scholarly journals Fluidization, resolidification, and reorientation of the endothelial cell in response to slow tidal stretches

2012 ◽  
Vol 303 (4) ◽  
pp. C368-C375 ◽  
Author(s):  
Ramaswamy Krishnan ◽  
Elizabeth Peruski Canović ◽  
Andreea L. Iordan ◽  
Kavitha Rajendran ◽  
Greeshma Manomohan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Mechanical Stretch ◽  
Vascular Endothelial ◽  
Cell Mapping ◽  
Traction Forces ◽  
Morphological Response ◽  
Umbilical Vein Endothelial Cells

Mechanical stretch plays an important role in regulating shape and orientation of the vascular endothelial cell. This morphological response to stretch is basic to angiogenesis, neovascularization, and vascular homeostasis, but mechanism remains unclear. To elucidate mechanisms, we used cell mapping rheometry to measure traction forces in primary human umbilical vein endothelial cells subjected to periodic uniaxial stretches. Onset of periodic stretch of 10% strain amplitude caused a fluidization response typified by attenuation of traction forces almost to zero. As periodic stretch continued, the prompt fluidization response was followed by a slow resolidification response typified by recovery of the traction forces, but now aligned along the axis perpendicular to the imposed stretch. Reorientation of the cell body lagged reorientation of the traction forces, however. Together, these observations demonstrate that cellular reorientation in response to periodic stretch is preceded by traction attenuation by means of cytoskeletal fluidization and subsequent traction recovery transverse to the stretch direction by means of cytoskeletal resolidification.

scholarly journals Proteome-Scale Profiling Reveals MAFG and MAFF as Two Novel Candidate Key Transcription Factors Involved in Palmitic acid Induced Umbilical Vein Endothelial Cells Apoptosis

2020 ◽  
Author(s):  
Mangyuan Wang ◽  
Fen Liu ◽  
Binbin Fang ◽  
Qiang Huo ◽  
Yining Yang
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
P Value ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Family Protein ◽  
Umbilical Vein Endothelial Cells

Abstract Backgrounds: Vascular endothelial cell apoptosis is the first risk factor of atherosclerosis (AS), and it can be induced by high doses of glucose and palmitic acid (PA). The purpose of our study is to use a new generation of high-throughput transcription factors (TFs) detecting method to identify novel candidate key TFs involved in PA-induced vascular endothelial cell apoptosis.Methods: Human umbilical vein endothelial cells (HUVECs) were treated with 0µM PA (control group), 250µM PA (group 1), or 500µM PA (group 2). Candidate TFs among the three groups were determined by significant changes according to t-test, and pathway enrichment, western blot (WB) and RT-qPCR were then performed.Results: Fifty-one TFs showing with significant p value were identified, and 24 TFs with significant p value plus fold change > 2 and with dose-dependence were identified with 12 TFs biologically validated in former studies. Two of the remaining 12 novel TFs, v-maf musculoaponeurotic fibrosarcoma oncogene family protein G (MAFG) and v-maf musculoaponeurotic fibrosarcoma oncogene family protein F (MAFF), were matched to AS known signalling pathways and were validated by WB and RT-qPCR in our study.Conclusions: We identified MAFG and MAFF as novel candidate key TFs in vascular endothelial cell apoptosis, which is the key initial process of AS.

scholarly journals miR-101-3p induces vascular endothelial cell dysfunction by targeting tet methylcytosine dioxygenase 2

2020 ◽  
Vol 52 (2) ◽  
pp. 180-191 ◽  
Author(s):  
Qiaoli Chen ◽  
Xiaoye Li ◽  
Lingjun Kong ◽  
Qing Xu ◽  
Zi Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Nuclear Factor Κb ◽  
Vascular Endothelial ◽  
Ros Production ◽  
Cell Dysfunction ◽  
Umbilical Vein Endothelial Cells

Abstract Endothelial cell (EC) dysfunction represents an early key event in atherosclerosis. Recently, MicroRNAs have been demonstrated to regulate EC function. miR-101-3p has been discovered to regulate cell apoptosis and proliferation in cardiovascular diseases. Therefore, the aim of the current study was to clarify whether miR-101-3p regulates the dysfunction of vascular endothelial cells. In this study, the transfection of human umbilical vein endothelial cells (HUVECs) with miR-101-3p mimic induced reactive oxygen species (ROS) production, EC dysfunction, and activated nuclear factor-κB (NF-κB), whereas transfection with miR-101-3p inhibitor alleviated these events. The antioxidant N-acetylcysteine alleviated miR-101-3p-induced EC dysfunction. Moreover, we observed that miR-101-3p inhibited the expression of tet methylcytosine dioxygenase 2 (TET2) at the posttranscriptional level, resulting in increased ROS production and activated NF-κB. TET2 overexpression inhibited ROS production, EC dysfunction, and NF-κB activation in miR-101-3p-transfected HUVECs. These results indicate that miR-101-3p induces EC dysfunction by targeting TET2, which regulates ROS production, EC dysfunction, and NF-κB activation. Taken together, our current study reveals a novel pathway associated with EC dysfunction. The modulation of miR-101-3p and TET2 expression levels may serve as a potential target for therapeutic strategies for atherosclerosis.

