RNA-binding protein SFPQ cooperates with HDAC1 to suppress CD40 transcription in pulmonary adventitial fibroblasts.

Pulmonary artery adventitial fibroblasts, the most abundant cellular constituent of adventitia, are often the first to be activated and reprogrammed to then influence the tone and structure of the vessel wall in pulmonary arterial hypertension (PAH). Our previous study found that interruption of CD40 ligand (CD40L)-CD40 signaling improves the efficacy of transplanted endothelial progenitor cells in monocrotaline induced-PAH. However, whether CD40L-CD40 signaling is involved in the activation of adventitial fibroblasts in PAH and whether Drosophila behavior human splicing (DBHS) protein family members have any roles during adventitial fibroblasts activation are completely unclear. Here, we show that soluble CD40L (sCD40L) stimulation progressively increases pro-inflammatory activity, proliferation, and migration of pulmonary adventitial fibroblasts. Besides, sCD40L stimulation decreases splicing factor proline- and glutamine-rich protein (SFPQ) protein (one member of DBHS protein family) expression, while SFPQ overexpression suppresses sCD40L stimulation-induced proliferation and migration of pulmonary adventitial fibroblasts by repressing CD40 transcription. Moreover, ChIP assays found that sCD40L stimulation promotes histone H3 tri-methylation at lysine 4 (H3K4me3), H3K36me3, and H3K27 acetylation (H3K27ac) modifications on CD40 promoter region in pulmonary adventitial fibroblasts, while SFPQ overexpression decreases H3K36me3 modification and increases H3K36ac on CD40 promoter region by interacting with histone deacetylase-1 (HDAC1) to inhibit CD40 transcription. This in-depth study shows that CD40L-CD40 signaling promotes activation of pulmonary adventitial fibroblasts by increasing proliferation, migration, and pro-inflammatory activity of adventitial fibroblasts, and SFPQ could inhibit CD40 transcription though switching H3K36me3 to H3K36ac modifications on its promoter by interacting with HDAC1. This study, first, uncovers the roles of SFPQ on CD40L-CD40 signaling-mediated activation of pulmonary adventitial fibroblasts.

Phomopsis liquidambari colonization promotes continuous cropping peanut growth by improving the rhizosphere microenvironment, nutrient uptake and disease incidence.

BACKGROUND: The continuous cropping of peanuts is a primary cause of yield and quality loss. Solutions to this problem should be therefore developed to ensure the sustainability of peanut production. RESULTS: In this study, colonization by the endophytic fungus Phomopsis liquidambari was detected, which led to significantly improved rhizosphere soil microenvironment, enhanced N, P and K assimilation and suppressed incidence of peanut disease. Statistical analysis demonstrated that the yield enhancement was significantly correlated with improvement of the rhizosphere soil microenvironment and the peanut's physiological status by P. liquidambari colonization. In addition, P. liquidambari colonization also significantly improved peanut quality. CONCLUSION: Our results indicate that the practical application of the endophytic fungus P. liquidambari has a strong potential to alleviate the obstacles associated with continuous peanut cropping under field conditions. © 2018 Society of Chemical Industry.

Tanshinone II A Attenuates TNF-α-Induced Expression of VCAM-1 and ICAM-1 in Endothelial Progenitor Cells by Blocking Activation of NF-κB.

