Blood Level of Osteonectin in Stenosing Atherosclerosis and Calcinosis of Coronary Arteries

Ragino, Yu. I.; Kashtanova, E.; Chernjavski, A. M.; Волков, А. М.; Polonskaya, Yа. V.; Tsimbal, S. Yu.; Eremenko, N.; Иванова, М. В.

doi:10.1007/s10517-011-1333-9

Cited by 4 publications

(4 citation statements)

References 12 publications

(18 reference statements)

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“…β‐actin and lamin‐B were blotted as cytoplasmic and nuclear loading control . Co‐immuno‐precipitation of Fas‐FasL, Fas‐FADD, and p53‐pp38MAPkinase (Thr180/Tyr182) were carried out by incubating followed by precipitating samples with anti‐Fas and anti‐p53 antibodies as per pure proteome protein A magnetic bead kit protocol, Merck Millipore . Immuno‐precipitates were then immunoblotted with anti‐FasL, anti‐FADD, anti‐pp38MAPK (Thr180/Tyr182) antibodies, and protein‐protein interactions were visualized by enzyme specific substrate (NBD‐BCIP or TMB) as required.…”

Section: Methodsmentioning

confidence: 99%

Association of p38MAPK‐p53‐Fas aggregation in S‐allyl cysteine mediated regulation of hepatocarcinoma

Chatterjee

Patra

Chakraborti

et al. 2019

Environmental Toxicology

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Bioactive components of dietary phytochemicals have been reported to possess antitumor activities. Evidences suggested key role of stress responsive p38MAPK in the induction of nutraceuticals mediated apoptosis in hepatocellular carcinoma (HCC). Current study demonstrated detailed molecular bagatelle associated with p38 MAPK mediated effective suppression of cell growth both in HepG2 and chemically induced liver carcinoma after S-allyl cysteine (SAC) treatment. SAC promoted p38MAPK activity responsible for p53 phosphorylation, its stabilization followed by nuclear translocation leading to induction in expression and oligomerization of Fas protein. Distinctive p38MAPK-p53 axis dependent Fas-FasL-FADD mediated caspase activities along with perturbed cell cycling became normalized with continuation of SAC treatment for another month to diethylnitrosamine induced liver carcinoma. Co-treatment with SB203580, the p38MAPK inhibitor, prevented pro-apoptotic effect of SAC by altering p53 phosphorylation and death inducing signaling complex conformation in HepG2 and induced HCC. Collectively study suggested significant contribution of p38MAPK-p53-DISC-Caspase pathway in the regulation of anti-neoplastic activity of SAC against HCC. K E Y W O R D S DEN, Fas, HepG2, p53, pp38MAPK, SAC

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Section: Methodsmentioning

confidence: 99%

Association of p38MAPK‐p53‐Fas aggregation in S‐allyl cysteine mediated regulation of hepatocarcinoma

Chatterjee

Patra

Chakraborti

et al. 2019

Environmental Toxicology

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“…The clinical implications of this remain unclear. SPARC levels are increased in patients with coronary artery disease [105,106] and predict adverse cardiovascular outcomes in moderate to severe heart failure [107] but have not proved useful in distinguishing patients with acute MI [108,109].…”

Section: Sparcmentioning

confidence: 99%

“…[ [105][106][107][108][109] Tenascin C (TN-C) Serum TN-C levels are increased in patients with coronary artery disease (n = 60) compared to controls (n = 20). In patients with ACS, TN-C levels are significantly higher in patients with ruptured plaque (n = 23) compared to those with non-ruptured plaques (n = 29).…”

Section: Sparcmentioning

confidence: 99%

The Role of Matrix Proteins in Cardiac Pathology

Trinh

Julovi

Rogers

2022

IJMS

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The extracellular matrix (ECM) and ECM-regulatory proteins mediate structural and cell-cell interactions that are crucial for embryonic cardiac development and postnatal homeostasis, as well as organ remodeling and repair in response to injury. These proteins possess a broad functionality that is regulated by multiple structural domains and dependent on their ability to interact with extracellular substrates and/or cell surface receptors. Several different cell types (cardiomyocytes, fibroblasts, endothelial and inflammatory cells) within the myocardium elaborate ECM proteins, and their role in cardiovascular (patho)physiology has been increasingly recognized. This has stimulated robust research dissecting the ECM protein function in human health and disease and replicating the genetic proof-of-principle. This review summarizes recent developments regarding the contribution of ECM to cardiovascular disease. The clear importance of this heterogeneous group of proteins in attenuating maladaptive repair responses provides an impetus for further investigation into these proteins as potential pharmacological targets in cardiac diseases and beyond.

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“…8 This protein plays an important role in atherogenesis and may be a biomarker of atherosclerosis and calcinosis in coronary arteries. 9 Bone sialoprotein (BSP) also is involved in the initiation of atherosclerosis. Microarray analysis reveals that BSP is overexpressed in human carotid plaques.…”

mentioning

confidence: 99%

Oxidized Low-Density Lipoprotein and Upregulated Expression of Osteonectin and Bone Sialoprotein in Vascular Smooth Muscle Cells

Farrokhi¹,

Samani

Chaleshtori³

2014

Lab Med

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Blood Level of Osteonectin in Stenosing Atherosclerosis and Calcinosis of Coronary Arteries

Cited by 4 publications

References 12 publications

Association of p38MAPK‐p53‐Fas aggregation in S‐allyl cysteine mediated regulation of hepatocarcinoma

Association of p38MAPK‐p53‐Fas aggregation in S‐allyl cysteine mediated regulation of hepatocarcinoma

The Role of Matrix Proteins in Cardiac Pathology

Oxidized Low-Density Lipoprotein and Upregulated Expression of Osteonectin and Bone Sialoprotein in Vascular Smooth Muscle Cells

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