Cellular Membrane Tether Retraction: Experiment and Model

2012 ◽  
Author(s):  
Jin-Yu Shao ◽  
Baoyu Liu
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cellular Membrane ◽  
Leukocyte Rolling ◽  
Tether Extraction ◽  
The Past ◽  
Selectin Ligand ◽  
Membrane Tethers ◽  
Membrane Tether

During leukocyte rolling on the endothelium, membrane tethers can be extracted simultaneously from both leukocytes and endothelial cells because of the force imposed by the blood flow [1]. Tether extraction has been shown to stabilize leukocyte rolling by increasing the lifetime of the adhesive selectin-ligand bonds that mediate leukocyte rolling [2]. Over the past two decades, tether extraction has been studied extensively, both experimentally and theoretically. In contrast, much less is known about tether retraction.

Sulfated Sialyl Lewis X, the Putative L-Selectin Ligand, Detected on Endothelial Cells of High Endothelial Venules by a Distinct Set of Anti-Sialyl Lewis X Antibodies

1997 ◽  
Vol 230 (3) ◽  
pp. 546-551 ◽  
Author(s):  
Chikako Mitsuoka ◽  
Naoko Kawakami-Kimura ◽  
Mikiko Kasugai-Sawada ◽  
Nozomu Hiraiwa ◽  
Ken'ichi Toda ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Sialyl Lewis X ◽  
Lewis X ◽  
High Endothelial Venules ◽  
Sialyl Lewis ◽  
Selectin Ligand

scholarly journals Blood flow boosts BMP signaling to keep vessels in shape

2016 ◽  
Vol 214 (7) ◽  
pp. 793-795 ◽  
Author(s):  
Claudio A. Franco ◽  
Holger Gerhardt
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Vascular Remodeling ◽  
Bmp Signaling ◽  
Mural Cells ◽  
Bone Morphogenic Proteins ◽  
Cell Biol ◽  
Suppress Cell Proliferation

Bone morphogenic proteins (BMPs) and blood flow regulate vascular remodeling and homeostasis. In this issue, Baeyens et al. (2016. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201603106) show that blood flow sensitizes endothelial cells to BMP9 signaling by triggering Alk1/ENG complexing to suppress cell proliferation and to recruit mural cells, thereby establishing endothelial quiescence.

DIAGNOSIS OF OVARIAN CANCER AND ACUTE ENDOMETRITIS BY NETWORK MODELING OF CHANGES IN BLOOD FLOW IN THE PELVIC ARTERIES

2021 ◽  
pp. 88-93
Author(s):  
Виталий Вячеславович Аксёнов ◽  
Николай Михайлович Агарков ◽  
Александра Игоревна Сурнина
Keyword(s):  
Ovarian Cancer ◽  
Blood Flow ◽  
Differential Diagnosis ◽  
Network Modeling ◽  
Correct Diagnosis ◽  
Arterial Blood Flow ◽  
Diagnostic Significance ◽  
The Past ◽  
Arterial Blood ◽  
High Level

Заболеваемость раком яичников в России в последнее время остается на высоком уровне. В мире более ста тысяч женщин умирают вследствие протекания данного заболевания. За последнее десятилетие заболеваемость острым эндометритом также неуклонно возрастает. Острый эндометрит обладает полиморфизмом симптомов, лабораторных и ультразвуковых изменений и вследствие этого тяжело поддается диагностике и дифференциальной диагностике. В условиях стационара обследованы 100 пациенток с раком яичников II-III стадии и 90 пациенток с диагнозом острого эндометрита. Им выполнялось ультразвуковое исследование. Полученные результаты подвергались обработке и математико-статистическому анализу, включающему расчёт показателей дезинтеграции, сетевое моделирование, математическое ранжирование. Изучение ультразвуковых изменений кровотока в маточных и яичниковых сосудах и венах у 100 заболевших раком яичников и 90 заболевших острым эндометритом дал возможность выделить ведущие дифференциально-диагностические аспекты. Характеристики дезинтеграции, в одном ряду со средними значениями локального кровотока, объективизируют дифференциацию рака яичников и острого эндометрита. В согласовании с дифференциально-диагностической значимостью ультразвуковых характеристик артериального кровотока в маточных и яичниковых сосудах построена сетевая модель дифференциальной диагностики рака яичников и острого эндометрита по более приоритетным переменам, собственно, что разрешает уменьшить размер и время обследования пациента и постановки верного диагноза The incidence of ovarian cancer in Russia has recently remained at a high level. In the world, more than a hundred thousand women die as a result of the course of this disease. The incidence of acute endometritis has also been steadily increasing over the past decade. Acute endometritis has a polymorphism of symptoms, laboratory and ultrasound changes and, as a result, is difficult to diagnose and differential diagnosis. 100 patients with stage II-III ovarian cancer and 90 patients with acute endometritis were examined in the hospital. They performed an ultrasound examination. The obtained results were processed and subjected to mathematical and statistical analysis, including the calculation of disintegration indicators, network modeling, and mathematical ranking. The study of ultrasound changes in blood flow in the uterine and ovarian vessels and veins in 100 patients with ovarian cancer and 90 patients with acute endometritis made it possible to identify the leading differential diagnostic aspects. The characteristics of disintegration, along with the average values of local blood flow, objectify the differentiation of ovarian cancer and acute endometritis. In accordance with the differential diagnostic significance of the ultrasound characteristics of arterial blood flow in the uterine and ovarian vessels, a network model for the differential diagnosis of ovarian cancer and acute endometritis is constructed according to higher priority changes, which actually allows reducing the size and time of the patient's examination and making the correct diagnosis

