Chemerin in caudal division of nucleus tractus solitarius increases sympathetic activity and blood pressure.

Chemerin is an adipokine that contributes to metabolism regulation. Nucleus tractus solitarius (NTS) is the first relay station in the brain for accepting various visceral afferent activities for regulating cardiovascular activity. However, the roles of chemerin in the NTS in regulating sympathetic activity and blood pressure are almost unknown. This study aimed to determine the role and potential mechanism of chemerin in the NTS in modulating sympathetic outflow and blood pressure. Bilateral NTS microinjections were performed in anaesthetized adult male Sprague-Dawley rats. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) were continuously recorded. Chemerin and its receptor chemokine-like receptor 1 (CMKLR1) were highly expressed in caudal NTS (cNTS). Microinjection of chemerin-9 to the cNTS increased RSNA, MAP and HR, which were prevented by CMKLR1 antagonist α-NETA, superoxide scavenger tempol or N-acetyl cysteine, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors diphenyleneiodonium or apocynin. Chemerin-9 increased superoxide production and NADPH oxidase activity in the cNTS. The increased superoxide production induced by chemerin-9 was inhibited by α-NETA. The effects of cNTS microinjection of chemerin-9 on the RSNA, MAP and HR were attenuated by the pretreatment with paraventricular nucleus (PVN) microinjection of NMDA receptor antagonist MK-801 rather than AMPA/kainate receptor antagonist CNQX. These results indicate that chemerin-9 in the NTS increases sympathetic outflow, blood pressure and HR via CMKLR1-mediated NADPH oxidase activation and subsequent superoxide production in anaesthetized normotensive rats. Glutamatergic inputs in the PVN are needed for the chemerin-9-induced responses.

Asprosin promotes vascular inflammation via TLR4-NFκB-mediated NLRP3 inflammasome activation in hypertension.

Objective: and design Mild vascular inflammation promotes the pathogenesis of hypertension. Asprosin, a newly discovered adipokine, is closely associated with metabolic diseases. We hypothesized that asprosin might led to vascular inflammation in hypertension via NLRP3 inflammasome formation. This study shows the importance of asprosin in the vascular inflammation of hypertension. Methods: Primary vascular smooth muscle cells (VSMCs) were obtained from the aorta of animals, including spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), NLRP3-/- and wild-type mice. Studies were performed in VSMCs in vitro, as well as WKY and SHR in vivo. Results: Asprosin expressions were up-regulated in VSMCs and media of arteries in SHR. Asprosin overexpression promoted NLRP3 inflammasome activation via Toll-like receptor 4 (TLR4), accompanied with activation of NFκB signaling pathway in VSMCs. Exogenous asprosin protein showed similar roles in promoting NLRP3 inflammasome activation. Knockdown of asprosin restrained NLRP3 inflammasome and p65-NFκB activation in VSMCs of SHR. NLRP3 inhibitor MCC950 or NFκB inhibitor BAY11-7082 attenuated asprosin-caused VSMC proliferation and migration. Asprosin-induced interleukin-1ß production, proliferation and migration were attenuated in NLRP3-/- VSMCs. Local asprosin knockdown in common carotid artery of SHR attenuated inflammation and vascular remodeling. Conclusions: Asprosin promoted NLRP3 inflammasome activation in VSMCs by TLR4-NFκB pathway, and thereby stimulates VSMCs proliferation, migration, and vascular remodeling of SHR.

Potential distribution and ecological impacts of Acmella radicans (Jacquin) R.K. Jansen (a new Yunnan invasive species record) in China.

