Corilagin Ameliorates Atherosclerosis in Peripheral Artery Disease via TLR4 Signal Pathway in vitro and in vivo

2019 ◽  
Author(s):  
Yi-Qing Li ◽  
Yu-Jie Wang ◽  
Yun-Fei Chen ◽  
Yao Wang ◽  
Shao-Jun Zhang ◽  
...  
Keyword(s):  
Peripheral Artery Disease ◽  
Signal Pathway ◽  
Peripheral Artery ◽  
Artery Disease

scholarly journals Polyunsaturated fatty acids and peripheral artery disease

2012 ◽  
Vol 17 (1) ◽  
pp. 51-63 ◽  
Author(s):  
S Marlene Grenon ◽  
Millie Hughes-Fulford ◽  
Joseph Rapp ◽  
Michael S Conte
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Peripheral Artery Disease ◽  
In Vivo Studies ◽  
Peripheral Artery ◽  
Beneficial Effects ◽  
Epidemiological Surveys ◽  
Artery Disease

There is substantial evidence that polyunsaturated fatty acids (PUFAs) such as n-3 and n-6 fatty acids (FAs) play an important role in prevention of atherosclerosis. In vitro and in vivo studies focusing on the interactions between monocytes and endothelial cells have explored the molecular effects of FAs on these interactions. Epidemiological surveys, followed by large, randomized, control trials have demonstrated a reduction in major cardiovascular events with supplementation of n-3 FAs in secondary prevention settings. The evidence of beneficial effects specific to patients with peripheral artery disease (PAD) remains elusive, and is the focus of this review.

scholarly journals Smoking and the Pathophysiology of Peripheral Artery Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Weiming Wang ◽  
Tingting Zhao ◽  
Kang Geng ◽  
Gang Yuan ◽  
Yue Chen ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Peripheral Artery Disease ◽  
Molecular Mechanisms ◽  
Vascular Diseases ◽  
Pathological Process ◽  
Peripheral Artery ◽  
Cell Remodeling ◽  
Artery Disease

Smoking is one of the most important preventable factors causing peripheral artery disease (PAD). The purpose of this review is to comprehensively analyze and summarize the pathogenesis and clinical characteristics of smoking in PAD based on existing clinical, in vivo, and in vitro studies. Extensive searches and literature reviews have shown that a large amount of data exists on the pathological process underlying the effects of cigarette smoke and its components on PAD through various mechanisms. Cigarette smoke extracts (CSE) induce endothelial cell dysfunction, smooth muscle cell remodeling and macrophage phenotypic transformation through multiple molecular mechanisms. These pathological changes are the molecular basis for the occurrence and development of peripheral vascular diseases. With few discussions on the topic, we will summarize recent insights into the effect of smoking on regulating PAD through multiple pathways and its possible pathogenic mechanism.

scholarly journals Oxygen availability and skeletal muscle oxidative capacity in patients with peripheral artery disease: implications from in vivo and in vitro assessments

2018 ◽  
Vol 315 (4) ◽  
pp. H897-H909 ◽  
Author(s):  
Corey R. Hart ◽  
Gwenael Layec ◽  
Joel D. Trinity ◽  
Yann Le Fur ◽  
Jayson R. Gifford ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Peripheral Artery Disease ◽  
Early Stage ◽  
Oxidative Capacity ◽  
Muscle Dysfunction ◽  
Peripheral Artery ◽  
Skeletal Muscle Dysfunction ◽  
Artery Disease

Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( Vmax) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O2 availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O2 delivery, tissue oxygenation, Vmax, and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O2 and RH + 100% O2). Compared with HC subjects, patients with PAD exhibited attenuated O2 delivery at the same absolute work rate and attenuated tissue reoxygenation and Vmax after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O2 significantly increased convective O2 delivery (~44%), tissue reoxygenation (~54%), and Vmax (~60%) in patients with PAD ( P < 0.05), such that Vmax was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O2. Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O2 supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. NEW & NOTEWORTHY Currently, there is little accord as to the role of O2 availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O2 supply and not the impact of an intrinsic mitochondrial defect in this pathology.

