scholarly journals Age-Dependent and -Independent Effects of Perivascular Adipose Tissue and Its Paracrine Activities during Neointima Formation

2019 ◽  
Vol 21 (1) ◽  
pp. 282 ◽  
Author(s):  
Eva Schütz ◽  
Rajinikanth Gogiraju ◽  
Maria Pavlaki ◽  
Ioannis Drosos ◽  
George S. Georgiadis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Smooth Muscle ◽  
Vascular Injury ◽  
Pcr Analysis ◽  
Aortic Tissue ◽  
Neointima Formation ◽  
Middle Aged ◽  
Perivascular Adipose Tissue ◽  
Independent Effects ◽  
And Function

Cardiovascular risk factors may act by modulating the composition and function of the adventitia. Here we examine how age affects perivascular adipose tissue (PVAT) and its paracrine activities during neointima formation. Aortic tissue and PVAT or primary aortic smooth muscle cells from male C57BL/6JRj mice aged 52 weeks (“middle-aged”) were compared to tissue or cells from mice aged 16 weeks (“adult”). Vascular injury was induced at the carotid artery using 10% ferric chloride. Carotid arteries from the middle-aged mice exhibited smooth muscle de-differentiation and elevated senescence marker expression, and vascular injury further aggravated media and adventitia thickening. Perivascular transplantation of PVAT had no effect on these parameters, but age-independently reduced neointima formation and lumen stenosis. Quantitative PCR analysis revealed a blunted increase in senescence-associated proinflammatory changes in perivascular tissue compared to visceral adipose tissue and higher expression of mediators attenuating neointima formation. Elevated levels of protein inhibitor of activated STAT1 (PIAS1) and lower expression of STAT1- or NFκB-regulated genes involved in adipocyte differentiation, inflammation, and apoptosis/senescence were present in mouse PVAT, whereas PIAS1 was reduced in the PVAT of patients with atherosclerotic vessel disease. Our findings suggest that age affects adipose tissue and its paracrine vascular activities in a depot-specific manner. PIAS1 may mediate the age-independent vasculoprotective effects of perivascular fat.

scholarly journals Role of Perivascular Adipose Tissue-Derived Adiponectin in Vascular Homeostasis

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1485
Author(s):  
Adrian Sowka ◽  
Pawel Dobrzyn
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Whole Body ◽  
Perivascular Adipose Tissue

Studies of adipose tissue biology have demonstrated that adipose tissue should be considered as both passive, energy-storing tissue and an endocrine organ because of the secretion of adipose-specific factors, called adipokines. Adiponectin is a well-described homeostatic adipokine with metabolic properties. It regulates whole-body energy status through the induction of fatty acid oxidation and glucose uptake. Adiponectin also has anti-inflammatory and antidiabetic properties, making it an interesting subject of biomedical studies. Perivascular adipose tissue (PVAT) is a fat depot that is conterminous to the vascular wall and acts on it in a paracrine manner through adipokine secretion. PVAT-derived adiponectin can act on the vascular wall through endothelial cells and vascular smooth muscle cells. The present review describes adiponectin’s structure, receptors, and main signaling pathways. We further discuss recent studies of the extent and nature of crosstalk between PVAT-derived adiponectin and endothelial cells, vascular smooth muscle cells, and atherosclerotic plaques. Furthermore, we argue whether adiponectin and its receptors may be considered putative therapeutic targets.

Abstract 5494: ADAMTS-7 is Critical for Vascular Smooth Muscle Cell Migration and Neointima Formation in Injured Rat Carotid Artery

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Wei Kong ◽  
Li Wang ◽  
Xue Bai ◽  
Bo Liu ◽  
Yi Zhu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Injury ◽  
Matrix Protein ◽  
Mrna Level ◽  
Balloon Catheter ◽  
Migration And Invasion ◽  
Neointima Formation ◽  
Subsequent Increase ◽  
Neointimal Thickening