Abstract 15312: Genetic Deletion of Toll-like Receptor 9 Accelerates Blood Flow Recovery after Hindlimb Ischemia

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Sachiko Nishimoto ◽  
Daiju Fukuda ◽  
Yasutomi Higashikuni ◽  
Kimie Tanaka ◽  
Yoichiro Hirata ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Femoral Artery ◽  
Cpg Odn ◽  
Toll Like Receptor ◽  
Artery Ligation ◽  
Ischemic Limb ◽  
Tnf Α ◽  
Genetic Deletion ◽  
Inflammatory Molecules

Background: Peripheral artery disease causes significant functional disability and results in impaired quality of life. Toll-like receptor (TLR)-2, 3 and 4 are suggested to participate in blood flow recovery in ischemic limb by modulating inflammation and angiogenesis, however, the role of TLR9 remains unknown. TLR9 recognizes bacterial unmethylated DNA and plays a role in innate defense, although it can also provoke inflammation in response to fragmented DNA released from regenerated mammalian cells. This study tested the hypothesis that genetic deletion of TLR9 accelerates blood flow recovery after femoral artery ligation by inhibiting inflammation and improving endothelial cell function. Methods and Results: Unilateral femoral artery ligation was performed in TLR9-deficient (TLR9KO) mice and wild type (WT) mice. Femoral artery ligation significantly increased RNA expression of TLR9 (20-times) in WT mice and plasma levels of single-stranded DNA and double-stranded DNA, endogenous ligands for TLR9, in both strains of mice compared with each sham-operated group (P<0.05). Laser Doppler perfusion imaging demonstrated that TLR9KO mice significantly improved the ratio of the blood flow in the ischemic to non-ischemic limb compared with WT mice at 2 weeks after ligation (P<0.05). TLR9KO mice showed less accumulation of macrophages and less expression of inflammatory molecules (e.g., TNF-α, MCP-1 and IL-1β in ischemic muscle compared with WT mice (P<0.05, respectively). In vitro experiments using thioglycolate-stimulated peritoneal macrophages demonstrated that CpG ODN, agonistic oligonucleotide for TLR9, promoted the expression of pro-inflammatory molecules (e.g., MCP-1 and TNF-α) in WT macrophages (P<0.05, respectively) but not in TLR9 KO macrophages. Furthermore, activation of TLR9 by CpG ODN inhibited migration and proliferation of endothelial cells as determined by scratch-wound assay and MTS assay, respectively (P<0.05). Conclusion: Our results suggested that TLR9 enhances inflammation and affects migration and proliferation of endothelial cells, leading to impaired blood flow recovery in ischemic limb. TLR9 may serve as a potential therapeutic target for ischemic limb disease.

scholarly journals Electro-Metabolic Sensing Through Capillary ATP-Sensitive K+ Channels and Adenosine to Control Cerebral Blood Flow

2021 ◽  
Author(s):  
Maria Sancho ◽  
Nicholas R. Klug ◽  
Amreen Mughal ◽  
Thomas J. Heppner ◽  
David Hill-Eubanks ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Function ◽  
Brain Activity ◽  
List Type ◽  
Capillary Endothelial Cells ◽  
Metabolic Sensing ◽  
Cellular Components

SUMMARYThe dense network of capillaries composed of capillary endothelial cells (cECs) and pericytes lies in close proximity to all neurons, ideally positioning it to sense neuro/glial-derived compounds that regulate regional and global cerebral perfusion. The membrane potential (VM) of vascular cells serves as the essential output in this scenario, linking brain activity to vascular function. The ATP-sensitive K+ channel (KATP) is a key regulator of vascular VM in other beds, but whether brain capillaries possess functional KATP channels remains unknown. Here, we demonstrate that brain capillary ECs and pericytes express KATP channels that robustly control VM. We further show that the endogenous mediator adenosine acts through A2A receptors and the Gs/cAMP/PKA pathway to activate capillary KATP channels. Moreover, KATP channel stimulation in vivo causes vasodilation and increases cerebral blood flow (CBF). These findings establish the presence of KATP channels in cECs and pericytes and suggest their significant influence on CBF.HIGHLIGHTSCapillary network cellular components—endothelial cells and pericytes—possess functional KATP channels.Activation of KATP channels causes profound hyperpolarization of capillary cell membranes.Capillary KATP channels are activated by exogenous adenosine via A2A receptors and cAMP-dependent protein kinase.KATP channel activation by adenosine or synthetic openers increases cerebral blood flow.