BACKGROUND ACMELLA RADICANS: (Jacquin) R.K. Jansen is a new invasive species record for Yunnan Province, China. Native to Central America, it has also been recently recorded invading other parts of Asia. To prevent this weed from becoming a serious issue, an assessment of its ecological impacts and potential distribution is needed. We predicted the potential distribution of A. radicans in China using the MaxEnt model and its ecological impacts on local plant communities and soil nutrients were explored. RESULTS: Simulated training using model parameters produced an area under curve value of 0.974, providing a high degree of confidence in model predictions. Environmental variables with the greatest predictive power were precipitation of wettest month, isothermality, topsoil TEB (total exchangeable bases), and precipitation seasonality, with a cumulative contribution of more than 72.70% and a cumulative permutation importance of more than 69.20%. The predicted potential suitable area of A. radicans in China is concentrated in the southern region. Projected areas of A. radicans ranked as high and moderately suitable comprised 5425 and 26,338 km2, accounting for 0.06 and 0.27% of the Chinese mainland area, respectively. Over the 5 years of monitoring, the population density of A. radicans increased while at the same time the population density and importance values of most other plant species declined markedly. Community species richness, diversity, and evenness values significantly declined. Soil organic matter, total N, total P, available N, and available P concentrations decreased significantly with increasing plant cover of A. radicans, whereas pH, total K and available K increased. CONCLUSION: Our study was the first to show that A. radicans is predicted to expand its range in China and may profoundly affect plant communities, species diversity, and the soil environment. Early warning and monitoring of A. radicans must be pursued with greater vigilance in southern China to prevent its further spread.

Asprosin contributes to vascular remodeling in hypertensive rats via superoxide signaling.

OBJECTIVE: Proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to vascular remodeling. Asprosin, a newly discovered protein hormone, is involved in metabolic diseases. Little is known about the roles of asprosin in cardiovascular diseases. This study focused on the role and mechanism of asprosin on VSMC proliferation and migration, and vascular remodeling in a rat model of hypertension. METHODS AND RESULTS: VSMCs were obtained from the aortic media of 8-week-old male Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Asprosin was upregulated in the VSMCs of SHR. For in vitro studies, asprosin promoted VSMC proliferation and migration of WKY and SHR, and increased Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) activity, NOX1/2/4 protein expressions and superoxide production. Knockdown of asprosin inhibited the proliferation, migration, NOX activity, NOX1/2 expressions and superoxide production in the VSMCs of SHR. The roles of asprosin in promoting VSMC proliferation and migration were not affected by hydrogen peroxide scavenger, but attenuated by superoxide scavenger, selective NOX1 or NOX2 inhibitor. Toll-like receptor 4 (TLR4) was upregulated in SHR, TLR4 knockdown inhibited asprosin overexpression-induced proliferation, migration and oxidative stress in VSMCs of WKY and SHR. Asprosin was upregulated in arteries of SHR, and knockdown of asprosin in vivo not only attenuated oxidative stress and vascular remodeling in aorta and mesentery artery, but also caused a subsequent persistent antihypertensive effect in SHR. CONCLUSIONS: Asprosin promotes VSMC proliferation and migration via NOX-mediated superoxide production. Inhibition of endogenous asprosin expression attenuates VSMC proliferation and migration, and vascular remodeling of SHR.

Intervention of Asprosin Attenuates Oxidative Stress and Neointima Formation in Vascular Injury.