Migration of vascular smooth muscle cells (VSMCs) plays an essential role during vascular development, in response to vascular injury and during atherogenesis. Extensive studies have implicated the importance of extracellular matrix (ECM)-degrading proteinases during VSMCs migration. ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs), a recently described family of proteinases, is capable of degrading vascular ECM proteins. However, the relevance of ADAMTS family members in cardiovascular disease is poorly understood. In this study, we sought to determine whether ADAMTS-7 is involved in VSMC migration and neointima formation in response to vascular injury. Denudation of rat carotid arteries with a balloon catheter led to an initial decrease of ADAMTS-7 protein level in injured compared with sham-operated arteries within the first 24 hours, followed by a subsequent increase during the 4 to 14 days after injury. In primary VSMCs, the pro-inflammatory cytokine TNF-α increased ADAMTS-7 mRNA level through transcriptional factors nuclear factor-kappa B and AP-1. VSMCs infected with ADAMTS-7 adenovirus (Ad-ADAMTS-7) greatly accelerated their migration and invasion in vitro . Conversely, suppression of ADAMTS-7 expression by small interfering RNA (siRNA) markedly retarded VSMC movement by 50% than that with scramble siRNA. At 7 days after injury, the neointimal area of the vascular wall was sixfold greater in Ad-ADAMTS-7-infected than that in Ad-GFP-infected vessels (3.10±0.88 vs. 0.52±0.28 ×10 4 μm 2 , n=8 per group, P <0.05). By contrast, perivascular administration of ADAMTS-7 siRNA, but not scramble siRNA to injured arteries resulted in prolonged ADAMTS-7 silencing and diminished neointimal thickening without affecting medial areas. This inhibitory effect was sustained up to 14 days after injury. As well, ADAMTS-7 mediated degradation of the vascular ECM cartilage oligomeric matrix protein (COMP) in injured vessels, which might facilitate VSMC migration and neointimal thickening. ADAMTS-7 directs VSMC migration and neointima formation and therefore may serve as a novel therapeutic target for vascular restenosis and atherogenesis.

scholarly journals Inhibition of Smooth Muscle β-Catenin Hinders Neointima Formation After Vascular Injury

2017 ◽  
Vol 37 (5) ◽  
pp. 879-888 ◽  
Author(s):  
Dario F. Riascos-Bernal ◽  
Prameladevi Chinnasamy ◽  
Jordana N. Gross ◽  
Vanessa Almonte ◽  
Lander Egaña-Gorroño ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Injury ◽  
Neointima Formation

scholarly journals Perivascular Adipose Tissue Potentiates Contraction of Coronary Vascular Smooth Muscle

Circulation ◽  
2013 ◽  
Vol 128 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Meredith Kohr Owen ◽  
Frank A. Witzmann ◽  
Mikaela L. McKenney ◽  
Xianyin Lai ◽  
Zachary C. Berwick ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Perivascular Adipose Tissue

Exosome‐like Vesicles Facilitate Intercellular Communication between Uterine Artery Smooth Muscle Cells and Perivascular Adipose Tissue

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Oluwatobiloba Osikoya ◽  
Spencer C. Cushen ◽  
Megan M. Raetz ◽  
Bhavani Nagarajan ◽  
Sangram Raut ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intercellular Communication ◽  
Uterine Artery ◽  
Muscle Cells ◽  
Perivascular Adipose Tissue

Tempol therapy attenuates medial smooth muscle cell apoptosis and neointima formation after balloon catheter injury in carotid artery of diabetic rats

2005 ◽  
Vol 289 (3) ◽  
pp. H1047-H1053 ◽  
Author(s):  
D. K. Jagadeesha ◽  
Timothy E. Lindley ◽  
Jason DeLeon ◽  
Ram V. Sharma ◽  
Francis Miller ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Injury ◽  
Critical Role ◽  
Balloon Catheter ◽  
Vascular Complications ◽  
Diabetic Rats ◽  
Neointima Formation ◽  
Muscle Cell Apoptosis

Accumulating data support the hypothesis that reactive oxygen species (ROS) play a critical role in the vascular complications observed in diabetes. However, the mechanisms of ROS-mediated vascular complications in diabetes are not clear. We tested the hypothesis that ROS-mediated increase in proapoptotic factor Bax expression leads to medial smooth muscle cell (SMC) apoptosis that is associated with neointima formation. We used a fructose-rich diet for 4 wk to model Type 2 diabetes in rats. SOD mimetic membrane-permeable 4-hydroxy-2,2,6,6,-tetramethylpiperidine-1-oxyl (Tempol, 1 mM) was administered in drinking water to scavenge superoxide starting 1 day before surgery and continued during the duration of the experiment. Vascular injury resulted in a significant increase in medial SMC apoptosis that was associated with neointima formation. The number of medial SMC positive for Bax immunostaining significantly increased in injured arteries compared with uninjured arteries. Superoxide scavenging by Tempol treatment inhibited both the Bax-positive index as well as the apoptotic index of medial SMC in response to vascular injury. Tempol treatment inhibited apoptotic loss of medial SMC, thus increasing their density in the injured arteries. These alterations in the media were associated with a marked decrease in neointima formation in injured arteries. We conclude that Bax expression may play an important role in vascular SMC apoptosis and, finally, that this regulatory mechanism is redox sensitive.

Sign in / Sign up

Export Citation Format

Share Document