scholarly journals Anti-inflammatory Effect of Salvia Miltiorrhiza is Mediated via IL-6, JAK, and STAT Pathway in a Dysfunctional Vascular Endothelial Cell

2021 ◽  
Vol 8 (3) ◽  
pp. 1-12
Author(s):  
Emmanuel Adikwu Orgah
Keyword(s):  
Diabetes Mellitus ◽  
Signal Transduction ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Salvia Miltiorrhiza ◽  
Vascular Endothelial Cell ◽  
Vascular Complication ◽  
Vascular Endothelial ◽  
Extracellular Medium

The vascular complication of diabetes mellitus is a problem for the patient, and the ability to cope with the disease and the associated inflammation is a critical aspect of diabetes. Cytokines-induced inflammation in vascular endothelial cells (VECs) plays an active role in chronic diseases such as atherosclerosis, diabetes mellitus, kidney injury, and stroke. We investigated the role of total salvianolic acids (TSA), total tanshinones (TTSN), and their combination (TSA/TTSN) on the activated vascular endothelial cell and its inhibitory effect on signal transduction and cytokines regulation. In the extracellular medium of the injury model of human umbilical vein endothelial cells (HUVECs) induced by thrombin, the human IL-6, VCAM-1, and ICAM-1 were significantly elevated (p ˂ 0.05). However, suppression in the TSA, TTSN, and TSA/TTSN (100 µg/L)-treated groups (p > 0.05) were notable. TSA alone but not TTSN and TSA/TTSN combination, inhibited the expression of P-selectin (p < 0.05) and E-selectin (p < 0.01) respectively, in VECs. Western blot analysis showed JAK and STAT expression in VECs however, the protein expression was modest in the Salvia miltiorrhiza-treated groups, indicating the potential of TSA/TTSN in the inflammatory pathways of IL-6, JAK, and STAT signal transduction in endothelial cells (ECs). This study has made novel observations regarding the components of Salvia miltiorrhiza regulatory effect on cytokines in Vascular Biology. Keywords: Atherosclerosis; Cytokines; Diabetes mellitus; HUVECs; Inflammation; Salvia militiorrhiza.

scholarly journals Co-Culture of Osteoblasts and Endothelial Cells on a Microfiber Scaffold to Construct Bone-Like Tissue with Vascular Networks

Materials ◽  
2019 ◽  
Vol 12 (18) ◽  
pp. 2869 ◽  
Author(s):  
Kouki Inomata ◽  
Michiyo Honda
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Osteoblastic Differentiation ◽  
Culture Conditions ◽  
Immunofluorescent Staining ◽  
Vascular Endothelial ◽  
Vascular Networks ◽  
Umbilical Vein Endothelial Cells ◽  
Hard Tissue Engineering

Bone is based on an elaborate system of mineralization and vascularization. In hard tissue engineering, diverse biomaterials compatible with osteogenesis and angiogenesis have been developed. In the present study, to examine the processes of osteogenesis and angiogenesis, osteoblast-like MG-63 cells were co-cultured with human umbilical vein endothelial cells (HUVECs) on a microfiber scaffold. The percentage of adherent cells on the scaffold was more than 60% compared to the culture plate, regardless of the cell type and culture conditions. Cell viability under both monoculture and co-culture conditions was constantly sustained. During the culture periods, the cells were spread along the fibers and extended pseudopodium-like structures on the microfibers three-dimensionally. Compared to the monoculture results, the alkaline phosphatase activity of the co-culture increased 3–6 fold, whereas the vascular endothelial cell growth factor secretion significantly decreased. Immunofluorescent staining of CD31 showed that HUVECs were well spread along the fibers and formed microcapillary-structures. These results suggest that the activation of HUVECs by co-culture with MG-63 could enhance osteoblastic differentiation in the microfiber scaffold, which mimics the microenvironment of the extracellular matrix. This approach can be effective for the construction of tissue-engineered bone with vascular networks.

scholarly journals KDR activation is crucial for VEGF165-mediated Ca2+mobilization in human umbilical vein endothelial cells

1999 ◽  
Vol 276 (1) ◽  
pp. C176-C181 ◽  
Author(s):  
Sonia A. Cunningham ◽  
Tuan M. Tran ◽  
M. Pia Arrate ◽  
Robert Bjercke ◽  
Tommy A. Brock
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Human Umbilical Vein ◽  
Intracellular Ca ◽  
Umbilical Vein Endothelial Cells