Aims: Asprosin, a newly discovered hormone, is linked to insulin resistance. This study shows the roles of asprosin in vascular smooth muscle cell (VSMC) proliferation, migration, oxidative stress, and neointima formation of vascular injury. Methods: Mouse aortic VSMCs were cultured, and platelet-derived growth factor-BB (PDGF-BB) was used to induce oxidative stress, proliferation, and migration in VSMCs. Vascular injury was induced by repeatedly moving a guidewire in the lumen of the carotid artery in mice. Results: Asprosin overexpression promoted VSMC oxidative stress, proliferation, and migration, which were attenuated by toll-like receptor 4 (TLR4) knockdown, antioxidant (N-Acetylcysteine, NAC), NADPH oxidase 1 (NOX1) inhibitor ML171, or NOX2 inhibitor GSK2795039. Asprosin overexpression increased NOX1/2 expressions, whereas asprosin knockdown increased heme oxygenase-1 (HO-1) and NADPH quinone oxidoreductase-1 (NQO-1) expressions. Asprosin inhibited nuclear factor E2-related factor 2 (Nrf2) nuclear translocation. Nrf2 activator sulforaphane increased HO-1 and NQO-1 expressions and prevented asprosin-induced NOX1/2 upregulation, oxidative stress, proliferation, and migration. Exogenous asprosin protein had similar roles to asprosin overexpression. PDGF-BB increased asprosin expressions. PDGF-BB-induced oxidative stress, proliferation, and migration were enhanced by Nrf2 inhibitor ML385 but attenuated by asprosin knockdown. Vascular injury increased asprosin expression. Local asprosin knockdown in the injured carotid artery promoted HO-1 and NQO-1 expressions but attenuated the NOX1 and NOX2 upregulation, oxidative stress, neointima formation, and vascular remodeling in mice. Innovation and Conclusion: Asprosin promotes oxidative stress, proliferation, and migration of VSMCs via TLR4-Nrf2-mediated redox imbalance. Inhibition of asprosin expression attenuates VSMC proliferation and migration, oxidative stress, and neointima formation in the injured artery. Asprosin might be a promising therapeutic target for vascular injury.

The genomic history and global migration of a windborne pest.

Many insect pests, including the brown planthopper (BPH), undergo windborne migration that is challenging to observe and track. It remains controversial about their migration patterns and largely unknown regarding the underlying genetic basis. By analyzing 360 whole genomes from around the globe, we clarify the genetic sources of worldwide BPHs and illuminate a landscape of BPH migration showing that East Asian populations perform closed-circuit journeys between Indochina and the Far East, while populations of Malay Archipelago and South Asia undergo one-way migration to Indochina. We further find round-trip migration accelerates population differentiation, with highly diverged regions enriching in a gene desert chromosome that is simultaneously the speciation hotspot between BPH and related species. This study not only shows the power of applying genomic approaches to demystify the migration in windborne migrants but also enhances our understanding of how seasonal movements affect speciation and evolution in insects.

GLP-1 in the Hypothalamic Paraventricular Nucleus Promotes Sympathetic Activation and Hypertension.

Glucagon-like peptide-1 (GLP-1) and its analogs are widely used for diabetes treatment. The paraventricular nucleus (PVN) is crucial for regulating cardiovascular activity. This study aims to determine the roles of GLP-1 and its receptors (GLP-1R) in the PVN in regulating sympathetic outflow and blood pressure. Experiments were carried out in male normotensive rats and spontaneously hypertensive rats (SHR). Renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded. GLP-1 and GLP-1R expressions were present in the PVN. PVN microinjection of GLP-1R agonist recombinant human GLP-1 (rhGLP-1) or EX-4 increased RSNA and MAP, which were prevented by GLP-1R antagonist exendin 9-39 (EX9-39) or GLP-1R antagonist 1, superoxide scavenger tempol, antioxidant N-acetylcysteine, NADPH oxidase (NOX) inhibitor apocynin, adenylyl cyclase (AC) inhibitor SQ22536 or protein kinase A (PKA) inhibitor H89. PVN microinjection of rhGLP-1 increased superoxide production, NADPH oxidase activity, cAMP level, AC, and PKA activity, which were prevented by SQ22536 or H89. GLP-1 and GLP-1R were upregulated in the PVN of SHR. PVN microinjection of GLP-1 agonist increased RSNA and MAP in both WKY and SHR, but GLP-1 antagonists caused greater effects in reducing RSNA and MAP in SHR than in WKY. The increased superoxide production and NADPH oxidase activity in the PVN of SHR were augmented by GLP-1R agonists but attenuated by GLP-1R antagonists. These results indicate that activation of GLP-1R in the PVN increased sympathetic outflow and blood pressure via cAMP-PKA-mediated NADPH oxidase activation and subsequent superoxide production. GLP-1 and GLP-1R upregulation in the PVN partially contributes to sympathetic overactivity and hypertension.

The Genetic Diversity of White-Backed Planthoppers (Sogatella furcifera) between Myanmar and Yunnan Province of China.

