Simvastatin reverses cardiomyocyte hypertrophy via the upregulation of phosphatase and tensin homolog expression.

The aim of the present study was to investigate the effects of simvastatin on the protein kinase B (PKB) signaling pathway and the expression of phosphatase and tensin homolog (PTEN). The effects of simvastatin were analyzed by administering the drug orally to male spontaneously hypertensive rats (SHRs) at a dose of 10 mg/kg/day, while the control animals received an equal volume of saline. The systolic pressure (mmHg) of the rat tail artery was measured prior to the initiation of the experiment, and once a week until the end of the experiment.

[Status of glucose metabolism in Chinese essential hypertensive patients].

Objective: To investigate glucose metabolism status and its relationship with blood pressure, obesity, renal function and cardio-cerebral vascular events in Chinese essential hypertensive patients.

Methods: Essential hypertensive patients without diabetic history were enrolled in this cross-sectional survey. All patients filled in questionnaires and received physical examination and laboratory tests.

Serum omentin-1 levels are inversely associated with the presence and severity of coronary artery disease in patients with metabolic syndrome.

Context: Omentin-1, an adipokine secreted from visceral adipose tissue, has been reported to be associated with coronary artery disease (CAD) and metabolic disorders.

Objective: To clarify the relationship between serum omentin-1 levels and the presence and severity of CAD in patients with metabolic syndrome (MetS).

Methods: We measured serum omentin-1 levels in 175 consecutive patients with MetS and in 46 controls.

[The relationship between reactive oxygen species-dependent activation of p38 MAPK and the expression of tumor necrosis factor-α in cultured cardiomyocytes].

Aim: To investigate the role of p38 mitogen-activated protein kinase(MAPK) in lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) expression in neonatal rat cardiomyocytes and to determine the relationship between reactive oxygen species (ROS) and p38 MAPK activation.

Methods: Cardiomyocytes were isolated from neonatal Sprague-Dawley rats and cultured by differential adhesion. Expression of TNF-α was determined in culture medium by ELISA.

Mitogenic effect of arginine vasopressin on adult rat cardiac fibroblast: involvement of PKC-erk1/2 pathway.

Arginine vasopressin (AVP) has been implicated in the pathophysiology of cardiac hypertrophy. We previously demonstrated that AVP is a mitogen for neonatal rat cardiac fibroblasts (CFs). In the present study, we extend our investigation to adult rat CFs to explore whether AVP could induce adult rat CFs proliferation and, if so, to identify the underlying mechanisms.

Involvement of ERK and AKT signaling in the growth effect of arginine vasopressin on adult rat cardiac fibroblast and the modulation by simvastatin.

Arginine vasopressin (AVP) has been shown to directly induce neonatal rat cardiac fibroblasts (CFs) proliferation, a major component involved in cardiac hypertrophy. Herein, we explored whether AVP is also a growth factor for adult rat CFs and, if so, whether the growth effect could be inhibited by simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. AVP significantly increased DNA synthesis in adult rat CFs by 73.

Arginine vasopressin stimulates proliferation of adult rat cardiac fibroblasts via protein kinase C-extracellular signal-regulated kinase 1/2 pathway.

Arginine vasopressin (AVP), a neurohormone and hemodynamic factor implicated in the pathophysiology of hypertension and congestive heart failure, can also act as a growth-stimulating factor. Our previous work demonstrated that AVP is a mitogen for neonatal rat cardiac fibroblasts (CFs). In the present study, we extended our investigations to adult rat CFs to explore whether AVP could induce adult rat CF proliferation and, if so, to identify the mechanism involved.

Chymase induces profibrotic response via transforming growth factor-beta 1/Smad activation in rat cardiac fibroblasts.

Mast cell-derived chymase is implicated in myocardial fibrosis (MF), but the underlying mechanism of intracellular signaling remains unclear. Transforming growth factor-beta 1 (TGF-beta1) is identified as the most important profibrotic cytokine, and Smad proteins are essential, but not exclusive downstream components of TGF-beta 1 signaling. Moreover, novel evidence indicates that there is a cross talk between Smad and mitogen-activated protein kinase (MAPK) signaling cascade.

Arginine vasopressin increases iNOS-NO system activity in cardiac fibroblasts through NF-kappaB activation and its relation with myocardial fibrosis.

Previous studies have shown that arginine vasopressin (AVP) promotes myocardial fibrosis (MF), whereas nitric oxide (NO) inhibits MF. Cardiac fibroblasts (CFs) are the main target cells of MF. However, the modulatory effect of AVP on NO production in CFs and the role of this effect in MF are still unknown.

Inhibitory effect of cyclosporin A on growth and collagen synthesis of rat cardiac fibroblasts induced by arginine vasopressin.

Aim: To investigate the effects of cyclosporin A (CsA) on growth and collagen synthesis of cardiac fibroblasts (CFs) induced by arginine vasopressin (AVP).

Methods: CFs of neonatal Sprague-Dawley rats were isolated by trypsinization and cultured; growth-arrested CFs were stimulated with 1 x 10(-7) mol x L(-1) AVP in the presence or absence of CsA (0.05, 0.

