Atherosclerosis

2014

DOI: 10.1016/j.atherosclerosis.2014.07.004

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Osteopontin – A multi-modal marker and mediator in atherosclerotic vascular disease

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Sdi≥32

Introduction1

Osteopontin In Vascular Calcification1

Erythropoietin1

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Cited by 129 publications

(119 citation statements)

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“…Osteopontin (OPN) is a multifunctional protein involved in several physiological and pathological events that serves as a biomarker or therapeutic target for such conditions as cancer, cardiovascular diseases, and various intractable inflammatory diseases [1][2][3][4] . Currently, OPN has been implicated in the pathogenesis of insulin resistance, obesity, and diabetes [5] .…”

Section: Introductionmentioning

confidence: 99%

Wogonin suppresses osteopontin expression in adipocytes by activating PPARα

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et al. 2015

Acta Pharmacol Sin

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Aim: Wogonin (5,7-dihydroxy-8-methoxyflavone), a major bioactive compound of the flavonoid family, is commonly extracted from the traditional Chinese medicine Scutellaria baicalensis and possesses antioxidant and anti-inflammatory activities and is assumed to have anti-diabetes function. Indeed, a current study has shown that it can possibly treat metabolic disorders such as those found in db/db mice. However, the underlying molecular mechanism remains largely unclear. The aim of this study was to investigate the impact of wogonin on osteopontin (OPN) expression in adipose tissue from type 1 diabetic mice and in 3T3-L1 adipocytes. Methods: Type 1 diabetes was induced by streptozotocin (STZ) injection. 3T3-L1 preadipocytes were converted to 3T3-L1 adipocytes through treatment with insulin, dexamethasone, and 3-isobutyl-1-methylxanthine (IBMX). Western blot analysis and RT-PCR were performed to detect protein expression and mRNA levels, respectively. Results: Wogonin treatment suppressed the increase in serum OPN levels and reduced OPN expression in adipose tissue from STZinduced type 1 diabetic mice. Administration of wogonin enhanced PPARα expression and activity. Silencing of PPARα diminished the inhibitory effects of wogonin on OPN expression in 3T3-L1 adipocytes. Furthermore, the levels of c-Fos and phosphorylated c-Jun were reduced in wogonin-treated adipose tissue and 3T3-L1 adipocytes. In addition, wogonin treatment dramatically mitigated p38 MAPK phosphorylation. Pharmacological inhibition of p38 MAPK by its specific inhibitor SB203580 increased PPARα activity and decreased OPN expression. Conclusion: Our results suggest that wogonin downregulated OPN expression in adipocytes through the inhibition of p38 MAPK and the sequential activation of the PPARα pathway. Given the adverse effects of high OPN levels on metabolism, our results provide evidence for the potential administration of wogonin as a treatment for diabetes.

“…Osteopontin (OPN) is a multifunctional protein involved in several physiological and pathological events that serves as a biomarker or therapeutic target for such conditions as cancer, cardiovascular diseases, and various intractable inflammatory diseases [1][2][3][4] . Currently, OPN has been implicated in the pathogenesis of insulin resistance, obesity, and diabetes [5] .…”

Section: Introductionmentioning

confidence: 99%

Wogonin suppresses osteopontin expression in adipocytes by activating PPARα

¹

,

²

,

³

et al. 2015

Acta Pharmacol Sin

View full text Add to dashboard Cite

Aim: Wogonin (5,7-dihydroxy-8-methoxyflavone), a major bioactive compound of the flavonoid family, is commonly extracted from the traditional Chinese medicine Scutellaria baicalensis and possesses antioxidant and anti-inflammatory activities and is assumed to have anti-diabetes function. Indeed, a current study has shown that it can possibly treat metabolic disorders such as those found in db/db mice. However, the underlying molecular mechanism remains largely unclear. The aim of this study was to investigate the impact of wogonin on osteopontin (OPN) expression in adipose tissue from type 1 diabetic mice and in 3T3-L1 adipocytes. Methods: Type 1 diabetes was induced by streptozotocin (STZ) injection. 3T3-L1 preadipocytes were converted to 3T3-L1 adipocytes through treatment with insulin, dexamethasone, and 3-isobutyl-1-methylxanthine (IBMX). Western blot analysis and RT-PCR were performed to detect protein expression and mRNA levels, respectively. Results: Wogonin treatment suppressed the increase in serum OPN levels and reduced OPN expression in adipose tissue from STZinduced type 1 diabetic mice. Administration of wogonin enhanced PPARα expression and activity. Silencing of PPARα diminished the inhibitory effects of wogonin on OPN expression in 3T3-L1 adipocytes. Furthermore, the levels of c-Fos and phosphorylated c-Jun were reduced in wogonin-treated adipose tissue and 3T3-L1 adipocytes. In addition, wogonin treatment dramatically mitigated p38 MAPK phosphorylation. Pharmacological inhibition of p38 MAPK by its specific inhibitor SB203580 increased PPARα activity and decreased OPN expression. Conclusion: Our results suggest that wogonin downregulated OPN expression in adipocytes through the inhibition of p38 MAPK and the sequential activation of the PPARα pathway. Given the adverse effects of high OPN levels on metabolism, our results provide evidence for the potential administration of wogonin as a treatment for diabetes.

