Berberine reduces both MMP-9 and EMMPRIN expression through prevention of p38 pathway activation in PMA-induced macrophages

Huang, Zhouqing; Wang, Liansheng; Shao, Meng; Wang, Yue; Chen, Ting; Wang, Changqian

doi:10.1016/j.ijcard.2009.06.023

Cited by 58 publications

(59 citation statements)

References 35 publications

(40 reference statements)

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“…27,44,45 For indirect inhibition, berberine, resveratrol, and curcumin have been reported to inhibit Bsg expression through regulation of mitogen-activated protein kinase and reactive oxygen species. [46][47][48][49] In this study, we showed that systemic Bsg inhibition showed resistance to chronic pressure overload in mice in vivo. Thus, inhibition of Bsg could be a promising therapeutic strategy for heart failure.…”

Section: Bsg As a Therapeutic Target And A Novel Biomarkermentioning

confidence: 63%

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Suzuki

Satoh

Ikeda

et al. 2016

ATVB

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Objective— Basigin (Bsg) is a transmembrane glycoprotein that activates matrix metalloproteinases and promotes inflammation. However, the role of Bsg in the pathogenesis of cardiac hypertrophy and failure remains to be elucidated. We examined the role of Bsg in cardiac hypertrophy and failure in mice and humans. Approach and Results— We performed transverse aortic constriction in Bsg +/– and in wild-type mice. Bsg +/– mice showed significantly less heart and lung weight and cardiac interstitial fibrosis compared with littermate controls after transverse aortic constriction. Both matrix metalloproteinase activities and oxidative stress in loaded left ventricle were significantly less in Bsg +/– mice compared with controls. Echocardiography showed that Bsg +/– mice showed less hypertrophy, less left ventricular dilatation, and preserved left ventricular fractional shortening compared with littermate controls after transverse aortic constriction. Consistently, Bsg +/– mice showed a significantly improved long-term survival after transverse aortic constriction compared with Bsg +/+ mice, regardless of the source of bone marrow ( Bsg +/+ or Bsg +/– ). Conversely, cardiac-specific Bsg-overexpressing mice showed significantly poor survival compared with littermate controls. Next, we isolated cardiac fibroblasts and examined their responses to angiotensin II or mechanical stretch. Both stimuli significantly increased Bsg expression, cytokines/chemokines secretion, and extracellular signal–regulated kinase/Akt/JNK activities in Bsg +/+ cardiac fibroblasts, all of which were significantly less in Bsg +/– cardiac fibroblasts. Consistently, extracellular and intracellular Bsg significantly promoted cardiac fibroblast proliferation. Finally, serum levels of Bsg were significantly elevated in patients with heart failure and predicted poor prognosis. Conclusions— These results indicate the crucial roles of intracellular and extracellular Bsg in the pathogenesis of cardiac hypertrophy, fibrosis, and failure in mice and humans.

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Section: Bsg As a Therapeutic Target And A Novel Biomarkermentioning

confidence: 63%

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Suzuki

Satoh

Ikeda

et al. 2016

ATVB

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“…According to our previous study, berberine dosage under 50 mM is not considered to affect cell viability (Huang et al, 2011). So doses ranged from 5 to 20 mM were used in the subsequent experiments.…”

Section: Berberine Protects H9c2 Cells From H/r-induced Cell Deathmentioning

confidence: 99%

Berberine alleviates cardiac ischemia/reperfusion injury by inhibiting excessive autophagy in cardiomyocytes

Huang

Han

et al. 2015

European Journal of Pharmacology

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110

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“…Recently, berberine has been found to have cholesterol- (Kong et al, 2004) and glucose-lowering effects (Yin et al, 2008). Further, when THP-1 cells differentiate into macrophages, berberine inhibits MMP-9 and EMMPRIN expression (Huang et al, 2009). However, the role of berberine on the expression of MMP-9 and EMMPRIN and its possible mechanism in oxLDL-stimulated macrophages remain unclear.…”

mentioning

confidence: 99%

Suppression of oxLDL‐Induced MMP‐9 and EMMPRIN Expression by Berberine via Inhibition of NF‐κB Activation in Human THP‐1 Macrophages

Huang

Shao

Wang

et al. 2011

The Anatomical Record

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Upregulation of matrix metalloproteinases (MMPs) and extracellular matrix metalloproteinase inducer (EMMPRIN) by macrophages leads to atherosclerotic plaque rupture by degradation of the extracellular matrix. NF-jB activation regulates many key inflammatory genes linked to atherosclerosis. In the present study, the function of berberine, a natural extract from Rhizoma coptidis, on MMP-9 and EMMPRIN expression, the role of NF-jB activation in oxLDL-stimulated macrophages, and the possible mechanism in which NF-jB activation is involved were investigated. Berberine inhibited the expression of MMP-9 and EMMPRIN at both mRNA and protein levels. The phosphorylation of IjB-a and nuclear translocation of p65 protein were reduced by berberine, suggesting that NF-jB activation was inhibited by berberine in oxLDL-stimulated macrophages. Overall, berberine suppressed the expression of MMP-9 and EMMPRIN by at least reducing partly the activity of NF-jB in oxLDL-induced macrophages. Anat Rec, 295:78-86, 2012. V V C 2011 Wiley Periodicals, Inc.

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Berberine reduces both MMP-9 and EMMPRIN expression through prevention of p38 pathway activation in PMA-induced macrophages

Cited by 58 publications

References 35 publications

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Basigin Promotes Cardiac Fibrosis and Failure in Response to Chronic Pressure Overload in Mice

Berberine alleviates cardiac ischemia/reperfusion injury by inhibiting excessive autophagy in cardiomyocytes

Suppression of oxLDL‐Induced MMP‐9 and EMMPRIN Expression by Berberine via Inhibition of NF‐κB Activation in Human THP‐1 Macrophages

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