Abstract 14820: Sirt7 Deficiency in Blood Vessel Components Impairs Vascular Function by Inhibiting Cell Cycle- and Inflammatory-Related Protein Expression

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Yuichi Kimura ◽  
Yasuhiro Izumiya ◽  
Satoshi Araki ◽  
Satoru Yamamura ◽  
Yoshiro Onoue ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Vascular Diseases ◽  
Tube Formation ◽  
Hindlimb Ischemia ◽  
Proliferation Assay

Introduction: Aging is a well-established cardiovascular risk factor and associated with vascular dysfunction. Sirt7, one of the members of mammalian sirtuin family, is thought to be involved in age-related diseases. However, little is known about the relative contribution of Sirt7 in vascular dysfunction. Hypothesis: Sirt7 maintains vascular cell functions and its deficiency plays a critical role in vascular diseases. Methods: Sirt7 loss- and gain-of-function experiments were performed with human aortic smooth muscle cells (HAoSMCs) and human umbilical vein endothelial cells (HUVECs). In vivo, blood flow recovery was evaluated by hindlimb ischemia model in homozygous Sirt7 deficient (Sirt7-/-) and wild-type (WT) mice. Irradiated WT mice were intravenously received bone marrow (BM) cells from WT or Sirt7 -/- mouse to achieve BM transfer. Results: An RNAi-medicated Sirt7 knockdown resulted in a significant inhibition of HAoSMCs proliferation following serum or Platelet-derived growth factor BB (PDGF-BB) stimulation as determined by cell count, BrdU cell proliferation assay and MTS proliferation assay. Knockdown of endogenous Sirt7 also reduced cell migration as revealed by Boyden chamber migration assay. The Cyclin D1 and Cyclin dependent kinase 2 (CDK2) protein levels were significantly decreased in Sirt7 siRNA-treated HAoSMCs in response to serum or PDGF-BB stimulation. In endothelial cells, knockdown of Sirt7 attenuated tube formation, proliferation and migration. These changes were accompanied by reduced ERK activation and VCAM-1 mRNA and protein expression in Sirt7 siRNA-treated HUVECs. Conversely, overexpression of Sirt7 by adenovirus enhanced tube formation and cell proliferation. In vivo, blood flow recovery in response to hindlimb ischemia was significantly attenuated in Sirt7-/- mice compared with WT mice. There was no difference in blood flow recovery between WT mice transplanted with WT or Sirt7-/- BM cells suggesting that Sirt7 deficiency in vascular cells have a predominant effect on attenuated blood flow recovery in response to hindlimb ischemia. Conclusions: Sirt7 in blood vessel components have an important role in maintenance of vascular function. Sirt7 could be a promising therapeutic target for vascular diseases.

Heat-Sterllized Pd Fluid Blocks Leukocyte Adhesion and Increases Flow Velocity in Rat Peritoneal Venules

1996 ◽  
Vol 16 (1_suppl) ◽  
pp. 137-141 ◽  
Author(s):  
Peter Jonasson ◽  
Ulf Bagge ◽  
Anders Wieslander ◽  
Magnus Braide
Keyword(s):  
Cell Culture ◽  
Blood Flow ◽  
Flow Velocity ◽  
Bacterial Infections ◽  
Degradation Products ◽  
Leukocyte Adhesion ◽  
Microvascular Blood Flow ◽  
Leukocyte Rolling ◽  
Rat Mesentery ◽  
Rolling Leukocytes

Data from cell culture experiments indicate that heat sterilization of peritoneal dialysis (PD) fluids produces cytotoxic glucose degradation products. The present vital microscopic study investigated the effects of different sterilization methods on the biocompatibility of PD fluids. Thus, heat-sterilized (commercially obtained and experimentally produced) and filter-sterilized PD fluids (pH = 5.30 5.40; 1.5% glucose) were compared with Tyrode buffer, with respect to the effects on microvascular blood flow velocity and leukocyte adhesion in the rat mesentery. Exteriorization of the mesentery produced a mild inflammation, known from the literature and characterized by the adhesive rolling of leukocytes along venular walls. Superfusion of the mesentery with filter-sterilized PD fluid had no significant effects on leukocyte rolling or flow velocity in venules 25 40 μm in diameter compared with buffer superfusion. Heat-sterilized PD fluid decreased the concentration of rolling leukocytes and increased flow velocity significantly, as compared with buffer and filter-sterilized PD fluid. The results indicate that heat sterilization of PD fluids produces substances that interact with microvascular tone and leukocyte-endothelial adhesion, which hypothetically could impair the acute, granulocyte-mediated defense against bacterial infections.

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