Basic fibroblast growth factor inhibits ventricular remodeling in Dahl salt-sensitive hypertensive rats

Suzuki, Takeya; Akasaka, Yoshikiyo; Namiki, Atsushi; Ito, Kinji; Ishikawa, Yukio; Yamazaki, Junichi; Ishii, Toshiharu

doi:10.1097/hjh.0b013e328312c889

Cited by 6 publications

(3 citation statements)

References 37 publications

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“…Our findings are consistent with the work of others who observed that FGF-2 regulates TGFβ1-mediated myofibroblast activity in non-cardiac derived cells [ 26 - 29 ]. Furthermore, and in support of our findings, Suzuki and co-workers documented an anti-fibrotic effect with addition of exogenous FGF-2 to the hearts of hypertensive rats [ 30 ]. To explain a possible mechanism of action, Cushing and co-workers showed that FGF-2 stimulates MAPK signaling and blocks the localization of SMADs into the nucleus.…”

Section: Discussionsupporting

confidence: 88%

Fibroblast growth factor-2 regulates human cardiac myofibroblast-mediated extracellular matrix remodeling

et al. 2015

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BackgroundTissue fibrosis and chamber remodeling is a hallmark of the failing heart and the final common pathway for heart failure of diverse etiologies. Sustained elevation of pro-fibrotic cytokine transforming growth factor-beta1 (TGFβ1) induces cardiac myofibroblast-mediated fibrosis and progressive structural tissue remodeling.ObjectivesWe examined the effects of low molecular weight fibroblast growth factor (LMW-FGF-2) on human cardiac myofibroblast-mediated extracellular matrix (ECM) dysregulation and remodeling.MethodsHuman cardiac biopsies were obtained during open-heart surgery and myofibroblasts were isolated, passaged, and seeded within type I collagen matrices. To induce myofibroblast activation and ECM remodeling, myofibroblast-seeded collagen gels were exposed to TGFβ1. The extent of ECM contraction, myofibroblast activation, ECM dysregulation, and cell apoptosis was determined in the presence of LMW-FGF-2 and compared to its absence. Using a novel floating nylon-grid supported thin collagen gel culture platform system, myofibroblast activation and local ECM remodeling around isolated single cells was imaged using confocal microscopy and quantified by image analysis.ResultsTGFβ1 induced significant myofibroblast activation and ECM dysregulation as evidenced by collagen gel contraction, structural ECM remodeling, collagen synthesis, ECM degradation, and altered TIMP expression. LMW-FGF-2 significantly attenuated TGFβ1 induced myofibroblast-mediated ECM remodeling. These observations were similar using either ventricular or atrial-derived cardiac myofibroblasts. In addition, for the first time using individual cells, LMW-FGF-2 was observed to attenuate cardiac myofibroblast activation and prevent local cell-mediated ECM perturbations.ConclusionsLMW-FGF-2 attenuates human cardiac myofibroblast-mediated ECM remodeling and may prevent progressive maladaptive chamber remodeling and tissue fibrosis for patients with diverse structural heart diseases.

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Section: Discussionsupporting

confidence: 88%

Fibroblast growth factor-2 regulates human cardiac myofibroblast-mediated extracellular matrix remodeling

et al. 2015

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“…But after tanshinone IIA treated, TGF-β1 secretion was decreased and bFGF secretion was increased significantly than 5%GS group. bFGF is capable of suppressing TGF-β1-induced fibroblast differentiation [53] and limiting progressive fibrosis [54]. TGF-β1, after binding to its receptors, activated downstream mediators that leaded to classic Smads signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

The Complex Regulation of Tanshinone IIA in Rats with Hypertension-Induced Left Ventricular Hypertrophy

Hui

Han

et al. 2014

PLoS ONE

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Tanshinone IIA has definite protective effects on various cardiovascular diseases. However, in hypertension-induced left ventricular hypertrophy (H-LVH), the signaling pathways of tanshinone IIA in inhibition of remodeling and cardiac dysfunction remain unclear. Two-kidney, one-clip induced hypertensive rats (n = 32) were randomized to receive tanshinone IIA (5, 10, 15 mg/kg per day) or 5% glucose injection (GS). Sham-operated rats (n = 8) received 5%GS as control. Cardiac function and dimensions were assessed by using an echocardiography system. Histological determination of the fibrosis and apoptosis was performed using hematoxylin eosin, Masson’s trichrome and TUNEL staining. Matrix metalloproteinase 2 (MMP2) and tissue inhibitor of matrix metalloproteinases type 2 (TIMP2) protein expressions in rat myocardial tissues were detected by immunohistochemistry. Rat cardiomyocytes were isolated by a Langendorff perfusion method. After 48 h culture, the supernatant and cardiomyocytes were collected to determine the potential related proteins impact on cardiac fibrosis and apoptosis. Compared with the sham rats, the heart tissues of H-LVH (5%GS) group suffered severely from the oxidative damage, apoptosis of cardiomyocytes and extracellular matrix (ECM) deposition. In the H-LVH group, tanshinone IIA treated decreased malondialdehyde (MDA) content and increased superoxide dismutase (SOD) activity. Tanshinone IIA inhibited cardiomyocytes apoptosis as confirmed by the reduction of TUNEL positive cardiomyocytes and the down-regulation of Caspase-3 activity and Bax/Bcl-2 ratio. Meanwhile, plasma apelin level increased with down-regulation of APJ receptor. Tanshinone IIA suppressed cardiac fibrosis through regulating the paracrine factors released by cardiomyocytes and the TGF-β/Smads signaling pathway activity. In conclusion, our in vivo study showed that tanshinone IIA could improve heart function by enhancing myocardial contractility, inhibiting ECM deposition, and limiting apoptosis of cardiomyocytes and oxidative damage.

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“…In contrast, others studies point to an anti-fibrotic effect of FGF-2. In Dahl salt-sensitive rats FGF-2 inhibited interstitial fibrosis and then the progression of ventricular remodeling [169] . Moreover, it was observed that lo-FGF-2 was able to attenuating ECM remodeling by myofibroblasts cultured within a 3D collagen matrix [170] .…”

Section: Fibrosismentioning

confidence: 96%

Neurotrophic Factors and Heart Diseases

Martinelli

Camargos

2016

Journal of Cardiology and Therapy

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Neurotrophic factors are well known for their action on the development, survival and regeneration of neurons. However, new functions have been assigned to those peptides not only during development but also throughout the postnatal life. The searches for new therapeutic strategies have highlighted the role of neurotrophic factors in various phenomena related to pathological and physiological processes. In this review will summarize the knowledge of the families of neurotrophic factors as well as other growth factors with known neurotrophic activity. We also aim to provide a synopsis of the involvement of those peptides in cardiac diseases since this knowledge undoubtedly contributes to the development of therapeutic strategies for prevention and treatment of heart diseases.

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Basic fibroblast growth factor inhibits ventricular remodeling in Dahl salt-sensitive hypertensive rats

Abstract: bFGF can inhibit the progression of ventricular remodeling by inhibiting interstitial fibrosis and promoting angiogenesis without decreasing blood pressure in hypertensive heart disease.

Cited by 6 publications

References 37 publications

Fibroblast growth factor-2 regulates human cardiac myofibroblast-mediated extracellular matrix remodeling

Fibroblast growth factor-2 regulates human cardiac myofibroblast-mediated extracellular matrix remodeling

The Complex Regulation of Tanshinone IIA in Rats with Hypertension-Induced Left Ventricular Hypertrophy

Neurotrophic Factors and Heart Diseases

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