Combination treatment of adipose-derived stem cells and adiponectin attenuates pulmonary arterial hypertension in rats by inhibiting pulmonary arterial smooth muscle cell proliferation and regulating the AMPK/BMP/Smad pathway

Lu, Luo; Zheng, Wuhong; Lian, Guili; Chen, Huaning; Li, Ling; Xu, Changsheng; Xie, Liangdi

doi:10.3892/ijmm.2017.3226

Cited by 17 publications

(23 citation statements)

References 52 publications

(58 reference statements)

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“…7,9,11,15 Evaluation of cardiac function Transthoracic echocardiography was performed on day 35 after the first MCT injection as described previously. 19 The rats were anesthetized with 2% sodium pentobarbital (50 mg/kg, IP) and were laid in the supine position. Echocardiography was performed using a GE Vivid-E9 ultrasound device (General Electric Co., Fairfield, CT, USA) with a 12.0 MHz linear array transducer.…”

Section: Animalsmentioning

confidence: 99%

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Pulmonary arterial hypertension induced by a novel method: Twice-intraperitoneal injection of monocrotaline

Zhuang

Lian

Huang

et al. 2018

Exp Biol Med (Maywood)

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Pulmonary arterial hypertension (PAH) in humans manifests as a chronic process. However, PAH induced by high-dose monocrotaline (MCT) in animals occurs as a subacute process. To establish a chronic PAH model, rats were randomly divided into three groups, control (ctrl), single injection (SI), and twice injection (TI) groups. Rats in the SI group received a single intraperitoneal injection of 40 mg/kg MCT on day 0. Rats in the TI group received twice injections of 20 mg/kg MCT on days 0 and 7. Survival percentage, characteristic changes of pulmonary arterial variables, and right ventricular features were evaluated. Thirty-five days after the first MCT injection, survival percentage in TI group was higher than that in the SI group. The mean pulmonary arterial pressure (mPAP), right ventricular hypertrophy index (RVHI), pulmonary vascular remodeling, serum tumor necrosis factor α (TNFα), and interleukin-6 (IL-6) were higher either in SI or in TI 28 and 35 days after the first MCT injection. The rats in the SI and TI groups exhibited higher right ventricle end diastolic diameter (RVEDD) and lower adjusted pulmonary artery acceleration time (PAAT/HR), tricuspid annular plane systolic excursion (TAPSE), cardiac output (CO) and right ventricle fractional shortening (RVFS) when compared with controls. However, mPAP, RVHI, TAPSE, PAAT/HR, CO, TNFα, and IL-6 were lower and RVEDD were higher in the TI group than in the SI group. Pulmonary macrophage infiltration and right ventricle (RV) fibrosis were lower in TI than SI groups. The cardiomyocyte cross-sectional area and the beta myosin heavy chain (MYH7) mRNA level of RV were lower in TI than SI, whereas alpha myosin heavy chain (MYH6) was increased. These results show that two intraperitoneal injections of 20 mg/kg MCT with seven days interval could induce a model similar to chronic PAH with increased survival percentage in rats. Impact statement We demonstrated previously that a single intraperitoneal injection of 40 mg/kg MCT produced a subacute, not chronic, PAH model in rats, and the short survival periods of these rats did not represent adequately the chronic PAH seen in humans. To overcome this limitation, in this study, the single dose of 40 mg/kg MCT was divided into twice injections of 20 mg/kg with an interval of seven days. This modified administration of MCT produced an animal model much more similar to chronic PAH with prolonged survival and characteristic changes of structures and function in pulmonary arteries and right ventricles.

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Section: Animalsmentioning

confidence: 99%

“…RVHI was calculated based on the ratio RV/(LVþS), which is considered as the level of right ventricular hypertrophy. 19…”

Section: Rvhimentioning

confidence: 99%

Pulmonary arterial hypertension induced by a novel method: Twice-intraperitoneal injection of monocrotaline

Zhuang

Lian

Huang

et al. 2018

Exp Biol Med (Maywood)

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“…Based on the molecular pathways mentioned above, tyrosine kinase inhibitors (platelet-derived growth factor inhibitors) and serotonin antagonists are being explored, but present outcomes are not ideal. Moreover, ROCK inhibitors, VEGF receptor inhibitors, stem cell therapy, mTOR inhibitors, PPAR- γ agonist, and strategies aiming at Warburg effect are all in the early phase of research [ 15 , 142 – 144 , 151 , 152 ].…”

Section: Potential Treatment To Pahmentioning

confidence: 99%

The Role and Regulation of Pulmonary Artery Smooth Muscle Cells in Pulmonary Hypertension

Zhu

Fang

2020

International Journal of Hypertension

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Pulmonary hypertension (PH) is one of the most devastating cardiovascular diseases worldwide and it draws much attention from numerous scientists. As an indispensable part of pulmonary artery, smooth muscle cells are worthy of being carefully investigated. To elucidate the pathogenesis of PH, several theories focusing on pulmonary artery smooth muscle cells (PASMC), such as hyperproliferation, resistance to apoptosis, and cancer theory, have been proposed and widely studied. Here, we tried to summarize the studies, concentrating on the role of PASMC in the development of PH, feasible molecular basis to intervene, and potential treatment to PH.

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“…Some researches showed that Ang(1-7) supplement significantly increases the levels of adiponectin [28,160], not only in circulation but also in the myocardial [161]. At the same time, more studies in recent years have reported that adiponectin may achieve its protective effect by activating AMPK [162][163][164][165]. Adiponectin or adiponectin receptors agonists activate several downstream signal transduction pathways mediated by AMPK and PPAR-α to improve fibrotic disorders [156].…”

Section: Adiponectinmentioning

confidence: 99%

AMPK: a balancer of the renin–angiotensin system

Liu

et al. 2019

Bioscience Reports

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The renin–angiotensin system (RAS) is undisputedly well-studied as one of the oldest and most critical regulators for arterial blood pressure, fluid volume, as well as renal function. In recent studies, RAS has also been implicated in the development of obesity, diabetes, hyperlipidemia, and other diseases, and also involved in the regulation of several signaling pathways such as proliferation, apoptosis and autophagy, and insulin resistance. AMP-activated protein kinase (AMPK), an essential cellular energy sensor, has also been discovered to be involved in these diseases and cellular pathways. This would imply a connection between the RAS and AMPK. Therefore, this review serves to draw attention to the cross-talk between RAS and AMPK, then summering the most recent literature which highlights AMPK as a point of balance between physiological and pathological functions of the RAS.

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Combination treatment of adipose-derived stem cells and adiponectin attenuates pulmonary arterial hypertension in rats by inhibiting pulmonary arterial smooth muscle cell proliferation and regulating the AMPK/BMP/Smad pathway

Cited by 17 publications

References 52 publications

Pulmonary arterial hypertension induced by a novel method: Twice-intraperitoneal injection of monocrotaline

Pulmonary arterial hypertension induced by a novel method: Twice-intraperitoneal injection of monocrotaline

The Role and Regulation of Pulmonary Artery Smooth Muscle Cells in Pulmonary Hypertension

AMPK: a balancer of the renin–angiotensin system

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