BACKGROUND/AIMS: Tanshinone IIA (Tan IIA) is effective in the treatment of inflammation and atherosclerosis. The adhesion of inflammatory cells to vascular endothelium plays important role in atherogenic processes. This study examined the effects of Tan IIA on expression of adhesion molecules in tumor necrosis factor-α (TNF-α)-induced endothelial progenitor cells (EPCs). METHODS: EPCs were pretreated with Tan IIA and stimulated with TNF-α. Mononuclear cell (MNC) adhesion assay was performed to assess the effects of Tan IIA on TNF-α-induced MNC adhesion. Expression of vascular cell adhesion molecule-1 (VCAM-1)/intracellular adhesion molecule-1 (ICAM-1) and activation of Nuclear factor κB (NF-κB) signaling pathway were measured. RESULTS: The results showed that the adhesion of MNCs to TNF-α-induced EPCs and expression of VCAM-1/ICAM-1 in EPCs were promoted by TNF-α, which were reduced by Tan IIA. TNF-α increased the amount of phosphorylation of NF-κB, IκB-α and IKKα/ß in cytosolic fractions and NF-κB p65 in nucleus, while Tan IIA reduced its amount. CONCLUSION: This study demonstrated a novel mechanism for the anti-inflammatory/anti-atherosclerotic activity of Tan IIA, which may involve down-regulation of VCAM-1 and ICAM-1 through partial blockage of TNF-α-induced NF-κB activation and IκB-α phosphorylation by the inhibition of IKKα/ß pathway in EPCs.

[Availability Changes in Different Exogenous Selenium Fertilizers in Soil and Their Effects on Selenium Accumulation in Wheat].

In order to understand the differences in the uptake and accumulation of several common exogenous selenium fertilizers by crops, a wheat pot experiment was conducted to study the availability changes in different selenium fertilizers (potassium selenate, potassium selenite, EDTA-chelated selenium, selenium powder, fly ash, and selenium-enriched straw) in soil and their effects on wheat growth and selenium uptake and distribution. The results showed that the change in availability of different exogenous selenium types in soil was different. During the whole growth period of wheat, the soil available selenium proportion of selenate, selenite, and EDTA-chelated selenium treatment was significantly higher than that of the control (CK), respectively, but there was no significant difference between the other treatments and the CK treatment. In the early stage of wheat growth, the soil available selenium proportion of selenate, selenite, and selenium powder treatment decreased gradually and tended to be stable in the later growth stage of wheat; however, the soil available selenium proportion of other exogenous selenium treatments showed a dynamic change of decreasing in the early period and increasing in the late period. The available selenium content in soil significantly affected the selenium uptake by wheat, and there was a significant positive correlation between them. Selenate application significantly increased the grain and leaf biomass of wheat, but other selenium fertilizers had no significant effect on wheat growth. The accumulation capacity of different exogenous selenium fertilizers for wheat followed the order of selenate>selenite, EDTA-chelated selenium>selenium powder, fly ash, and selenium-enriched straw. There was no significant difference between the selenium powder, fly ash, and selenium-enriched straw treatments and the CK treatment. Selenium was more easily transferred to and accumulated in the stems and leaves of wheat after the application of selenate, whereas selenium was more easily transferred to and accumulated in grains after the application of selenite and EDTA-chelated selenium.

Unique Huygens-Fresnel electromagnetic transportation of chiral Dirac wavelet in topological photonic crystal.

Light propagates in various ways depending on environment, including uniform medium, surface/interface and photonic crystals, which appears ubiquitously in daily life and has been exploited for advanced optics technology. We unveiled that a topological photonic crystal exhibits unique electromagnetic (EM) transport properties originating from the Dirac frequency dispersion and multicomponent spinor eigenmodes. Measuring precisely local Poynting vectors in microstrips of honeycomb structure where optics topology emerges upon a band gap opening in the Dirac dispersion and a p-d band inversion induced by a Kekulé-type distortion respecting C6v symmetry, we showed that a chiral wavelet induces a global EM transportation circulating in the direction counter to the source, which is intimately related to the topological band gap specified by a negative Dirac mass. This brand-new Huygens-Fresnel phenomenon can be considered as the counterpart of negative refraction of EM plane waves associated with upwardly convex dispersions of photonic crystals, and our present finding is expected to open a new window for photonic innovations.

Superparamagnetic iron oxide nanoparticles may affect endothelial progenitor cell migration ability and adhesion capacity.

