alexa Osteopontin in Vascular Calcification: A Central Player or Accidental Witness? | Open Access Journals
ISSN: 2161-0444
Medicinal Chemistry
Like us on:
Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on
Medical, Pharma, Engineering, Science, Technology and Business

Osteopontin in Vascular Calcification: A Central Player or Accidental Witness?

Alexander E Berezin1,2*

1Consultant of Therapeutic Unit, Private Hospital “Vita Center”, 3, Sedova str., Zaporozhye, Ukraine

2Consultant of Therapeutic Unit, Internal Medicine Department, State Medical University, 26, Mayakovsky av., Zaporozhye, Ukraine

*Corresponding Author:
Alexander E Berezin
Consultant of Therapeutic Unit, Internal Medicine Department
State Medical University, 26, Mayakovsky av., Zaporozhye, Ukraine
Tel: +380612894585
E-mail: [email protected] (or) [email protected]

Received date: March 29, 2017; Accepted date: April 12, 2017; Published date: April 17, 2017

Citation: Berezin AE (2017) Osteopontin in Vascular Calcification: A Central Player or Accidental Witness? Med Chem (Los Angeles) 7:106-107. doi: 10.4172/2161-0444.1000439

Copyright: © 2017 Berezin AE. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Medicinal Chemistry

Abstract

Osteopontin (OPN) is an integrin-binding ligand belonged to the family of N-linked glycoprotein, which is produced by activated mononuclears and linking systemic inflammation, atherosclerosis, and vascular remodeling. There is a large body of evidence regarding the controversial role of OPN in vascular calcification, while OPN is considered a pretty accurate biomarker of vascular remodeling with promising predictive value for cardiovascular (CV) disease and CV events. The short communication depicts the discussion about some controversies regarding exclusive role of OPN in several phases of vascular remodeling.

Keywords

Hypertension; Vascular remodeling; Inflammation; Calcification; Osteopontin; Regulation

Osteopontin in Vascular Calcification

Recent preclinical and clinical studies have shown that vascular calcification is inexorable pathological process leading to mechanical rigidity and stiffness of vascular wall, endothelial dysfunction, development and accelerating atherosclerosis even in the absence of established cardiovascular (CV) disease [1-3]. Ectopic calcification is represented by several mutually counteracting molecular mechanisms, i.e., oxidative stress, microvascular inflammation, immune cell-to-cell cooperation, accumulation of lipids and extracellular proteins, vascular reparative systems, and metabolic disorders [4-6]. All these processes are under tight regulation of vitamin D, parathyroid hormone-related peptides (fibroblast growth factor, transcription factor Sox2, betacatenin, etc.) and matricellular proteins such as osteopontin (OPN) and phosphate [7-10].

OPN is an integrin-binding ligand belonged to the family of N-linked glycoprotein, which is produced by activated mononuclears and linking systemic inflammation, atherosclerosis, and vascular remodeling via regulating ectopic calcification and extracellular matrix accumulation [11]. Indeed, OPN corresponded to hyperphosphatemia, conventional and nonconventional CV risk factors and CV disease mortality [10]. It has been postulated that OPN appeared to block vascular calcification most likely by preventing calcium phosphate crystal growth and inducing cellular mineral resorption. However, the role of OPN in vascular calcification is pretty controversial. The first controversy is based on opinion regarding that the OPN was found in elevated concentration in patients with established vascular calcification, atherosclerosis, and CV disease associated with severe vascular remodeling including hypertension, chronic kidney disease, diabetes mellitus [4,9,12]. In this context, OPN is an accurate biomarker of vascular remodeling closely relating to inflammation intensity, glucose level and pro-thrombotic state with promising predictive value for CV events [13].

However, there is large body of evidence that OPN could be an inducible inhibitor of vascular calcification in vivo and that the elevation of OPN level in serum reflects an involvement of protective mechanisms against ectopic calcium deposition [14]. Indeed, OPN deficiency may attenuate development and accelerating atherosclerosis increasing susceptibility to calcium deposition in smooth muscle cells [15,16].

Second controversy relates to a widely known fact regarding that the OPN is strongly induced in mononuclear and myeloid cells acting as pro-inflammatory mediator of direct and indirect vascular injury leading to endothelial dysfunction [9,17,18]. Interestingly, exogenous OPN is able to inhibit a differentiation of activated macrophages into osteoclasts in vascular wall and attenuate shaping M2-phenotype of macrophages with anti-inflammatory ability [9]. Thus, mononuclears obtained from patients with and without established vascular calcification may reply to OPN in different way that confirms being alternatively shaping mononuclears in vascular wall during ectopic calcification. Probably, OPN exerts a pivotal role in turning M1 phenotype of macrophages into M2 phenotype in vascular calcification that coordinates reducing expression of several pro-inflammatory factors and attenuating vascular osteoclast formation.

The next controversy allows us considering about a cause of interrelationship between inflammatory cytokines, overproduction of reactive oxygen species and OPN expression in individuals with established CV diseases. Inflammatory-induced OPN through NADPH oxidase signaling cascade may regulate an activation of pro-matrix metalloproteinase 9 in aortic mesenchymal cells, which play a central role in vascular reparation [19] acting as endogenous repair system together endothelial progenitor cells [6]. Moreover, deficiency of OPN presentation in aorta associated with increased risk of aneurism formation, thrombosis and fissuring plaque cap [20]. Whether OPN is a primary regulator of exaggerated inflammation cascade in the target cells via control of proliferative response or non-specific messenger, which protects vascular wall against calcium deposition through blockage of tissue metalloproteinases is not fully understood. However, there is evidence that inhibition of OPN prevented vascular calcification [21]. How similar evidence relates to clinical findings regarding predictive value of circulating OPN in individuals with and without established CV diseases is not clear [22]. Large clinical studies are required in future to explain in details the role of OPN as a biomarker of CV events and CV diseases and as well as a possible target of medical care.

Conclusion

OPN is considered a multi-directed factor contributing in several phases of vascular remodeling including calcium accumulation, atherosclerosis, vascular reparation and microvascular inflammation. The role of OPN as a pretty accurate biomarker of CV risk, CV diseases and CV events are actively investigated, while there are several controversies in final effects of OPN regarding vascular calcification based on multimodal pathogenetic capabilities of the molecule. Future investigations are needed to understand the possible role of OPN in biomarker-guided therapy of the CV disease and assay of vascular remodeling risk.

References

Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Recommended Conferences

Article Usage

  • Total views: 376
  • [From(publication date):
    April-2017 - Sep 23, 2017]
  • Breakdown by view type
  • HTML page views : 335
  • PDF downloads :41
 

Post your comment

captcha   Reload  Can't read the image? click here to refresh

Peer Reviewed Journals
 
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
 
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

[email protected]

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

[email protected]

1-702-714-7001Extn: 9037

Business & Management Journals

Ronald

[email protected]

1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

[email protected]

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

[email protected]

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

[email protected]

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

[email protected]

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

[email protected]

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

[email protected]

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

[email protected]

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

[email protected]

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

[email protected]

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

[email protected]

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

[email protected]

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

[email protected]

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

[email protected]

1-702-714-7001 Extn: 9042

 
© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version
adwords