Specific Overexpression of YAP in Vascular Smooth Muscle Attenuated Abdominal Aortic Aneurysm Formation by Activating Elastic Fiber Assembly via LTBP4.

Abdominal aortic aneurysm (AAA) is a fatal vascular disease. Vascular smooth muscle cells (VSMCs) play a crucial role in the pathogenesis of AAA. Increasing evidence has shown that Yes-associated protein (YAP) is involved in diverse vascular diseases.

Brown Adipose Tissue Activation Is Involved in Atherosclerosis of ApoE Mice Induced by Chronic Intermittent Hypoxia.

Obstructive sleep apnea is an atherogenesis factor of which chronic intermittent hypoxia is a prominent feature. Chronic intermittent hypoxia (CIH) exposure can sufficiently activate the sympathetic system, which acts on the β3 adrenergic receptors of brown adipose tissue (BAT). However, the activity of BAT and its function in CIH-induced atherosclerosis have not been fully elucidated.

Mirabegron Ameliorated Atherosclerosis of ApoE Mice in Chronic Intermittent Hypoxia but Not in Normoxia.

Purpose: It has been established that obstructive sleep apnea (OSA) is an independent risk factor for atherosclerosis. Chronic intermittent hypoxia (CIH) activates sympathoadrenal system and upregulates β3 adrenergic receptor (β3 AR). However, the effect of selective β3 AR agonist mirabegron in CIH-induced atherosclerosis remains unknown.

The establishment of a homozygous SNTA1 knockout human embryonic stem cell line (WAe009-A-50) using the CRISPR/Cas9 system.

SNTA1 encodes α1-syntrophin, a scaffold protein, which is a component of the dystrophin-associated protein complex. Additionally, α1-syntrophin interacts with SCN5A and nNOS-PMCA4b complex in cardiomyocytes. SNTA1 is a susceptibility locus for arrhythmia and cardiomyopathy.

Ascorbic acid can promote the generation and expansion of neuroepithelial-like stem cells derived from hiPS/ES cells under chemically defined conditions through promoting collagen synthesis.

Introduction: Spinal cord injury (SCI) is a neurological, medically incurable disorder. Human pluripotent stem cells (hPSCs) have the potential to generate neural stem/progenitor cells (NS/PCs), which hold promise in the treatment of SCI by transplantation. In our study, we aimed to establish a chemically defined culture system using serum-free medium and ascorbic acid (AA) to generate and expand long-term self-renewing neuroepithelial-like stem cells (lt-NES cells) differentiated from hPSCs effectively and stably.

Lipidomics reveals the dynamics of lipid profile altered by omega-3 polyunsaturated fatty acid supplementation in healthy people.

Glycerophospholipids (GPs) and sphingolipids (SPs) are important lipid components in the body and play biological functions. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) are important nutrients, and their supplements are commonly used for preventing some diseases. However, the effect of n-3 PUFAs on the human glycerophospholipidome and sphingolipidome is unclear.

Thoracic Endoscopic-Assisted Mini-Open Surgery for Thoracic and Thoracolumbar Spinal Cord Compression.

Intervertebral disc herniation is a common cause of spinal cord compression, especially for the thoracic and thoracolumbar spinal cord, which has limited buffer space in the spinal canal. Spinal cord compression usually causes decreased sensation and paralysis of limbs below the level of compression, urinary and fecal incontinence, and/or urinary retention, which brings great suffering to the patients and usually requires surgical intervention. Thoracotomy or abdominothoracic surgery is usually performed for the thoracolumbar cord compression caused by hard intervertebral disc herniation.

Cardiomyocyte-specific loss of diacylglycerol acyltransferase 1 (DGAT1) reproduces the abnormalities in lipids found in severe heart failure.

Diacylglycerol acyltransferase 1 (DGAT1) catalyzes the final step in triglyceride synthesis, the conversion of diacylglycerol (DAG) to triglyceride. Dgat1(-/-) mice exhibit a number of beneficial metabolic effects including reduced obesity and improved insulin sensitivity and no known cardiac dysfunction. In contrast, failing human hearts have severely reduced DGAT1 expression associated with accumulation of DAGs and ceramides.