In order to clarify the migration route and the source of white-backed planthopper (WBPH) (Sogatella furcifera) between Myanmar and Yunnan Province, China, we collected six populations throughout Myanmar and five populations around the border areas in Yunnan Province, China. A total of 790 base pairs in the mtDNA COI genes from 416 individuals were obtained. A total of 43 haplotypes were identified, among which 37 were unique haplotypes, and the remaining 6 were shared among different populations. Two common shared haplotypes (H_1 and H_2) had a widespread distribution in all populations and accounted for 88.8% of the total haplotype frequency, suggesting a high-level gene flow among the Myanmar and Yunnan populations. Bayesian skyline plot (BSP) analysis results indicated that the effective population size of WBPH expanded between about 10,000 and 7000 years ago, and S. furcifera might follow the post-LGM (Last Glacial Maximum) expansion pattern. Based on the total migrant (Nem) value, it can be deduced that north and northeast Myanmar were the primary migration sources for WBPH populations in the southwest and south Yunnan regions. This study aims to contribute to the sustainable regional management of this important rice pest and provide new insights into the genetic diversity of WBPH in Southeast Asia.

[Angiotensin-(1-7) improves endothelium-dependent vasodilation in rats with monocrotaline-induced pulmonary arterial hypertension].

In this study, we used a rat model of pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) to investigate the role and mechanism of angiotensin (Ang)-(1-7) in regulating pulmonary artery diastolic function. Three weeks after subcutaneous injection of MCT or normal saline, the right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) of rats were detected using a right heart catheter. Vascular endothelium-dependent relaxation was evaluated by acetylcholine (ACh)-induced vasodilation. The relaxation function of vascular smooth muscle was evaluated by sodium nitroprusside (SNP)-induced vasodilation. Human pulmonary artery endothelial cells (HPAECs) were incubated with Ang-(1-7) to measure nitric oxide (NO) release levels. The results showed that compared with control rats, RVSP and RVHI were significantly increased in the MCT-PAH rats, and both ACh or SNP-induced vasodilation were worsened. Incubation of pulmonary artery of MCT-PAH rats with Ang-(1-7) (1 × 10-9-1 × 10-4 mol/L) caused significant vaso-relaxation. Pre-incubation of Ang-(1-7) in the pulmonary artery of MCT-PAH rats significantly improved ACh-induced endothelium-dependent relaxation, but had no significant effect on SNP-induced endothelium-independent relaxation. In addition, Ang-(1-7) treatment significantly increased NO levels in HPAECs. The Mas receptor antagonist A-779 inhibited the effects of Ang-(1-7) on endothelium-dependent relaxation and NO release from endothelial cells. The above results demonstrate that Ang-(1-7) promotes the release of NO from endothelial cells by activating Mas receptor, thereby improving the endothelium-dependent relaxation function of PAH pulmonary arteries.

Red imported fire ant nesting affects the structure of soil microbial community.

The red imported fire ants (RIFA, Solenopsis invicta) have become a well-known invasive species that poses significant ecological and economic threats globally. As of recent times, the geographic scope of its invasion in China is rapidly expanding, thereby aggravating the extent and severity of its detrimental effects. The importance of soil microorganisms for maintaining soil health and ecosystem function has been widely acknowledged. However, the negative impact of RIFAs on soil microbial communities and their functions has not yet been fully understood. In this study, we sequenced the V3-V4 variable region of the bacterial 16S rRNA gene in soil samples collected from three types of RIFA nests to investigate the impact of RIFA invasion on soil microbial diversity and composition. The results of alpha diversity analysis showed that the normal soil without nests of RIFAs exhibited the highest level of diversity, followed by the soil samples from RIFA-invaded nests and abandoned nests. Taxonomy and biological function annotation analyses revealed significant differences in microbial community structure and function among the different samples. Our findings demonstrate that RIFA invasion can significantly alter soil microbial community composition, which could ultimately affect ecosystem function. Therefore, effective management strategies are urgently needed to mitigate the negative impact of invasive species on native ecosystems.