“…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][8][9][10].…”

Section: Osteopontin In Vascular Calcificationmentioning

confidence: 99%

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

2017

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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.

“…OPN levels have previously been linked to manifestations on the arterial side, such as the severity of coronary atherosclerosis, increased risk for major adverse cardiac events and peripheral arterial disease [107,108]. The role of OPN in cardiovascular disease is not clear.…”

Section: Sdi≥3mentioning

confidence: 99%

“…Some studies suggest OPN as a pro-inflammatory enhancer of atherosclerosis [107,109], while other propose OPN as a protector in post-myocardial infarction by recruiting macrophages and neutrophils to clean-up dead cell debris [110].…”

Section: Sdi≥3mentioning

confidence: 99%

Biomarkers of disease activity and organ damage in systemic lupus erythematosus

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Jag tror att när vi går igenom tiden att allt det bästa inte hänt än Håkan Hellström ABSTRACTSystemic lupus erythematosus (SLE) is a systemic inflammatory disease. Clinically, the distinction between ongoing inflammation attributed to SLE, and organ damage due to medication or co-morbidities remains challenging. In addition, SLE is a heterogeneous disease where the various disease phenotypes complicate the search for biomarkers that adequately reflect disease activity and/or signs of increasing organ damage. The aim of the thesis was to investigate and evaluate potential new biomarkers of disease activity and/or organ damage in SLE patients.High mobility group box protein-1 (HMGB1) is a nuclear non-histone protein that can shuttle to the cytoplasm, become secreted extracellularly, and participate in systemic inflammation.Administration of monoclonal anti-HMGB1 antibodies has been reported both to attenuate and intensify disease in animal models of arthritis and lupus. In Paper I of the thesis, circulating anti-HMGB1 was found in 23% of the SLE patients and correlated with disease activity variables. The biological role of these autoantibodies remains to be elucidated.As a consequence of massive circulating levels of cellular debris and immune complexes, SLE patients have insufficient capacity to remove such material via the reticuloendothelial system. Pentraxin 3 (PTX3) may possibly protect against lupus flares due to classical complement activation, opsonization of apoptotic cells, and cytokine induction. In Paper II, circulating PTX3 was found to be inhibited or exhausted by interferon (IFN)-α, a key cytokine of SLE pathogenesis, and serum levels of PTX3 in SLE patients were inversely related to IFN-α levels.Suppressed PTX3 levels may contribute to a vicious circle resulting in impaired waste clearance, autoantigen exposure and autoantibody production, and sustained disease activity.Osteopontin (OPN), a protein known to influence cell signaling and apoptosis, has been proposed as a marker of organ damage in pediatric lupus. In a Swedish cross-sectional study, circulating OPN levels were found to be raised in SLE (Paper III). In patients with recent-onset disease, OPN reflected disease activity, while in established disease, OPN appeared to mirror damage accrual and cardiovascular damage. In Paper IV, OPN was instead analyzed in an international longitudinal multi-center study based on patients with recent-onset SLE and follow-up data. OPN turned out to be a poor predictor of organ damage, but significant associations were observed between OPN and disease activity both at disease onset, as well as over 5 years of follow-up.In conclusion, increased anti-HMGB1 antibody and decreased PTX3 levels could potentially sustain the impaired waste-disposal. Of the molecules analyzed in this thesis, OPN seems to be the best marker of disease activity. Further studies of these proteins may help to better understand SLE pathogenesis and to optimize treatment of patients.

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