Adrenomedullin(27-52) inhibits vascular calcification in rats.

Adrenomedullin (ADM) has the vasodilatory properties and involves in the pathogenesis of vascular calcification. ADM could be degraded into more than six fragments in the body, including ADM(27-52), and we suppose the degrading fragments from ADM do the same bioactivities as derived peptides from pro-adrenomedullin. The present study carries forward by assessing the effects on vascular calcification of the systemic administration of ADM(27-52).

Plasma mitochondrial coupling factor 6 in patients with acute myocardial infarction.

Previous studies have shown that mitochondrial coupling factor 6 (CF6) is an endogenous peptide that inhibits prostacyclin (PGI2) synthesis in vascular endothelial cells. In this study, we measured the plasma CF6 level of patients with acute myocardial infarction (AMI) to observe dynamic changes of CF6. All patients showed elevated plasma CF6 levels upon admission for treatment of AMI.

Changes in production and metabolism of brain natriuretic peptide in rats with myocardial necrosis.

In this study, we employed rat model of acute myocardial necrosis induced by isoproterenol (ISO) to study the possible roles of corin, the protease uniquely distributing in myocardium to convert pro-brain natriuretic peptide (proBNP) to BNP, and neutral endopeptidase (NEP), the major enzyme to degrade BNP, in changing the levels of BNP. In rats with isoproterenol alone, the myocardium necrosis occurred and the cardiac function was inhibited; the BNP contents in plasma and myocardium were upregulated, so did the myocardial corin mRNA level; the NEP activity in plasma and myocardium were downregulated. Omapatrilat (OMA) treatment relieved myocardial lesions and improved cardiac function.

[Hydrogen sulfide: a novel cardiovascular functional regulatory gas factor].

Hydrogen sulfide (H(2)S) may be endogenously produced by cystathionine beta-lyase (CBS) and cystathionine gamma-lyase (CSE) as a cardiovascular physiological functional factor. On the hypoxic pulmonary hypertension (HPH) animal model, the plasma H(2)S concentration, the gene expression and the activity (CSE) were decreased in lung tissues In L-NAME induced hypertension and spontaneous hypertension rats (SHR) models, the plasma H(2)S concentration, vascular CSE activity and mRNA expression were obviously decreased. When H(2)S was exogenously supplied, systolic pressure obviously decrease.

Endothelin-1 is a potent regulator in vivo in vascular calcification and in vitro in calcification of vascular smooth muscle cells.

We observed changes of endothelin content and endothelin mRNA in vivo in vascular calcification and in vitro in calcification of vascular smooth muscle cells to explore the role of endothelin in vascular calcification. Calcification model in vivo was induced by administration of Vitamin D(3) plus nicotine. Calcification of vascular smooth muscle cells (VSMCs) was induced by beta-glycerophosphate.

Dysfunction of myocardial and vascular taurine transport in spontaneously hypertensive rats.

The alterations of taurine transport and the expression of taurine transporter (TAUT) mRNA in myocardium and aortic wall were investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. It was demonstrated that plasma taurine concentration and taurine release from myocardium and aortic wall in SHR were higher than those in WKY rats, whereas taurine content, taurine uptake and TAUT mRNA in myocardium and aortic wall of SHR were lower than those of WKY rats. In SHR, the maximal velocity (V(max)) of taurine transportation in myocardium and aortic wall was lower by 24% (P<0.

[Changes in adrenomedullin and receptor activity-modifying protein 2 mRNA in myocardium and vessels during L-NNA-induced hypertension in rats].

To explore the changes in adrenomedullin (ADM) and receptor activity-modifying protein 2 (RAMP2) mRNA in myocardium and vessels in hypertension, a hypertensive rat model was prepared by administering L-NNA. Contents of ADM in plasma, myocardium and vessels were measured by radioimmunoassay (RIA). The levels of pro-ADM mRNA of myocardium and vessels were determined by competitive quantitative RT-PCR.