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

Suzuki, Kota; Satoh, Kimio; Ikeda, Shohei; Sunamura, Shinichiro; Otsuki, Tomohiro; Satoh, Taijyu; Kikuchi, Nobuhiro; Omura, Junichi; Kurosawa, Ryo; Nogi, Masamichi; Numano, Kazuhiko; Sugimura, Koichiro; Aoki, Tatsuo; Tatebe, Shunsuke; Miyata, Satoshi; Mukherjee, Rupak; Spinale, Francis G.; Kadomatsu, Kenji; Shimokawa, Hiroaki

doi:10.1161/atvbaha.115.306686

Cited by 49 publications

(35 citation statements)

References 55 publications

(34 reference statements)

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“…BSG also exhibited high expression in LV of patients with cardiomyopathy [18,19]. Moreover, upregulation of serum or plasma sBSG was observed in patients with heart failure and ACS [20,26]. High expression of sBSG indicates an unfavorable prognosis in heart failure [20].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, upregulation of serum or plasma sBSG was observed in patients with heart failure and ACS [20,26]. High expression of sBSG indicates an unfavorable prognosis in heart failure [20]. In aging mice, cardiac-restricted overexpression of BSG caused adverse myocardial remodeling consisting of LV dilatation, hypertrophy, and fibrosis along with increase and activation of MMPs [21].…”

Section: Discussionmentioning

confidence: 99%

“…Also, BSG is highly expressed in left ventricle (LV) of patients with myocardial infarction [16,17], inflammatory cardiomyopathy [18], and dilated cardiomyopathy [19]. Serum levels of sBSG were significantly elevated in patients with heart failure and were predictive of poor prognosis [20]. In mice model, persistent cardiomyocyte-specific overexpression of BSG increases MMPs levels and promotes cardiac fibrosis, adverse LV remodeling, and heart failure in response to chronic pressure overload and during aging [20,21].…”

Section: Introductionmentioning

confidence: 99%

“…Serum levels of sBSG were significantly elevated in patients with heart failure and were predictive of poor prognosis [20]. In mice model, persistent cardiomyocyte-specific overexpression of BSG increases MMPs levels and promotes cardiac fibrosis, adverse LV remodeling, and heart failure in response to chronic pressure overload and during aging [20,21]. On the contrary, BSG knockdown contributes to decrease in MMPs levels and resistance to pressure overload induced cardiac hypertrophy [20,22].…”

Section: Introductionmentioning

confidence: 99%

“…In mice model, persistent cardiomyocyte-specific overexpression of BSG increases MMPs levels and promotes cardiac fibrosis, adverse LV remodeling, and heart failure in response to chronic pressure overload and during aging [20,21]. On the contrary, BSG knockdown contributes to decrease in MMPs levels and resistance to pressure overload induced cardiac hypertrophy [20,22]. Cardiac BSG knockdown also improves adverse remodeling induced by IL-18 in the post-infarcted mice heart [23].…”

Section: Introductionmentioning

confidence: 99%

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Basigin rs8259 Polymorphism Confers Decreased Risk of Chronic Heart Failure in a Chinese Population

et al. 2017

IJERPH

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Left ventricular remodeling is an essential risk factor contributing to the pathogenesis of chronic heart failure (CHF). Basigin (BSG) promotes cardiovascular inflammation and myocardial remodeling processes by induction of extracellular matrix metalloproteinases and inflammatory cytokines. BSG rs8259 polymorphism was associated with BSG expression and risk of acute coronary syndrome. Therefore, we investigated whether rs8259 polymorphism contributes to risk and prognosis of CHF in Chinese patients. In total 922 adult patients with CHF and 1107 matched healthy controls were enrolled. BSG rs8259 polymorphism was genotyped using PCR-restriction fragment length polymorphism. Whole blood BSG mRNA expression data from Genotype-Tissue Expression project was accessed. Evaluation of follow-up data was performed in only 15.2% (140) of the patients with CHF. BSG rs8259 TT genotype was associated with a decreased risk of CHF (OR = 0.83, 95% CI = 0.72–0.96, p = 0.010), especially in patients with hypertension (OR = 0.80, 95% CI = 0.68–0.95, p = 0.011) and coronary heart disease (OR = 0.81, 95% CI = 0.69–0.96, p = 0.013) after adjustment for multiple cardiovascular risk factors. Rs8259 T allele was associated with decreased BSG mRNA in whole blood from 338 healthy normal donors (p = 1.31 × 10−6). However, rs8259 polymorphism failed to exhibit an association with cardiovascular mortality (p = 0.283). BSG rs8259 polymorphism may contribute to decreased risk of CHF in a Chinese Han population.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Basigin rs8259 Polymorphism Confers Decreased Risk of Chronic Heart Failure in a Chinese Population

et al. 2017

IJERPH

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Glycosylated CD147 reduces myocardial collagen cross‐linking in cardiac hypertrophy

