation. Transplanted kidneys' function assessed by serum creatinine was 75% higher in the cold-stored transplanted kidneys treated with DFO compared with untreated kidneys. Moreover, the DFO treatment was attended by a significant reduction in apoptotic and necrotic tubular injury. Thus, our consistent findings from two sets of studies in a transplant model suggest that a simple strategy of including DFO in the cold-storage solution reduces cold ischemia-associated renal transplant damage and improves renal function. Our findings have potentially important ramifications for cold preservation of kidneys, and possibly other organs, in clinical transplantation.

Animals↗
PubMed2003

Integrin-mediated suppression of endotoxin-induced DNA damage in lung endothelial cells is sensitive to poly(ADP-ribose) polymerase-1 gene deletion.

Endotoxin (LPS) is a cause of adult respiratory distress syndrome (ARDS), a disease which is preceded by acute lung injury involving the pulmonary endothelium. Experimentally, LPS causes acute DNA strand breakage in mouse lung endothelial cells (MLEC). Engagement of integrin cell adhesion receptors inhibits acute DNA breakage, which could be of use in reducing lung injury. Because integrins presumably inhibit DNA damage or activate repair, we hypothesized that the DNA-damage response protein, poly(ADP-ribose) polymerase-1 (PARP-1), regulates the protective action of integrins, as well as sensitivity to LPS. Therefore, the effect of LPS on MLEC cultured from wild-type and PARP-1 knockout mice was determined. Fluorescence microscopic measures were used to assess plasma membrane integrity, PARP activity, DNA strand breakage and DNA repair in attached cells. LPS caused a concentration-dependent increase in the permeability of wild-type MLEC. Engagement of beta1 integrins with an antibody protected wild-type MLEC from this LPS-induced injury. Wild-type cells treated with the PARP-inhibitor, 3-aminobenzamide, and PARP-1 knockout MLEC were also resistant. LPS caused acute DNA breakage in both wild-type and knockout MLEC, but PARP was activated only in wild-type cells. LPS-induced DNA breakage was inhibited by 3-aminobenzamide, but not by knockout. Anti-beta1 integrin antibody also inhibited the DNA breakage and PARP activation caused by LPS in wild-type MLEC. However, integrin engagement did not prevent DNA breakage in PARP-1 knockout cells, despite a similar level of beta1 integrin in wild-type and knockout cells. Thus, integrin engagement, 3-aminobenzamide, and PARP-1 deletion protected MLEC from increases in membrane permeability caused by LPS. PARP-1 deletion also impaired the ability of integrin engagement to inhibit LPS-induced DNA breakage, suggesting that knockout may affect nuclear factors necessary for integrin-mediated suppression of LPS-induced DNA breakage.

Animals↗
PubMed2003

[HDAC1 expression and effect of TSA on proliferation and apoptosis of A549 cells].

BACKGROUND & OBJECTIVE: Histone deacetylase (HDAC) shows a high expression in many cancer cells and the inhibitor of HDAC1, trichostatin A (TSA), can inhibit the growth of cancer cells. Hypoxia is a common feature of malignant tumors. This paper was designed to investigate the expression of HDAC1 of A549 cell strains in hypoxia condition and the effect of TSA on their proliferation and apoptosis. METHODS: The authors designed 1 normoxia group (control group) and 5 hypoxia groups (test groups): hypoxia 6h group (A), TSA + hypoxia 6h (B), hypoxia 12h group (C), hypoxia 24h group (D), TSA + hypoxia 24h (E), hypoxia 48h group (F). The expression of HDAC1 in A549 cells was examined using Western blot analysis. Proliferation, the apoptotic rates of A549 cells and the effect of TSA on them were determined using MTT method, immunohistochemistry, TUNEL method, and flow cytometry. The expression of mRNA of HDAC1 and the effect of TSA on it were determined using reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The A values expressed by HDAC1 in A549 cell strains were 138+/-11 in the control group, 78+/-4, 86+/-5, 124+/-3, and 120+/-9 in test groups A, C, D, and F, respectively. The A values of HDAC1mRNA versus the A values of beta-Atin mRNA were 0.68+/-0.03 in the control group, 0.46+/-0.03, 0.45+/-0.02, 0.70+/-0.03, and 0.33+/-0.02 in test groups A, C, D, and F, respectively. The A values of the expression of PCNA in A549 cell strains were 0.13+/-0.03 in the control group, 0.10+/-0.02, 0.11+/-0.02, 0.16+/-0.02, and 0.11+/-0.03 in test groups A, B, D, and E, respectively. The A values of MTT in A549 cell strains were 0.50+/-0.06 in the control group, 0.41+/-0.04, 0.45+/-0.03, 0.59+/-0.02, and 0.45+/-0.03 in test groups A, B, D, and E, respectively. The A values of positive cells of apoptosis in A549 cell strains were 0.16+/-0.04 in the control group, 0.18+/-0.02, 0.18+/-0.05, 0.20+/-0.05, and 0.23+/-0.05 in test groups A, B, D, and E, respectively. The apoptotic rates in A549 cells were 1.11% in the control group, 18.91%,14.30%, 36.99%, and 51.92% in test groups A, B, D, and E, respectively. CONCLUSION: The expression of HDAC1 plays an important role in the proliferation and apoptosis of A549 cells, which is regulated by hypoxia. TSA may serve as a new target for therapy of lung cancer.