Sweet potato (Ipomoea batatas) and hyacinth bean (Lablab purpureus) in combination provide greater suppression of mile-a-minute (Mikania micrantha) than either crop alone.

Introduction: In natural systems, diverse plant communities tend to prevent a single species from dominating. Similarly, management of invasive alien plants may be achieved through various combinations of competing species. Methods: We used a de Wit replacement series to compare different combinations of sweet potato (Ipomoea batatas (L.) Lam), hyacinth bean (Lablab purpureus (L.) Sweet) and mile-a-minute (Mikania micrantha Kunth) through measures of photosynthesis, plant growth, nutrient levels in plant tissue and soil, and competitive ability. Results: Cultured alone sweet potato and hyacinth beans exhibited higher total biomass, leafstalk length, and leaf area than mile-a-minute. In mixed culture, either sweet potato or hyacinth bean or both together significantly suppressed the mile-a-minute parameters, i.e., plant height, branch, leaf, adventitious root, and biomass (P<0.05). Based on a significantly lower than 1.0 relative yield of the three plant species in mixed culture, we showed intraspecific competition to be less than interspecific competition. Calculated indices (relative yield, relative yield total, competitive balance index, and change in contribution) demonstrated a higher competitive ability and higher influence of either crop compared to mile-a-minute. The presence of sweet potato and hyacinth bean, especially with both species in combination, significantly reduced (P<0.05) mile-a-minute's net photosynthetic rate (Pn), antioxidant enzyme activities (superoxide dismutase, peroxidase, catalase, and malondialdehyde), chlorophyll content, and nutrient content (N, P, and K). In soil with mile-a-minute in monoculture soil organic matter, total and available N, total and available K, and available P were significantly greater (P<0.05) than in soil with sweet potato grown in monoculture, but less than in soil with hyacinth bean grown in monoculture soil. Nutrient soil content was comparatively reduced for plant mixtures. Plant height, leaf, biomass, Pn, antioxidant enzyme activities, and plant and soil nutrient contents of sweet potato and hyacinth bean tended to be much greater when grown with two crops compared to in mixture with just sweet potato or hyacinth bean. Discussion: Our results suggest that the competitive abilities of both sweet potato and hyacinth bean were greater than that of mile-a-minute, and also that mile-a-minute suppression was significantly improved via a combination of the two crops compared to either sweet potato or hyacinth bean alone.

A chromosome-level genome assembly of tomato pinworm, Tuta absoluta.

The tomato pinworm, Tuta absoluta, or Phthorimaea absouta, is native to South America, but quickly spread to other regions of world, including Europe, Africa, and Asia, devastating to global tomato production. However, a lack of high-quality genome resources makes it difficult to understand its high invasiveness and ecological adaptation. Here, we sequenced the genome of the tomato pinworm using Nanopore platforms, yielding a genome assembly of 564.5 Mb with contig N50 of 3.33 Mb. BUSCO analysis demonstrated that this genome assembly has a high-level completeness of 98.0% gene coverage. In total, 310 Mb are repeating sequences accounting for 54.8% of genome assembly, and 21,979 protein-coding genes are annotated. Next, we used the Hi-C technique to anchor 295 contigs to 29 chromosomes, yielding a chromosome-level genome assembly with a scaffold N50 of 20.7 Mb. In sum, the high-quality genome assembly of the tomato pinworm is a useful gene resource that contributes to a better understanding of the biological characteristics of its invasiveness and will help in developing an efficient control policy.

Upregulated expression of a TOR2A gene product-salusin-ß in the paraventricular nucleus enhances sympathetic activity and cardiac sympathetic afferent reflex in rats with chronic heart failure induced by coronary artery ligation.