BACKGROUND AIMS: Cell labeling with superparamagnetic iron oxide (SPIO) nanoparticles enables non-invasive tracking of transplanted cells. The aim of this study was to investigate whether SPIO nanoparticles have an effect on endothelial progenitor cell (EPC) functional activity and the feasibility of a protocol for labeling swine- and rat-origin EPC using SPIO nanoparticles at an optimized low dosage. METHODS: EPC were isolated from the peripheral blood of swine and bone marrow of rat and characterized. After ex vivo cultivation, EPC were labeled with SPIO nanoparticles (to make a series of final concentrations, 50, 100, 200 and 400 microg/mL) or vehicle control. We also investigated the long-term effects of 200 microg/mL SPIO nanoparticles on EPC (4, 8, 12 and 16 days after labeling). The labeling efficiency was tested through Prussian blue (PB) staining and the intracellular iron uptake was also measured quantitatively and confirmed. EPC proliferation and migration were determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell chamber assay, respectively. An EPC adhesion assay was performed by replating the cells on fibronectin-coated dishes and then counting the adherent cells. EPC apoptosis was evaluated using an Annexin V-FITC apoptosis kit. RESULTS: SPIO nanoparticles impaired EPC migration and promoted EPC adhesion. EPC proliferation and apoptosis were not affected. SPIO nanoparticles could label EPC efficiently at 200 microg/mL overnight without significantly affecting EPC functional activity. CONCLUSIONS: SPIO nanoparticles impaired the EPC migration ability and promoted the EPC adhesion capacity. EPC could be labeled efficiently at an appropriate concentration (200 microg/mL) without significantly affecting their functional activity.

Primary percutaneous coronary intervention in a COVID-19 patient with ST-segment elevation myocardial infarction after lung transplantation: a case report.

We present an unusual case of a patient with bilateral-lung transplantation due to severe coronavirus disease 2019 (COVID-19), who subsequently suffered complications with acute myocardial infarction and underwent primary percutaneous coronary intervention (PCI).

A high-performance topological bulk laser based on band-inversion-induced reflection.

Topological insulators are materials that behave as insulators in the bulk and as conductors at the edge or surface due to the particular configuration of their bulk band dispersion. However, up to date possible practical applications of this band topology on materials' bulk properties have remained abstract. Here, we propose and experimentally demonstrate a topological bulk laser. We pattern semiconductor nanodisk arrays to form a photonic crystal cavity showing topological band inversion between its interior and cladding area. In-plane light waves are reflected at topological edges forming an effective cavity feedback for lasing. This band-inversion-induced reflection mechanism induces single-mode lasing with directional vertical emission. Our topological bulk laser works at room temperature and reaches the practical requirements in terms of cavity size, threshold, linewidth, side-mode suppression ratio and directionality for most practical applications according to Institute of Electrical and Electronics Engineers and other industry standards. We believe this bulk topological effect will have applications in near-field spectroscopy, solid-state lighting, free-space optical sensing and communication.

Endothelial progenitor cells may inhibit apoptosis of pulmonary microvascular endothelial cells: new insights into cell therapy for pulmonary arterial hypertension.

BACKGROUND AIMS: Endothelial apoptosis underlies the pathophysiology of pulmonary arterial hypertension (PAH). Some factors/cytokines released by endothelial progenitor cells (EPC) have been revealed as potent inhibitors of apoptosis. The aim of this study was to investigate the effects of EPC on pulmonary microvascular endothelial cell (PMVEC) survival with the PAH condition. METHODS: PMVEC apoptosis was induced by high shear stress (HSS) with serum starvation or pro-inflammatory factors in an artificial capillary system. EPC were delivered into monocrotaline-induced PAH nude rats. RESULTS: PMVEC apoptosis under HSS and serum starvation conditions was significantly inhibited by EPC conditioned medium (CM). It was attenuated by vascular endothelial growth factor (VEGF)-A or -B blocking. EPC CM promoted PMVEC proliferation, which was weakened by VEGF-A or interleukin (IL)-8 blocking. The EPC CM caused less apoptosis of PMVEC induced by HSS plus pro-inflammatory factors. The anti-apoptotic effect of EPC CM was attenuated by blockade of either vascular endothelial growth factor receptor (VEGFR)-1 or -2. However, the pro-proliferating effect appeared to be weakened only by VEGFR-2 blocking. Both Erk1/2 and Akt phosphorylation were enhanced by EPC CM. VEGFR-2 blockage led to significant inhibition of Erk1/2 and Akt activation; VEGFR-1 blockage only of Erk1/2 activation. Human-origin VEGF co-localized with incorporated EPC in small pulmonary arterioles, and EPC transplantation resulted in down-regulation of caspase-3 expression. CONCLUSIONS: The VEGF-A/B-VEGFR-1/2-Erk1/2 signal pathway took major responsibility for the anti-apoptotic effects of EPC on PMVEC, and VEGF-A-VEGFR-2-Akt for pro-proliferating effects. Growth factors, secreted in a paracrine manner by transplanted EPC, inhibited cell apoptosis in PAH lung.