Simvastatin attenuates hypertrophic responses induced by cardiotrophin-1 via JAK-STAT pathway in cultured cardiomyocytes.

Unlabelled: Cardiotrophin-1 (CT-1) is a cytokine involved in the growth and survival of cardiac cells via activation of the Janus activated kinase/signal transducer activator of transcription (JAK/STAT). Statins, 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, have effects that extend beyond cholesterol reduction and inhibit vascular smooth muscle cell (VSMC) proliferation and cardiac hypertrophy. However, whether stains also can inhibitin vitromyocardial hypertrophy or not still remains elusive.

[Effects of simvastatin on DNA synthesis in rat cardiac fibroblasts].

Objective: To investigate the effects of simvastatin (Sim) and the interference by mevalonate (MVA) against its effect on DNA synthesis in rat cardiac fibroblasts (CFs).

Methods: CFs were isolated from neonatal SD rats by trypsin digestion and growth-arrested CFs were stimulated with Sim and/or MVA at varied concentrations for different time lengths, and the DNA synthesis in the cells was measured by (3)H-thymidine ((3)H-TdR) incorporation assay.

Results: Sim decreased (3)H-TdR incorporation in the CFs in a concentration-dependent manner, and (3)H-TdR incorporation was significantly lower in cells treated with 1 x 10(-6) and 1 x 10(-5) mol/L Sim (1,175+/-202.

[Effects of simvastatin on the left ventricular hypertrophy in spontaneously hypertensive rats and its relationship with the expression of protein kinase B].

Objective: To investigate the effects of simvastatin on left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs) and its possible mechanism.

Methods: Sixteen male SHRs were randomly divided into 2 equal groups: treatment group and SHR control to be given simvastatin or glucose-normal saline by oral gavage for 10 weeks. Eight Wistar-Kyoto (WKY) rats were given normal saline as normal controls.

[Expression of cellular repressor of E1A-stimulated genes in vascular smooth muscle cells of different phenotypes].

Objectives: The phenotypic modulation of vascular smooth muscle cells (VSMC) plays a central role in the pathogenesis of arteriosclerosis. The purpose of this study was to investigate the expression of the cellular repressor of E1A-activated genes (CREG) at the transcriptional and protein level in human internal thoracic artery smooth muscle cells (HITASY), which express different patterns of differentiation markers after serum withdrawal.

Methods: After cloning and recombining the CREG vector, the antiserum against the CREG protein was produced from the rabbits immunized by the purification CREG protein.

[Arginine vasopressin-induced nitric oxide content changes in cultured cardiac fibroblasts and its relation to nuclear factor-kappaB].

To investigate the changes in the nitric oxide (NO) contents, nitric oxide synthase (NOS) activity and inducible nitric oxide (iNOS) mRNA expression in arginine vasopressin (AVP)-induced cardiac fibroblasts (CFs) in vitro and its relation to nuclear factor-kappaB (NF-kappaB), CFs were isolated by trypsin digestion method. Nitric acid reductase method, spectrophotometry, reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence-interactive laser cytometer techniques and Western blotting were used respectively to detect NO contents, NOS activity, iNOS mRNA expression and the activation of NF-kappaB in CFs. AVP increased NO contents, NOS activity and iNOS mRNA expressions in a concentration-dependent manner; NF-kappaB was activated and mobilized from cytoplasm to nucleus in AVP-induced CFs; PDTC, one of the inhibitors of NF-kappaB, could inhibit aforementioned increments.

Effects of arginine vasopressin on growth of rat cardiac fibroblasts: role of V1 receptor.

The abnormal proliferation of cardiac fibroblasts is involved in the pathophysiologic process of left ventricular hypertrophy (LHV) associated with essential hypertension. Arginine vasopressin (AVP) has been reported to contribute significantly to the pathogenesis of hypertension. In this study, the authors investigated the effects of AVP and its V1 receptor antagonist [d(CH2)5Tyr2(Me)]AVP on the growth of rat cardiac fibroblasts.

[Effects of chelerythrine on cell proliferation and p27 expression of cardiac fibroblasts modulated by arginine vasopressin].

Objective: To study the effects of chelerythrine, a protein kinase C (PKC) inhibitor, on the cell proliferation and p27 expression of cardiac fibroblasts (CFs) modulated by arginine vasopressin (AVP) and to investigate the intracellular signal transduction mechanisms of AVP in CFs.

Methods: The cultured CFs of neonatal Sprague-Dawley rats were divided into 3 groups: AVP group (10(-7) mol/L AVP was added into the culture), chelerythrine group (10(-6) mol/L chelerythrine and 10(-7) mol/L AVP were added into the culture), and control group. MTT assay was used to evaluate the cell proliferation.

[Effects of atorvastatin on the proliferation and collagen synthesis of rat cardiac fibroblasts].

Objective: To investigate the effects of atorvastatin on the proliferation and collagen synthesis of rat cardiac fibroblasts (CFs).

Methods: Isolated and cultured CFs of neonatal Sprague-Dawley (SD) rats were isolated and cultured. The DNA synthesis of CFs was measured by (3)H-TdR uptake test.