Soluble CD40L in peripheral artery disease

2005 ◽  
Vol 93 (03) ◽  
pp. 578-583 ◽  
Author(s):  
Kiat Tan ◽  
Muzahir Tayebjee ◽  
Indran Davagnanam ◽  
Mark Moss ◽  
Gregory Lip ◽  
...  
Keyword(s):  
Peripheral Artery Disease ◽  
Sole Source ◽  
Clinical Severity ◽  
Healthy Controls ◽  
Peripheral Artery ◽  
Platelet Surface ◽  
Soluble Cd40l ◽  
Soluble P ◽  
Artery Disease

SummaryAlthough soluble CD40L (sCD40L, possibly derived from platelets and pro-inflammatory in vitro) may be implicated in thrombosis and haemostasis, there are little data in peripheral artery disease (PAD). We hypothesised the following: (a) that sCD40L relates to the clinical severity of PAD; and (b) that peripheral artery angioplasty acutely raises sCD40L levels. sCD40L was compared to established platelet markers soluble P selectin, platelet microparticles and platelet surface expression of CD62 and CD63. We recruited 36 healthy controls, 33 patients with intermittent claudication (IC), and 33 with symptomatically more severe critical limb is chaemia (CLI), measuring plasma markers by ELISA and membrane markers by flow cytometry. Eleven patients with CLI subsequently underwent peripheral artery angioplasty: blood was taken before and 10 minutes after the intervention. Results show that sCD40L was raised in IC at median 68 (IQR 28–333) pg/ml and in CLI at 64 (34–282) pg/mL compared to 35 (IQR 28–55) pg/ml in the healthy controls (p=0.009). Levels were no different between IC and CLI. The same distribution pattern was present for soluble P selectin, %platelets CD62+ve and CD63+ve. sCD40L failed to correlate significantly with ABPI (p=0.264), unlike %platelets CD62+ve (p=0.0032) and CD63+ve (p=0.009). Pre-angioplasty sCD40L level of 72 (35–610) ng/ml rose to 100 ng/ml (IQR=60–237)(p=0.018) post–angioplasty. Plasma sCD40L, in addition to other platelet indices, is raised in peripheral atherosclerosis and is increased by peripheral artery angioplasty, although levels seem unrelated to clinical severity. Failure to correlate with other markers suggest the platelet may not be the sole source of sCD40L, and that other cells may contribute to plasma levels.

scholarly journals Dual specificity phosphatase 5 regulates perfusion recovery in experimental peripheral artery disease

2019 ◽  
Vol 24 (5) ◽  
pp. 395-404 ◽  
Author(s):  
Satyanarayana Alleboina ◽  
Dawit Ayalew ◽  
Rahul Peravali ◽  
Lingdan Chen ◽  
Thomas Wong ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Peripheral Artery Disease ◽  
Molecular Mechanisms ◽  
Endothelial Cell Proliferation ◽  
Peripheral Artery ◽  
Vessel Occlusion ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity ◽  
Artery Disease

Peripheral artery disease (PAD) is caused by atherosclerotic occlusions of vessels outside the heart, particularly those of the lower extremities. Angiogenesis is one critical physiological response to vessel occlusion in PAD, but our understanding of the molecular mechanisms involved in angiogenesis is incomplete. Dual specificity phosphatase 5 (DUSP5) has been shown to play a key role in embryonic vascular development, but its role in post-ischemic angiogenesis is not known. We induced hind limb ischemia in mice and found robust upregulation of Dusp5 expression in ischemic hind limbs. Moreover, in vivo knockdown of Dusp5 resulted in impaired perfusion recovery in ischemic limbs and was associated with increased limb necrosis. In vitro studies showed upregulation of DUSP5 in human endothelial cells exposed to ischemia, and knockdown of DUSP5 in these ischemic endothelial cells resulted in impaired endothelial cell proliferation and angiogenesis, but did not alter apoptosis. Finally, we show that these effects of DUSP5 on post-ischemic angiogenesis are a result of DUSP5-dependent decrease in ERK1/2 phosphorylation and p21 protein expression. Thus, we have identified a role of DUSP5 in post-ischemic angiogenesis and implicated a DUSP5-ERK-p21 pathway that may serve as a therapeutic target for the modulation of post-ischemic angiogenesis in PAD.