A combination of left ventricular noncompaction and double orifice mitral valve.

A 24-year-old woman admitted with mild chest distress associated with activity without chest complaint for twenty days. Two orifices were visible at the level of the mitral valve with a transthoracic short-axis view of the two-dimensional and three-dimensional echocardiography. The left ventricle was mildly dilatated and the left ventricular wall was thickened, especially at the apex and anterolateral wall, and appeared sponge-like. There were numerous, excessively prominent trabeculations associated with intertrabecular recesses. Although the coexistence of NVM and DOMV could be a coincidence, we believe that both defects were probably caused by a developmental arrest of the left ventricular myocardium in the present case.

Resveratrol attenuates thromboxane A2 receptor agonist-induced platelet activation by reducing phospholipase C activity.

Resveratrol (3,5,4'-trihydroxystilbene) is a naturally occurring compound shown to decrease the incidence of thromboembolic disease. Although considerable data are available as to the inhibitory effect of resveratrol on the platelet aggregation and thrombopoiesis in human, its underlying mechanism, at the cellular level, has not been rigorously studied. In this experiment, we studied the effect of resveratrol and 1-[6-[[17-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione, a phospholipase C inhibitor (U-73122) on the thromboxane A2 receptor agonist (9,11-dideoxy-11 alpha,9 alpha-epoxymethanoprostaglandin F(2 alpha), U46619)-induced platelet aggregation, platelet P-selectin expression, and the activity of phospho-phospholipase C beta 3 (P-PLC beta 3) and total-phospholipase C beta 3 (T-PLC beta 3), which play key roles in the signal transduction system of platelet in human. It was found that resveratrol blocked platelet aggregation and platelet P-selectin expression induced by U46619 in a concentration-dependent manner. U-73122 and resveratrol had additive effect in inhibiting platelet aggregation and platelet P-selectin expression. Resveratrol (final concentration was 50 microM) could reduce the ratio of P-PLC beta 3 to T-PLC beta 3. Taken together, these results show that resveratrol suppresses U46619-induced platelet aggregation and P-selectin expression partly through the decrease of the activity of phospholipase C beta of platelets.

Safety and efficacy of autologous endothelial progenitor cells transplantation in children with idiopathic pulmonary arterial hypertension: open-label pilot study.

Experimental data suggest that transplantation of EPCs attenuates monocrotaline-induced pulmonary hypertension in rats and dogs. In addition, our previous studies suggested that autologous EPC transplantation was feasible, safe, and might have beneficial effects on exercise capacity and pulmonary hemodynamics in adults with IPAH. Thus, we hypothesized that transplantation of EPCs would improve exercise capacity and pulmonary hemodynamics in children with IPAH. Thirteen children with IPAH received intravenous infusion of autologous EPCs. The right-sided heart catheterization and 6-MWD test were performed at baseline and at the time of 12 wk after cell infusion. At the time of 12 wk, mPAP decreased by 6.4 mmHg from 70.3 +/- 19.0 to 63.9 +/- 19.3 mmHg (p = 0.015). PVR decreased by approximately 19% from 1118 +/- 537 to 906 +/- 377 dyn s/cm(5) (p = 0.047). CO increased from 3.39 +/- 0.79 to 3.85 +/- 0.42 L/min (p = 0.048). The 6-MWD increased by 39 m from 359 +/- 82 to 399 +/- 74 m (p = 0.012). NYHA functional class also improved. There were no severe adverse events with cell infusion. The small pilot study suggested that intravenous infusion of autologous EPCs was feasible, safe, and associated with significant improvements in exercise capacity, NYHA functional class, and pulmonary hemodynamics in children with IPAH. Confirmation of these results in a randomized controlled trial are essential.