Apoptosis↗
PubMed2003

[Heterogeneity of human breast cancer cells and their biological behavior].

OBJECTIVE: To investigate the heterogeneity of human breast cancer cells, their influence on biological behavior of tumor cells and clinical implications. METHODS: The subpopulations of MCF-7 breast cancer cells were isolated by Percoll gradient centrifugation. DNA content and cell cycle distribution were detected with flow cytometry. Tumor chemosensitivity analysis was performed with MTT assay. RESULTS: Heterogeneity was observed in DNA content and cell cycle distribution among four subpopulations of breast cancer cells, which were related to their proliferation ability and chemosensitivity results. CONCLUSION: Hereditary instability and intrinsic characteristics of most tumor cells, not only lead to tumor progression and heterogeneity but also cause the loss of monoclonality and the generation of subclones. Further study on some profiles of tumor heterogeneity such as DNA content, cell cycle distribution and their influence on tumor proliferation and chemosensitivity may very well improve the clinical treatment.

Breast Neoplasms↗
PubMed2003

Experimental study on cheng zai wan for treatment of necrosis of the femoral head.

Cheng Zai Wan ([symbol: see text]), a Chinese herbal preparation was administrated in the two-leg rat model of aseptic necrosis of the femoral head established by taking prednisone acetate for a long period and the osteoporosis model rat by castration in order to explore the effects of the prescription on necrosis of the femoral head. The results showed that after treatment, the pitting on the surface of the femoral head disappeared, the reticular structure with filling cells was restored; the fat droplets in bone cells or cartilage cells of the femoral head were significantly reduced; sparse capillaries were improved, density and width of the bone trabecula were increased somewhat; bone mineral density, bone weight, bone strength and rigidity were significantly increased; and the low level of estrin was improved. It is suggested that Cheng Zai Wan has definite therapeutic effects on aseptic necrosis of the femoral head.

Animals↗
PubMed2002

Vasodilator response assessment in porcine myocardium with magnetic resonance relaxometry.

BACKGROUND: This research describes an early preclinical study of the biophysical mechanisms governing changes in myocardial T2 during vasodilation in normal myocardium. METHODS AND RESULTS: Theoretical modeling and experimental studies in an instrumented pig model (n=7) provided measures of changes in myocardial T2, relative blood volume (BV), and microcirculation oxygen levels (%O2) during intracoronary adenosine infusion. Intracoronary adenosine increases perfusion without increasing blood volume or cardiac metabolic rate; thus, T2 elevations should reflect elevated microcirculation oxygen levels. Robust strategies were used for magnetic resonance imaging (MRI) data collection. Measures of myocardial and vascular T1 before and after Clariscan (Amersham Health) injection provided blood volume assessment. Changes in microcirculation oxygen levels were estimated via direct blood sampling from the left anterior descending (LAD) coronary vein. Perfusion changes were monitored using a Doppler flow wire within the left main coronary artery. Myocardial T2 elevations (DeltaT2=17+/-8%) within the LAD arterial perfusion bed were related to elevations in perfusion (coronary velocity reserve=3.2+/-0.4) and coronary venous %O2 [Delta(LAD CV%O2) =56+/-11%], whereas blood volume (DeltaBV=0 +/-2%) and cardiac metabolic rate [Delta(heart rate x blood pressure) = -4+/-11%] remained constant. CONCLUSIONS: Myocardial T2 elevation during intracoronary adenosine infusion was significant and repeatable, caused by increases in microcirculation oxygen levels. Changes in microcirculation oxygen levels of approximately 40%O2 should be detectable by this technique. This sensitivity should suffice for differentiating normal from abnormal myocardium via measurement of myocardial perfusion reserve.

Adenosine↗
PubMed2002

Cold induces catalytic iron release of cytochrome P-450 origin: a critical step in cold storage-induced renal injury.