We have prepared a polyclonal mouse antibody directed against the first three immunoglobulin-like domains of the kinase insert domain-containing receptor (KDR) tyrosine kinase. It possesses the ability to inhibit binding of the 165-amino acid splice variant of vascular endothelial cell growth factor (VEGF165) to recombinant KDR in vitro as well as to reduce VEGF165binding to human umbilical vein endothelial cells (HUVEC). These results confirm that the first three immunoglobulin-like domains of KDR are involved in VEGF165interactions. The anti-KDR antibody is able to completely block VEGF165-mediated intracellular Ca2+mobilization in HUVEC. Therefore, it appears that binding of VEGF165to the fms-like tyrosine kinase (Flt-1) in these cells does not translate into a Ca2+response. This is further exemplified by the lack of response to placental growth factor (PlGF), an Flt-1-specific ligand. Additionally, PlGF is unable to potentiate the effects of submaximal concentrations of VEGF165. Surprisingly, the VEGF-PlGF heterodimer was also very inefficient at eliciting a Ca2+signaling event in HUVEC. We conclude that KDR activation is crucial for mobilization of intracellular Ca2+in HUVEC in response to VEGF165.

scholarly journals UNC5B Promotes Vascular Endothelial Cell Senescence via the ROS-Mediated P53 Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Zhen Yang ◽  
Han Li ◽  
Pengcheng Luo ◽  
Dan Yan ◽  
Ni Yang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Cell Number ◽  
Cell Senescence ◽  
Vascular Endothelial ◽  
Vascular Disorders ◽  
P53 Pathway ◽  
Age Related

Vascular endothelial cell senescence is involved in human aging and age-related vascular disorders. Guidance receptor UNC5B is implicated in oxidative stress and angiogenesis. Nonetheless, little is known about the role of UNC5B in endothelial cell senescence. Here, we cultured primary human umbilical vein endothelial cells to young and senescent phases. Subsequently, the expression of UNC5B was identified in replicative senescent cells, and then, its effect on endothelial cell senescence was confirmed by UNC5B-overexpressing lentiviral vectors and RNA interference. Overexpression of UNC5B in young endothelial cells significantly increased senescence-associated β-galactosidase-positive cells, upregulated the mRNAs expression of the senescence-associated secretory phenotype genes, reduced total cell number, and inhibited the potential for cell proliferation. Furthermore, overexpression of UNC5B promoted the generation of intracellular reactive oxygen species (ROS) and activated the P53 pathway. Besides, overexpression of UNC5B disturbed endothelial function by inhibiting cell migration and tube formation. Nevertheless, silencing UNC5B generated conflicting outcomes. Blocking ROS production or inhibiting the function of P53 rescued endothelial cell senescence induced by UNC5B. These findings suggest that UNC5B promotes endothelial cell senescence, potentially by activating the ROS-P53 pathway. Therefore, inhibiting UNC5B might reduce endothelial cell senescence and hinder age-related vascular disorders.

Carbon monoxide liberated from carbon monoxide-releasing molecule CORM-2 attenuates inflammation in the liver of septic mice

2008 ◽  
Vol 294 (1) ◽  
pp. G184-G191 ◽  
Author(s):  
Gediminas Cepinskas ◽  
Kazuhiro Katada ◽  
Aurelia Bihari ◽  
Richard F. Potter
Keyword(s):  
Carbon Monoxide ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Cecal Ligation ◽  
Cell Phenotype ◽  
Vascular Endothelial ◽  
Proinflammatory Responses ◽  
Umbilical Vein Endothelial Cells

Recent studies suggest that exogenously administered CO is beneficial for the resolution of acute inflammation. In this study, we assessed the role of CO liberated from a systemically administered tricarbonyldichlororuthenium-(II)-dimer (CORM-2) on modulation of liver inflammation during sepsis. Polymicrobial sepsis in mice was induced by cecal ligation and perforation (CLP). CORM-2 (8 mg/kg iv) was administered immediately after CLP induction, and neutrophil [polymorphonuclear leukocyte (PMN)] tissue accumulation, activation of transcription factor, NF-κB, and changes in adhesion molecule ICAM-1 expression (inflammation-relevant markers) were assessed in murine liver 24 h later. In addition, the effects and potential mechanisms of CORM-2-released CO in modulation of vascular endothelial cell proinflammatory responses were assessed in vitro. To this end, human umbilical vein endothelial cells (HUVEC) were stimulated with LPS (1 μg/ml) in the presence or absence of CORM-2 (10–100 μM) and production of intracellular reactive oxygen species (ROS), (DHR123 oxidation) and NO (DAF-FM nitrosation) and subsequent activation of NF-κB were assessed 4 h later. In parallel, expression of ICAM-1 and inducible NO synthase (iNOS) proteins along with PMN adhesion to LPS-challenged HUVEC were also assessed. Induction of CLP resulted in increased PMN accumulation, ICAM-1 expression, and activation of NF-κB in the liver of septic mice. These effects were significantly attenuated by systemic administration of CORM-2. In in vitro experiments, CORM-2-released CO attenuated LPS-induced production of ROS and NO, activation of NF-κB, increase in ICAM-1 and iNOS protein expression and PMN adhesion to LPS-stimulated HUVEC. Taken together, these findings indicate that CO released from systemically administered CORM-2 provides anti-inflammatory effects by interfering with NF-κB activation and subsequent downregulation of proadhesive vascular endothelial cell phenotype in the liver of septic mice.

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