Cui

Jiao

et al. 2018

J of Cellular Biochemistry

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The mechanism of transition from chronic pressure overload-induced cardiac hypertrophy to heart failure is still unclear. Angiotensin II (Ang II) may be an important factor that mediates the transition in the end-stage of cardiac hypertrophy. In the present study, Goldblatt two-kidney one-clip (2K1C) rat model was used to simulate Ang II-induced hypertension. The elevated Ang II not only induced the concentric hypertrophy of left ventricle and cardiac fibrosis, but also increased the expression and glycosylation of CD147 in 2K1C rats. The left ventricular structure and function detected by echocardiogram showed a sign of the transition from cardiac hypertrophy to heart failure in 16 weeks of 2K1C rats. Ang II can activate N-acetylglucosamine transferase V (GnT-V), a key enzyme for CD147 glycosylation. Retinoic acid, an agonist of GnT-V, further increased glycosylated CD147, and activated matrix metalloproteinase-2/-9 (MMP-2 and MMP-9) in the hypertrophied left ventricle of 2K1C rat. Meanwhile, collagen cross-linking in the hypertrophied left ventricle significantly reduced in 2K1C rats. On the contrary, tunicamycin, an inhibitor of N-glycan biosynthesis, inhibited glycosylation of CD147 and activity of MMP-2 and MMP-9, and then maintained a stable of collagen cross-linking in the 2K1C rat hearts. The above results suggested that Ang II increased glycosylated CD147 which activated MMP-2 and MMP-9. Collagens were degraded by the activated MMPs and then reduced collagen cross-linking. Finally, the hypertrophied left ventricle was progressively dilated in chronic pressure overload due to losing the limitation of collagen cross-linking. Therefore, the compensated hypertrophy of left ventricle gradually transited to congestive heart failure.

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Serum–glucocorticoid-regulated kinase 1 contributes to mechanical stretch-induced inflammatory responses in cardiac fibroblasts

Gan

Ren

et al. 2017

Mol Cell Biochem

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Excessive mechanical stretch induces production of proinflammatory mediators in cardiac fibroblasts, which could act as inflammatory supporter cells in heart failure. Accumulation evidence and our previous studies suggest that serum-glucocorticoid-regulated kinase 1 (SGK1) contributes to cardiac remodeling and fibrosis, development of heart failure. However, the role and mechanism of SGK1 in mechanical stretch-induced inflammation of cardiac fibroblasts remain unclear. Here, cardiac fibroblasts isolated from wild-type (WT) and SGK1 knockout (SGK1) mice were stimulated by 18% cyclic stretch, under static condition as the control. The results showed that mechanical stretch increased SGK1 expression and activation in WT cardiac fibroblasts but not its isoform, SGK2 or SGK3 expression. Bio-Plex array revealed hyperstretch could enhance chemokines release in WT cardiac fibroblasts, but SGK1 knockout significantly attenuated chemokines production through blocking activation of nuclear factor-kappa B (NF-κB). Moreover, supernatants from WT cardiac fibroblasts subjected to hyperstretch promoted macrophage migration, enhanced expression of macrophage-derived profibrotic mediators, whereas supernatants from SGK1 deficiency suppressed these effects. Although SGK1 did not directly affect mechanical stretch-induced myofibroblast differentiation, SGK1 activation of cardiac fibroblasts facilitated myofibroblast differentiation through the upregulation of the profibrotic mediators secreted by macrophages. These results suggest that SGK1 may play a critical role in the inflammatory cascade of cardiac fibroblasts triggered by mechanical stretch; SGK1 could be used as a potential target for treatment of cardiac fibrosis and heart failure.

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

Cited by 49 publications

References 55 publications

Basigin rs8259 Polymorphism Confers Decreased Risk of Chronic Heart Failure in a Chinese Population

Basigin rs8259 Polymorphism Confers Decreased Risk of Chronic Heart Failure in a Chinese Population

Glycosylated CD147 reduces myocardial collagen cross‐linking in cardiac hypertrophy

Serum–glucocorticoid-regulated kinase 1 contributes to mechanical stretch-induced inflammatory responses in cardiac fibroblasts

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