Earlier experimental studies have suggested a role for iron in cold-storage-induced organ injury. Whether the cytochrome P-450 enzymes, shown to be a source for iron in several injury models, contribute to cold-induced iron release is not known. Storage of human proximal tubular epithelial (RPTE) cells at 4 degrees C in the University of Wisconsin (UW) solution caused a significant and time-dependent increase in bleomycin-detectable iron (BDI). To identify the cellular source of BDI, RPTE cells were subfractionated and stored at 4 degrees C for 4 h. Bleomycin-detectable iron release was highest in the microsomes, next in the cytosol and none in the mitochondria. As microsomes are rich in iron-containing cytochrome P-450 enzymes, microsomes were cold stored with P-450 inhibitors, cimetidine and piperonyl butoxide. P-450 inhibitors significantly reduced cold-induced BDI release. Furthermore, cimetidine and iron chelator deferoxamine (DFO) significantly reduced cold-induced cell injury, suggesting a role for P-450-derived iron in cold-induced cell injury. In rat kidney experiments, BDI and LDH release were significantly higher in cold-stored kidneys than in control kidneys. Inclusion of cimetidine and DFO in the cold-storage solution significantly suppressed the BDI and LDH release, and reduced the ultrastructural changes. Our data demonstrate for the first time that cold-induced catalytic iron release may be at least in part of microsomal cytochrome P-450 origin, and that it participates in cold-storage-induced renal injury. In the clinical setting, sequestering free iron released during cold storage is possible and may prove to be useful in limiting organ injury.

Adenosine↗
PubMed2002

The abnormal expression of retinoic acid receptor-beta, p 53 and Ki67 protein in normal, premalignant and malignant esophageal tissues.

AIM: Esophageal cancer remains a significant health problem worldwide. It is important to investigate alterations in expression of retinoic acid receptor-beta, p 53 and Ki67 proteins in esophageal carcinogenesis. METHODS: To find biomarkers for early identification of esophageal cancer, we analyzed the retinoic acid receptor-beta, p 53 protein and the proliferation marker Ki67 in surgical specimens of normal, mildly, and severely dysplastic and malignant esophageal tissues by in situ hybridization of RNA and immunohistochemistry. RESULTS: RAR-beta was expressed in 94.3%(33/35) of normal mucosae, 67.8%(19/28) of the mild, 58.1% (18/31) of the severe lesions and 53.2%(116/218) of tumor samples. RAR-beta mRNA was expressed in 62.7%(42/67), 55.1%(43/78) and 29.2%(7/24) of well, moderated and poorly differentiated SSCs. The p 53 and Ki67 proteins were 5.9%(2/34) of the normal mucosa. P53 and Ki67 stained positively in 10.7%(3/28) and 21.4% (6/28) of mild dysplasia, and 51.6%(16/31) and 58.1% (18/31) of severely dysplasia respectively. Samples from esophageal cancer showed no higher levers of p 53 and Ki67 expression than seen in severely dysplastic lesions. There was significant difference of RAR-beta p 53 and Ki67 expression between normal mucosa and dysplastic tissue or esophageal cancer. CONCLUSION: Loss of RAR-beta expression and accumulation of p 53 and Ki67 proteins may serve as biomarkers for early identification of esophageal cancer in the high-risk populations.

Biomarkers, Tumor↗
PubMedDate not supplied

An efficient, nonenzymatic method for isolation and culture of murine aortic endothelial cells and their response to inflammatory stimuli.

Given the utility of murine models and the physiological and pathological significance of the aortic endothelium, we developed a simplified, nonenzymatic method for isolation and culture of murine aortic endothelial cells (MAECs). Aortic explants were initially cultured on fibronectin-coated plastic. Murine aortic endothelial cells migrated from the explants and proliferated. This expansion allowed for cultures to be established from the aortas of one or three mice. Murine aortic endothelial cells were then purified from expanded cultures by fluorescence-activated cell sorting for the uptake of 1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate-labeled acetylated low-density lipoprotein. The majority of the cells in expanded cultures were as positive as human umbilical vein endothelial cells labeled in the same way. The most positive half of the labeled MAEC population was placed back in culture, and the cells formed "cobblestone" monolayers at confluence. Smooth muscle alpha-actin, which was present in aortic tissue and to a lesser extent in explant cultures before sorting, was not detected in selected MAECs. Western blotting and immunostaining also demonstrated the presence of the endothelial markers, platelet endothelial cell adhesion molecule-1, factor VIII-related antigen, and Bandeiraea simplicifolia lectin 1 binding. Murine aortic endothelial cells retained expected inflammatory functions: vascular cell adhesion molecule-1 protein was induced by bacterial endotoxin, and NO production was synergistically induced by the combination of endotoxin and interferon-gamma. Our simple, efficient method will facilitate investigations of aortic endothelial cell function in vitro using murine models.

Animals↗