AIM: Enhanced cardiac sympathetic afferent reflex (CSAR) promotes sympathetic hyperactivation in chronic heart failure (CHF). Salusin-ß is a torsin family 2 member A (TOR2A) gene product and a cardiovascular active peptide closely associated with cardiovascular diseases. We aimed to determine the roles of salusin-ß in the paraventricular nucleus (PVN) in modulating enhanced CSAR and sympathetic hyperactivation in rats with CHF induced by coronary artery ligation and elucidate the underlying molecular mechanisms. METHODS: CSAR was evaluated based on the responses of mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) to the epicardial administration of capsaicin in rats under anesthesia. RESULTS: Salusin-ß protein expression was upregulated in the PVN of the CHF compared with sham-operated rats. Salusin-ß microinjection into the PVN dose-dependently increased MAP and RSNA and enhanced CSAR, while anti-salusin-ß IgG exerted opposite effects. The effect of salusin-ß was inhibited by reactive oxygen species (ROS) scavenger or NAD(P)H oxidase inhibitor but promoted by superoxide dismutase inhibitor. The effect of anti-salusin-ß IgG was interdicted by nitric oxide (NO) synthase inhibitor. Furthermore, chronic salusin-ß gene knockdown in PVN attenuated CSAR, reduced sympathetic output, improved myocardial remodeling and cardiac function, decreased NAD(P)H oxidase activity and ROS levels, and increased NO levels in the CHF rats. CONCLUSION: Increased salusin-ß activity in the PVN contributes to sympathetic hyperactivation and CSAR in CHF by inhibiting NO release and stimulating NAD(P)H oxidase-ROS production. Reducing endogenous central salusin-ß expression might be a novel strategy for preventing and treating CHF in the future.

Population Growth of Fall Armyworm, Spodoptera frugiperda Fed on Cereal and Pulse Host Plants Cultivated in Yunnan Province, China.

The fall armyworm, Spodoptera frugiperda is a major agricultural pest in China, and has migrated from its continuous breeding area to other parts of China. In our study, the biological behaviors of S. frugiperda fed on maize, wheat, barley, faba beans, and soya beans were evaluated in a growth chamber. Results indicated that maize-fed S. frugiperda larvae performed well, as evidenced by shorter larva-adult periods, adult pre-oviposition period (APOP), total pre-oviposition period (TPOP), and generation time (T), and a higher survival rate, intrinsic (r) and finite (λ) rate of increase, and net reproductive rate (Ro), However, S. frugiperda larvae performed weakly when fed barley and faba bean plants, as indicated by lower survival rates, r, and λ, and longer pre-adult period, TPOP, and T. A heavier pupal weight of both sexes was recorded on faba beans (0.202 g) and a lighter weight on barley (0.169 g). Fecundity was higher when fed faba beans and maize, and lower when fed wheat and barley. Thus, maize was the most optimal and barley was the least optimal host plant, followed by faba beans, for S. frugiperda larvae growth and development. This study enhances our knowledge of S. frugiperda in these host plants and can help in the design of management approaches.

Salusin-ß, a TOR2A gene product, promotes proliferation, migration, fibrosis, and calcification of smooth muscle cells and accelerates the imbalance of vasomotor function and vascular remodeling in monocrotaline-induced pulmonary hypertensive rats.