Resveratrol attenuates adenosine diphosphate-induced platelet activation by reducing protein kinase C activity.

Inappropriate platelet activation is the key point of thrombogenesis. The aim of the present study was to investigate the effects of resveratrol (RESV), a compound extracted from the Chinese medicinal herb Polygonum cuspidatum sieb et Zucc, on the platelet activation induced by adenosine diphosphate (ADP) and its possible mechanism. The percentage of platelet aggregation and surface P-selectin-positive platelets, and the activity of protein kinase C (PKC) of platelet were observed with platelet aggregometer, flow cytometry and phosphorimaging system, respectively. RESV at 25, 50 and 100 microM showed anti-platelet aggregation and inhibition of surface P-selectin-positive platelets in a concentration-dependent manner. RESV (50 microM) inhibited the activity of PKC in the membrane fraction of platelets and decreased the percentage of membrane associated PKC activity in total PKC activity. Moreover, DL-erythro-1,3-Dihydroxy-2-aminooctadecane, an elective protein kinase C inhibitor (PKCI), and RESV had additive effects of inhibiting the percentage of platelet aggregation and surface P-selectin-positive platelets. It is suggested that RESV may inhibit platelet aggregation, the percentage of surface P-selectin-positive platelets and subsequent thrombus formation. The mechanisms may be partly relative to the decrease of the activity of PKC of platelets.

[Inhibitory effect of resveratrol on cardiac fibroblast proliferation induced by angiotensin II].

OBJECTIVE: To observe the effect and mechanism of resveratrol on cardiac fibroblast (cFs) proliferation induced by angiotensin II (Ang II). METHODS: The in vitro cFs proliferation model was established by stimulating cultured cFs of new born rats with Ang II by differential attachment method. Cell proliferation was measured by MTT assay, and the effect of resveratrol, L-NAME and ODQ on cell proliferation were observed respectively. Besides, the hypertrophic response of cFs was estimated by measuring expressions of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) mRNA, with the levels of ANP and BNP in culture medium determined by radioimmunoassay and ELISA respectively; and their mRNA expressions determined by reverse transcription polymerase chain reaction (RT-PCR). Level of nitric oxide (NO) in the culture medium was measured by Griess reagent; nitric oxide synthase (NOS) level by chemical colorimetric method; and cGMP by radioimmunoassay. RESULTS: Resveratrol at the dose of 25-100 micromol/L inhibited cFs proliferation in a time and dose dependent manner, which could be partially blocked by pretreatment with L-NAME or ODQ. NO and cGMP levels increased, ANP, BNP levels and their mRNA expression lowered after resveratrol treatment. CONCLUSION: Resveratrol in a definite concentration range could inhibit cFs proliferation and hypertrophic response induced by Ang II, up-regulating the signal pathway of NO and cGMP might be one of the acting paths of the inhibitory effects.

[Quantitative and functional changes of circulating endothelial progenitor cells in dogs with dehydromonocrotaline-induced pulmonary artery hypertension].

