Objective: To observe the effect of rosiglitazone on the production of nitric oxide (NO) and the expression of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) /the endothelial nitric oxide synthase (eNOS) in cultured human umbilical vein endothelial cells(HUVECs), and to investigate the mechanism of signal transduction of rosiglitazone in improving the endothelial function.
Methods: HUVECs were treated with various concentrations of rosiglitazone. The NO level was measured using Griess Reaction in cell culture supernatants; the expressions of PI3K-, PKB- and eNOS mRNA were measured using RT-PCR; and the expressions of PKB, eNOS, and phosphorylation of PKB-Ser473, eNOS-Ser1177 were measured using Western Blot.
Results: Rosiglitazone increased the endothelial NO production in a dose- and time-dependent manner in cultured HUVECs, and also increased the expression of PI3K mRNA and the phosphorylation of PKB-Ser473 and eNOS-Ser1177 in a concentration-dependent manner, with no alteration in the expression of PKB and eNOS in cultured HUVECs. N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone.
Conclusion: Treatment with rosiglitazone can increase the NO production and improve the endothelial function through up-regulating the PI3K/PKB/eNOS signal pathways in cultured HUVECs.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
[Xinfeng Capsule alleviates RA-FLS-induced angiogenesis in HUVEC cells by inhibiting the lncRNA HOTAIR/PI3K/AKT pathway].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
December 2024
Department of Rheumatology, First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031, China.
Objective To investigate the effect of serum containing Xinfeng capsule (XFC) on the angiogenesis of human umbilical vein endothelial cells (HUVEC) induced by rheumatoid arthritis fibroblast-like synoviocytes (RA-FLS) and its mechanism of action. Methods An in vitro co-culture model of RA-FLS and HUVEC was established. Serum containing XFC was prepared by oral gavage of SD rats.
View Article and Find Full Text PDFInhibiting autophagy selectively prunes dysfunctional tumor vessels and optimizes the tumor immune microenvironment.
Theranostics
January 2025
State Key Laboratory of Biotherapy and Cancer Center, West China Hospital, Sichuan University, and Collaborative Innovation Center for Biotherapy, Chengdu, Sichuan Province, People's Republic of China.
Dysfunctional tumor vasculature, hypoxia, and an immunosuppressive microenvironment are significant barriers to effective cancer therapy. Autophagy, which is critical for maintaining cellular homeostasis and apoptosis resistance, is primarily triggered by hypoxia and nutrient deprivation, conditions prevalent in dysfunctional tumor vessels due to poor circulation. However, the role of autophagy in dysfunctional tumor endothelial cells and its impact on treatment and the tumor microenvironment (TME) remain poorly understood.
View Article and Find Full Text PDFCo-culture of natural killer cells and tumor spheroids on a heterogeneous multilayer paper stack.
J Zhejiang Univ Sci B
December 2024
Key Laboratory of Luminescence Analysis and Molecular Sensing, Ministry of Education, Institute for Clean Energy and Advanced Materials, School of Materials and Energy, Southwest University, Chongqing 400715, China.
Multilayer paper-based cell culture, as an in vitro three-dimensional (3D) cell culture method, has been frequently used to research drug bioavailability, therapeutic efficacy, and dose-limiting toxicity in malignant tumors. This paper proposes a heterogenous multilayer paper stacking co-culture system to establish a model of natural killer (NK) cells moving through the endothelium layer and attacking tumor spheroids. This system consists of three layers: a bottom tumor-spheroid layer, a middle invasion layer, and a top endothelium layer.
View Article and Find Full Text PDFAtorvastatin Attenuates Endothelial Cell Injury in Atherosclerosis Through Inhibiting ACSL4-Mediated Ferroptosis.
Cardiovasc Ther
January 2025
Department of Cardiology The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
This study is aimed at investigating the effects of atorvastatin (ATV) on endothelial cell injury in atherosclerosis (AS) through inhibiting acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated ferroptosis. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to establish an in vitro model of AS. The cell viability, lactate dehydrogenase (LDH) release, apoptosis, and expression levels of apoptotic proteins were assessed.
View Article and Find Full Text PDFOncogene 5'-3' exoribonuclease 2 enhances epidermal growth factor receptor signaling pathway to promote epithelial-mesenchymal transition and metastasis in non-small-cell lung cancer.
Cytojournal
November 2024
Department of Respiratory and Critical Care Medicine, Wuyi County First People's Hospital, Jinhua, Zhejiang, China.
Objective: Epithelial-mesenchymal transition (EMT) and metastasis are the primary causes of mortality in non-small-cell lung cancer (NSCLC). 5'-3' exoribonuclease 2 (XRN2) plays an important role in the process of tumor EMT. Thus, this investigation mainly aimed to clarify the precise molecular pathways through which XRN2 contributes to EMT and metastasis in NSCLC.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!