Purpose: The hyper-proliferation, promoted migration, fibrosis, and calcification of pulmonary arterial smooth muscle cells (PASMCs) play critical roles in pulmonary artery (PA) continuous contraction and vascular remodeling, leading to elevated pulmonary arterial resistance and pulmonary hypertension (PH). In this study, we sought to ascertain the effects of a TOR2A gene product, salusin-ß, on PASMCs' proliferation, migration, fibrosis, calcification, and the imbalance of vasomotor function as well as pulmonary vascular remodeling in monocrotaline (MCT)-induced PH rats and their underlying mechanisms. Methods: Knockdown or overexpression of salusin-ß in rats or PASMCs was performed through tail vein injection or cell transfection of virus. The right ventricular systolic pressure (RVSP) of the rat was measured by right ventricle catheterization. Sodium nitroprusside (SNP) or acetylcholine (ACh)-induced dose-dependent relaxation was used to evaluate the vasodilatation function. Primary PASMCs were isolated from the PAs of control and PH rats. Results: The salusin-ß protein expressions were significantly increased in PAs and PASMCs isolated from PH rats compared with control rats. Knockdown of salusin-ß in rats decreased high K+ solution-induced contraction, RVSP and RV hypertrophy index, improved SNP or ACh-induced vascular relaxation of PAs, and relieved vascular remodeling and calcification of PAs from PH rats. Silencing salusin-ß in PASMCs isolated from PH rats alleviated the proliferation, migration, fibrosis, and calcification, as well as the NAD(P)H oxidase activity and reactive oxygen species (ROS) level. Overexpression of salusin-ß exerted the opposite effects on vasomotor function and vascular remodeling, and PASMCs proliferation, migration, fibrosis and calcification. Conclusion: Increased salusin-ß activity in PAs from PH rats contributes to PASMCs proliferation, migration, fibrosis, and calcification, leading to the imbalance of vascular contraction and relaxation and vascular remodeling through stimulating the production of NAD(P)H oxidase derived ROS.

Saluisn-ß contributes to endothelial dysfunction in monocrotaline-induced pulmonary arterial hypertensive rats.

BACKGROUND: The endothelial dysfunction and the consequent attenuated pulmonary vasodilatation are the major causes of elevated pulmonary arterial resistance and pressure in pulmonary arterial hypertension (PAH). Current study aimed to explore the effects of a TOR2A gene product, salusin-ß, on endothelium-dependent vascular relaxation and the progression of PAH in monocrotaline (MCT)-induced PAH rats as well as the relevant signaling pathway. METHODS: Acetylcholine (ACh)-induced dose-dependent relaxation was used to evaluate the endothelium-dependent vasodilatation function. RESULTS: The salusin-ß level in plasma and pulmonary artery (PA) in MCT-PAH rats were significantly increased, while the ACh-induced endothelium-dependent vasodilatation was attenuated. After salusin-ß incubation or overexpression of salusin-ß gene, the endothelium-dependent relaxation was further deteriorated, while anti-salusin-ß IgG incubation or knockdown of salusin-ß improved it in PAH rats. The superoxide anions scavenger NAC or the antioxidant apocynin inhibited the effect of salusin-ß, while the SOD inhibitor DETC further enhanced it. The nitric oxide (NO) synthase inhibitor L-NAME almost blocked the effect of anti-salusin-ß IgG. Silencing of salusin-ß in PAH rats decreased right ventricular (RV) systolic pressure, RV hypertrophy index, NAD(P)H oxidase activity and ROS level, and increased the eNOS activity and NO level of PA. Overexpression of salusin-ß played opposite roles. CONCLUSIONS: The elevated saluisn-ß level in PAH rats plays important roles in the reduction of endothelium-dependent vasodilatation and participates in the progression of PAH through stimulating NAD(P)H oxidase-ROS production and inhibiting eNOS-NO release.

Immigration Pathways of White-Backed Planthopper in the Confluence Area of the Two Monsoon Systems.

The white-backed planthopper, WBPH, Sogatella furcifera (Horváth) is a plant pest that migrates long-distances. The migration pathway of WBPH in eastern China coincides with the north-south round trip of the East Asian monsoon. However, in Yunnan China, which is affected by two monsoon systems, the migration pathway is unclear. Light-trap data and analysis of female ovarian development showed that the peak period of immigration of WBPH into western Yunnan was earlier than in eastern Yunnan. Using meteorological reanalysis data and flight parameters of WBPH, trajectory modeling showed that there are two immigration pathways to Yunnan. One is from Myanmar to western Yunnan, and the other is from Vietnam and Laos to eastern Yunnan. The reason for the differences in source areas and immigration pathways between eastern and western Yunnan is that the west wind prevails in western Yunnan and is controlled by South Asian monsoon, while southwesterly winds prevail in eastern Yunnan due to the combined influence of South Asian monsoon and East Asian monsoon. The results indicate that WBPH invades Yunnan via two pathways under a two-monsoon system. These data will allow earlier prediction and population management of WBPH.

