The Urotensin II System and Carotid Atherosclerosis: A Role in Vascular Calcification

Albanese, Isabella; Daskalopoulou, Stella S.; Yu, Bin; You, Zhipeng; Genest, Jacques; Alsheikh‐Ali, Alawi A.; Schwertani, Adel

doi:10.3389/fphar.2016.00149

Cited by 13 publications

(7 citation statements)

References 45 publications

(54 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, we now have the means to study calcification in AVS using human tissues [14,15,29], which according to our results, may be the only effective way to study the disease. Our study is limited, however, in that it only explores ALP-dependent calcification and does not address other molecular contributors including Runx2 [30], Wnts [4], UII [15], BMPs [31], and TGF-β [32]. Furthermore, we cultured our cells in OSM for 7 days for HAVICs and 12 days for BAVICs, while other studies assess calcification onset after much longer incubation times [33].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Assessing Calcification Onset in Aortic Valve Interstitial Cells

Khan¹,

B²,

Al‐Kindi³

et al. 2017

Cardiovasc Pharm Open Access

View full text Add to dashboard Cite

IntroductionAortic valve stenosis (AVS) is a complex disease, characterized by the thickening of the aortic valve with significant fibrosis and/or calcification [1]. Short-term symptoms include shortness of breath and fainting, while more long-term symptoms include heart failure and inevitably, death [2]. Treatment for AVS remains non-existent, with surgical intervention being the only viable option for at-risk patients. Thus, there has been interest in finding innovative approaches to treating this perilous disease [3,4].The pathogenesis of AVS is an active process involving multiple cell types and complexed underlying mechanisms [5,6]. Upon differentiation of mesenchymal-like cells to chondrogenic cells, matrix vesicles are released, containing enzymes and other factors that lead to the onset of calcification [7]. One of these enzymes, alkaline phosphatase (ALP), is a metalloenzyme that has been shown to play a profound role in calcification onset by concentrating calcium [8], mineralizing hydroxyapatite crystals [8], and inactivating inhibitory polyphosphates [9]. In humans, there are four ALP isozymes: alkaline phosphatase, tissue-nonspecific isozyme (TNALP), intestinal-type alkaline phosphatase, placental-type alkaline phosphatase, and placental-like alkaline phosphatase [10]. Two isoforms of TNALP exist: bone-specific TNALP and liver-specific TNALP, both of which are abundantly found in the serum [10]. Within the context of vascular calcification, bone TNALP is highly expressed in calcifying vascular smooth muscle cells and is likely to be responsible for calcium deposition and AVS pathogenesis [10].A multitude of studies draw conclusions regarding the pathogenesis of AVS in humans by utilizing aortic valve interstitial cells from bovine [11][12][13]. The ultimate goal of these studies is to identify mechanisms that will help us better understand calcification onset in humans. However, there is a need to directly compare these animal models to humans and assess whether or not it is plausible to make such a AbstractAortic valve stenosis (AVS) is one of the most common heart valve diseases, and surgical intervention remains the only viable treatment option. Thus, there is a need for novel and innovative treatments. One approach is to study the biological pathogenesis of this disease in hopes of finding new targets for drug therapy. Although this may be a viable option, it faces some methodological concerns. Many studies attempted to address the underlying mechanisms of this disease using aortic valves from bovine models. Although these may be viable models in certain diseased conditions, this may not be the case when studying calcification in AVS. Thus, the aim of our study was to assess the significance of drawing conclusions from bovine models to humans in the context of AVS, and investigate the role of alkaline phosphatase (ALP), an enzyme that increases calcium mineralization and deposition in aortic valve calcification. We also wanted to identify any differences in calcification when using different os...

show abstract

Section: Discussionmentioning

confidence: 99%

“…Primary HAVIC lines were generated as previously described [14,15]. Cultured HAVICs showed positive staining for alpha smooth muscle actin, indicating myofibroblast phenotype after 2 passages.…”

Section: Isolation and Culture Of Valve Interstitial Cellsmentioning

confidence: 99%

Assessing Calcification Onset in Aortic Valve Interstitial Cells

Khan¹,

B²,

Al‐Kindi³

et al. 2017

Cardiovasc Pharm Open Access

View full text Add to dashboard Cite

show abstract

“…In addition, macrophages and lymphocytes secrete pro-inflammatory cytokines such as IL-6, IL-1β and IFN-γ in atherosclerotic plaques. These cytokines further upregulate the expression of UII and UT and accelerate the formation of atherosclerotic plaques (Birker-Robaczewska et al 2003, Johns et al 2004, with the autocrine/paracrine effects of macrophage UII significantly increasing macrophage-positive areas (Zhao et al 2015) and destabilizing atherosclerotic plaques , Albanese et al 2016. Reports in recent years show that UII can induce the expression and secretion of various inflammatory cytokines, such as MCP-1 and TGF-β, causing arterial inflammatory injury (You et al 2012.…”

Section: Atherosclerosismentioning

confidence: 99%

Urotensin II: an inflammatory cytokine

Sun

Liu²

2019

Journal of Endocrinology

View full text Add to dashboard Cite

Urotensin II (UII) is a polypeptide molecule with neurohormone-like activity. It has been confirmed that UII is widely distributed in numerous organs of different animal species from fish to mammals, including humans. The UII receptor is orphan G-protein-coupled receptor 14, also known as UT. The tissue distribution of UII and UT is highly consistent, and their expression may be regulated by autocrine and paracrine mechanisms. In the body, UII has many physiological and pathophysiological activities, such as vasoconstrictor and vasodilatory actions, cell proliferation, pro-fibrosis, neuroendocrine activity, insulin resistance and carcinogenic and inflammatory effects, which have been recognized only in recent years. In fact, UII is involved in the process of inflammatory injury and plays a key role in the onset and development of inflammatory diseases. In this paper, we will review the roles UII plays in inflammatory diseases.

show abstract

“…Meanwhile, patients with reduced urotensin II levels have increased cardiovascular mortality rates, and urotensin II may provide cardiovascular protection and predict cardiovascular deaths in patients with CKD [ 50 ]. Urotensin II correlates with ventricular function and vascular atherosclerosis in patients with CKD [ 66 ]. Additionally, RAAS plays a significant role in mediating the heart and kidney and promotes the development of CRS [ 1 ].…”

Section: Renal Biomarkersmentioning

confidence: 99%

Biomarkers in Cardiorenal Syndromes

Zhao

Luo

2018

BioMed Research International

View full text Add to dashboard Cite

There is a consensus that cardiorenal syndromes (CRS) are defined as the disorders of heart and kidney where acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in another. Patients with CRS have increased hospitalization and mortality rates, and thus their identification is of great implication. Biomarkers are not only predictive in heart failure or renal diseases, but also useful in identifying cardiac dysfunction in renal diseases and renal injury in heart failure. Thus, they may be applied in order to identify patients with CRS and even assess prognosis and guide therapy in these patients. However, studies on biomarkers have just begun in CRS. Future studies are essential to observe current biomarkers and find novel biomarkers in CRS so as to improve diagnosis, therapy, and prognosis of CRS.

show abstract

The Urotensin II System and Carotid Atherosclerosis: A Role in Vascular Calcification

Cited by 13 publications

References 45 publications

Assessing Calcification Onset in Aortic Valve Interstitial Cells

Assessing Calcification Onset in Aortic Valve Interstitial Cells

Urotensin II: an inflammatory cytokine

Biomarkers in Cardiorenal Syndromes

Contact Info

Product

Resources

About