scholarly journals DUAL CT AND MRI IN VIVO TRACKING OF STEM CELL THERAPY IN PERIPHERAL ARTERY DISEASE

2010 ◽  
Vol 55 (10) ◽  
pp. A176.E1654
Author(s):  
Yibin Xie ◽  
Yingli Fu ◽  
Ronald Ouwerkerk ◽  
Steven M. Shea ◽  
Tina Ehtiati ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Therapy ◽  
Peripheral Artery Disease ◽  
Stem Cell Therapy ◽  
Peripheral Artery ◽  
Artery Disease ◽  
Ct And Mri

scholarly journals Involvement of CD8+ T cell subsets in early response to vascular injury in patients with peripheral artery disease in vivo

2018 ◽  
Vol 194 ◽  
pp. 26-33 ◽  
Author(s):  
Pawel Maga ◽  
Tomasz P. Mikolajczyk ◽  
Lukasz Partyka ◽  
Mateusz Siedlinski ◽  
Mikolaj Maga ◽  
...  
Keyword(s):  
T Cell ◽  
Peripheral Artery Disease ◽  
Vascular Injury ◽  
Cd8 T Cell ◽  
Early Response ◽  
T Cell Subsets ◽  
Peripheral Artery ◽  
Artery Disease

scholarly journals Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells

2016 ◽  
Vol 40 (5) ◽  
pp. 1005-1012 ◽  
Author(s):  
Patrycja Sosińska ◽  
Ewa Baum ◽  
Beata Maćkowiak ◽  
Magdalena Maj ◽  
Katarzyna Sumińska-Jasińska ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Peripheral Artery Disease ◽  
Interleukin 1 ◽  
Secretory Activity ◽  
Dependent Manner ◽  
Peripheral Artery ◽  
Expression Of Genes ◽  
Artery Disease ◽  
Arterial Endothelial Cells

Background/Aims: Dysfunction of the arterial endothelial cells promotes the progression of atherosclerosis. We studied how exposure of human arterial endothelial cells to atherosclerotic serum from patients with peripheral artery disease changes the secretory activity of these cells, and whether that reaction is modified by sulodexide. Methods: Endothelial cells in in vitro culture were exposed to standard culture medium ± 100pg/mL Interleukin-1(IL-1) or to medium supplemented with 20% atherosclerotic serum. Afterwards, the expression of genes responsible for the synthesis of Interleukin-6 (IL-6), Vascular Cell Adhesion Protein-1 (VCAM-1) and Von Willebrand Factor (VWF) was evaluated, together with the secretion of these compounds. Additionally, the effect of sulodexide on these processes was studied. Results: Atherosclerotic serum stimulated the expression of IL6, VCAM-1 and VWF genes in endothelial cells, which was followed by increased secretion of these compounds by 179%, 121% and 116%, respectively. Sulodexide (0.5 LRU/mL) reduced atherosclerotic serum-induced increased expression of genes for IL-6 (-32%), VCAM-1 (-20%) and VWF (-42%), and lowered secretion of these molecules: IL-6 (-27%), VCAM-1(-27%), VWF (-25%). Sulodexide also reduced, in a dose- dependent manner, secretion of IL6 from unstimulated and stimulated with IL-1 endothelial cells. Conclusions: Atherosclerotic serum induces proinflammatory and prothrombotic phenotype in arterial endothelium, which is partially reduced by sulodexide, via inhibition of genes expression, and in consequence lower secretory activity.

scholarly journals Long-Term In Vivo Oxygen Sensors for Peripheral Artery Disease Monitoring

2018 ◽  
pp. 351-356 ◽  
Author(s):  
Scott P. Nichols ◽  
Mary K. Balaconis ◽  
Rebecca M. Gant ◽  
Kit Y. Au-Yeung ◽  
Natalie A. Wisniewski
Keyword(s):  
Peripheral Artery Disease ◽  
Oxygen Sensors ◽  
Disease Monitoring ◽  
Peripheral Artery ◽  
Artery Disease
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