OBJECTIVE: To determine the quantitive and functional changes of circulating endothelial progenitor cells (EPCs) in dogs with dehydromonocrotaline-induced pulmonary artery hypertension (PAH). METHODS: Dehydromonocrotaline was injected into the canine right ventricle to induce pulmonary hypertension. Circulating EPCs were enumerated as AC+(113), KDR+ cells by fluorescence-activated cell sorter using counting beads, and the number and activity of EPCs after in vitro expansion were determined by acLDL uptake/lectin staining assay and in vitro tubule forming assay. RESULTS: Nine of the 10 beagles survived after dehydromonocrotaline injection. Six weeks later, mean pulmonary artery pressure increased from (11.3 +/- 2.0) mm Hg (1 mm Hg = 0.133 kPa) to (20.2 +/- 1.6) mm Hg (t =10.307, P < 0.01), and the AC+(133) and KDR+ cells decreased from (632.8 +/- 42.8) cells/ml to (206.1 +/- 26.8) cells/ml (t = 25.361, P < 0.01). UEA- I and DiLDL positive cells deceased from (41 +/- 6) EPCs/ x 200 field to (22 +/- 6) EPCs/ x 200 field (t = 6.510, P < 0.01). In addition, in vasculogenesis assay, PAH EPCs formed less quantitative (11.2 +/- 2.8 vs 21.1 +/- 2.8 tubules/ x 200 field, respectively, t = 7. 583, P <0. 01) and less qualitive tubules than baseline EPCs. CONCLUSION: The number and vessel forming ability of EPCs are impaired in this canine model of dehydromonocrotaline-induced pulmonary hypertension.

[Inhibitory effects of emodin on proliferation of rat vascular smooth muscle cell induced by angiotensin II].

OBJECTIVE: To investigate the effects of emodin on the proliferation of cultured rat vascular smooth muscle cell (VSMC) induced by angiotensin II. METHOD: VSMCs were cultured by explant method. Cell proliferation model was established by stimulation with Ang II. Cell proliferation was measured by MTT assay to observe the effects of emodin (10, 20, 40 and 80 micromol x L(-1)) and N(G)-nitro-L-arginine methyl ester (L-NAME, 100 micromol x L(-1)) on VSMC proliferation induced by Ang II. The expression of PCNA was measured by immunohistochemical staining. Nitric oxide (NO) level was measured by Griess reagent. Nitric oxide synthase (NOS) and inducible nitric oxide synthase (iNOS) levels were detected by chemical colorimetric method. mRNA expression of iNOS was measured by reverse transcription polymerase chain reaction (RT-PCR). RESULT: Emodin at the doses range from 10 to 80 mol x L(-1) inhibited cell proliferation in a dose and time-dependent manner. The inhibitory effects were partly blocked by 100 mol x L(-1) of L-NAME. Emodin markedly decreased the expression of PCNA in VSMC, increased NO, NOS and iNOS levels, and increased iNOS mRNA expression in VSMC. CONCLUSION: Emodin could inhibite VSMCs proliferation induced by Ang II. Inhibiting the expression of PCNA, increasing the NO secretion and upregulating the iNOS gene expression might be associated with the inhibitory effects.

Endothelial progenitor cells in age-related vascular remodeling.

Accumulating evidence has demonstrated that endothelial progenitor cells (EPCs) could facilitate the reendothelialization of injured arteries by replacing the dysfunctional endothelial cells, thereby suppressing the formation of neointima. Meanwhile, other findings suggest that EPCs may be involved in the pathogenesis of age-related vascular remodeling. This review is presented to summarize the characteristics of EPCs and age-related vascular remodeling. In addition, the role of EPCs in age-related vascular remodeling and possible solutions for improving the therapeutic effects of EPCs in the treatment of age-related diseases are discussed.

Proteomic analysis of the serum in patients with idiopathic pulmonary arterial hypertension.

Idiopathic pulmonary arterial hypertension (IPAH) is a rare disease of unknown etiology. The exact pathogenesis of pulmonary arterial hypertension is still not well known. In the past decades, many protein molecules have been found to be involved in the development of IPAH. With proteomic techniques, profiling of human plasma proteome becomes more feasible in searching for disease-related markers. In present study, we showed the protein expression profiles of the serum of IPAH and healthy controls after depleting a few high-abundant proteins in serum. Thirteen spots had changed significantly in IPAH compared with healthy controls and were identified by LC-MS/MS. Alpha-1-antitrypsin and vitronectin were down-regulated in IPAH and may be valuable candidates for further explorations of their roles in the development of IPAH.