Allelochemicals Identified From Sweet Potato (Ipomoea batatas) and Their Allelopathic Effects on Invasive Alien Plants.

Sweet potato [Ipomoea batatas (L.) Lam] is grown as important cash and food crop worldwide and has been shown to exhibit allelopathic effects on other plants. However, its metabolome has not been studied extensively, particularly with respect to the production of phytotoxic bioactive secondary products. In this study, the chemical composition of petroleum ether extract of sweet potato was characterized, and the morphological and physiological effects of some individual components against four invasive alien weeds Bidens pilosa L., Galinsoga parviflora Cav., Lolium multiflorum Lam., and Phalaris minor Retz. were determined. Twenty-one components were identified by GS-MS, constituting 96.08% of petroleum ether extract in sweet potato. The major components were palmitic acid (PA) (17.48%), ethyl linoleate (EL) (13.19%), linoleic acid (LA) (12.55%), ethyl palmitate (EP) (11.77%), ethyl linolenate (ELL) (8.29%) oleic acid (5.82%), ethyl stearate (4.19%), and 3-methylphenol acetate (3.19%). The five most abundant compounds exhibited strong inhibition activity against the four invasive weeds tested. The highest inhibition rates were seen for LA, followed by PA and EP, respectively. Catalase (CAT), malondialdehyde (MDA), and peroxidase (POD) content of L. multiflorum were increased by the three allelochemicals, i.e., LA, PA and EP, but superoxide dismutase (SOD), chlorophyll-a and chlorophyll-b levels declined. Overall, the combined impact of all five compounds could be quite effective in suppressing the invasive weeds of concern.

Research Progress on Pulmonary Arterial Hypertension and the Role of the Angiotensin Converting Enzyme 2-Angiotensin-(1-7)-Mas Axis in Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) is a progressive disease with a complex aetiology and high mortality. Functional and structural changes in the small pulmonary arteries lead to elevated pulmonary arterial pressure, resulting in right heart failure. The pathobiology of PAH is not fully understood, and novel treatment targets in PAH are desperately needed. The renin-angiotensin system is critical for maintaining homeostasis of the cardiovascular system. The system consists of the angiotensin converting enzyme (ACE)-angiotensin (Ang) II-angiotensin type 1 receptor (AT1R) axis and the ACE2-Ang-(1-7)-Mas receptor axis. The former, the ACE-Ang II-AT1R axis, is involved in vasoconstrictive and hypertensive actions along with cardiac and vascular remodelling. The latter, the ACE2-Ang-(1-7)-Mas axis, generally mediates counterbalancing effects against those mediated by the ACE-Ang II-AT1R axis. Based on established functions, the ACE2-Ang-(1-7)-Mas axis may represent a novel target for the treatment of PAH. This review focuses on recent advances in pulmonary circulation science and the role of the ACE2-Ang-(1-7)-Mas axis in PAH.

Erianin: A Direct NLRP3 Inhibitor With Remarkable Anti-Inflammatory Activity.

Erianin (Eri) is the extract of Dendrobium chrysotoxum Lindl. The NLRP3 inflammasome is a multiprotein complex that plays key roles in a wide variety of chronic inflammation-driven human diseases. Nevertheless, little is known about the protection of Eri against NLRP3 inflammasome-related diseases. In this study, we demonstrated that Eri inhibited NLRP3 inflammasome activation in vitro and in vivo. Mechanistically, Eri directly interacted with NLRP3, leading to inhibition of NLRP3 inflammasome assembly. Eri associated with the Walker A motif in the NACHT domain and suppressed NLRP3 ATPase activity. In mouse models, Eri had therapeutic effects on peritonitis, gouty arthritis and type 2 diabetes, via NLRP3. More importantly, Eri was active ex vivo for synovial fluid cells and monocytes from patients with IAV infection and gout. Eri may serve as a potential novel therapeutic compound against NLRP3-driven diseases.