The Golgi-localized transporter OsPML3 is involved in manganese homeostasis and complex N-glycan synthesis in rice.

Manganese (Mn) is involved in many biochemical pathways as an enzyme cofactor, and is essential for maintaining metabolic processes in various plant cell compartments. Here, we determined the function of a rice (Oryza sativa) Mn transporter, PHOTOSYNTHESIS-AFFECTED MUTANT 71-LIKE 3 (OsPML3), belonging to the UNCHARACTERIZED PROTEIN FAMILY 0016 (UPF0016), in regulating Mn homeostasis and late-stage Golgi N-glycosylation. OsPML3 was highly expressed in rapidly developing tissues such as young leaves, root caps, lateral root primordia, and young anthers. Heterologous expression of OsPML3 restored the growth of Mn uptake-defective yeast strain Δsmf1 under Mn-limited conditions. Sub-cellular localization analysis revealed that OsPML3 localizes in the Golgi apparatus. At the vegetative stage, we observed necrotic root tips and lateral root primordia, and chlorotic young leaves in OsPML3 knockout lines under Mn-deficient conditions. Knocking out OsPML3 reduced the Mn content in the young leaves but did not affect the older leaves. Additionally, knocking out OsPML3 reduced the deposition of cell wall polysaccharides and the content of Lea (Lewis A structure)-containing N-glycan in roots and young leaves. OsPML3 knockout lines grown in the paddy field had reduced pollen fertility. Moreover, we found that the Lewis A structure was reduced in young anthers of OsPML3 knockout lines. Collectively, our results indicate that OsPML3 maintains Mn homeostasis in the Golgi apparatus of the rapidly developing rice tissues, and regulates the deposition of cell wall polysaccharides and late-stage Golgi N-glycosylation, especially biosynthesis of the Lewis A structure.

The tonoplast-localized transporter OsNRAMP2 is involved in iron homeostasis and affects seed germination in rice.

Vacuolar storage of iron (Fe) is important for Fe homeostasis in plants. When sufficient, excess Fe could be stored in vacuoles for remobilization in the case of Fe deficiency. Although the mechanism of Fe remobilization from vacuoles is critical for crop development under low Fe stress, the transporters that mediate vacuolar Fe translocation into the cytosol in rice remains unknown. Here, we showed that under high Fe2+ concentrations, the Δccc1 yeast mutant transformed with the rice natural resistance-associated macrophage protein 2 gene (OsNRAMP2) became more sensitive to Fe toxicity. In rice protoplasts and transgenic plants expressing Pro35S:OsNRAMP2-GFP, OsNRAMP2 was localized to the tonoplast. Vacuolar Fe content in osnramp2 knockdown lines was higher than in the wild type, while the growth of osnramp2 knockdown plants was significantly influenced by Fe deficiency. Furthermore, the germination of osnramp2 knockdown plants was arrested. Conversely, the vacuolar Fe content of Pro35S:OsNRAMP2-GFP lines was significantly lower than in the wild type, and overexpression of OsNRAMP2 increased shoot biomass under Fe deficiency. Taken together, we propose that OsNRAMP2 transports Fe from the vacuole to the cytosol and plays a pivotal role in seed germination.

Traffic-related air pollution is associated with cardio-metabolic biomarkers in general residents.

PURPOSE: The study was conducted to explore the mechanisms linking traffic-related air pollution and cardio-metabolic risk. METHODS: The participants included 371 men and women aged from 45 to 75 in an urban residential area in Shanghai, China. The participants were divided into four categories (≤50, 51-100, 101-200 and >200 m) according to the residential distance to major road. Additionally, the personal fine particulate matter (PM2.5) was measured from 8:00 am to 6:00 pm to assess the PM2.5 exposure in general residents. Then, the continuous subclinical measurements and biological effects related to cardio-metabolic disorders were detected. The generalized linear regression analysis was applied for estimating the adjusted hazards ratio for cardio-metabolic disorders relative to traffic-related air pollution. RESULTS: The average personal PM2.5 is 111.1 µg/m(3) in the participants living within 50 m to major road, which is significantly higher than the personal PM2.5 (68.2 µg/m(3)) in the participants living more than 200 m away from the major road. The participants living within 50 m to major road compared with those living more than 200 m away have 1.15 times higher of heart rate (HR), 1.95 times higher of fasting insulin, 1.30 times higher of homeostasis model assessment of insulin resistance (HOMA-IR), 1.56 times higher of low-density lipoprotein cholesterol (LDL-C), 8.39 times higher of interleukin 6 (IL-6), 4.30 times higher of augmentation index (AI), 1.60 times higher of systolic blood pressure (SBP) and 1.91 times higher of diastolic blood pressure (DBP). Contrary to the increase in above biological effects, there were 1.06 times lower of low frequency (LF), 1.05 times lower of high frequency (HF), 2.54 times lower of IL-10, 4.61 times lower of nitric oxide (NO), 1.19 times lower of superoxide dismutase (SOD) and 1.85 times lower of total antioxidant capacity (T-AOC). There was no clear exposure-response relationship can be observed in the fasting glucose, LF/HF, cholesterol and high-density lipoprotein (HDL). CONCLUSION: Long-term exposure to traffic-related air pollution may contribute to the development or exacerbation of cardio-metabolic disorders. The mechanisms linking air pollution and cardio-metabolic disorders may be associated with the increased systemic inflammation and oxidative stress, reduced insulin sensitivity and elevated arterial stiffness and blood pressure.

[Effects and mechanism of inflammation and energy metabolism in mice caused by PM_(2. 5) exposure].

OBJECTIVE: The current study was conducted to observe the effects of fine particles( PM_(2. 5)) on energy metabolism and inflammation. The potential mechanism linking PM_(2. 5)and type 2 diabetes was explored. METHODS: C57 BL /6 mice were randomly assigned to 2 groups. The mice in exposure group were intratracheal instilled of 15 mg / kg BW PM_(2. 5). The mice in control were instilled with saline. The instillation were conducted three times per week for 18 weeks. Insulin resistance test( ITT) and introperitoneal glucose tolerance test( IPGTT) were determined after the last exposure. The mRNA expression of IL-6, IL-17 A, MAPK, NF-κB and TNF-α were analyzed in liver and white adipose tissue. RESULTS: The body weight of mice in PM_(2. 5)group [( 24. 976 ± 0. 571) g] showed significant decrease compared to that in control mice [( 28. 452 ± 1. 520) g]( P < 0. 05). Blood glucose significantly increased in exposure group. The mice in exposure group showed insulin resistance and glucose tolerance impairment. The expression of IL-6 mRNAexpression in liver( 0. 373 ± 0. 185) and in white adipose tissue( 0. 364 ± 0. 089)increased along with the increase of TNF-α mRNA expression( 0. 008 ± 0. 002) in white adipose tissue. CONCLUSION: The PM_(2. 5)exposure may be associated with the development of diabetes. The potential mechanism could be the impaired glucose tolerance, elevated insulin resistance and the increase of inflammatory response.

Treg responses are associated with PM2.5-induced exacerbation of viral myocarditis.

The adverse cardiovascular events induced by ambient fine particles (PM2.5) are paid more attention in the world. The current study was conducted to explore the mechanisms of T regulatory cells (Treg) responses in PM2.5-induced exacerbation of viral myocarditis. The male BALB/c mice were administered an intratracheal (i.t.) instillation of 10 mg/kg b.w. PM2.5 suspension. Twenty-four hours later, the mice were injected intraperitoneally (i.p.) with 100 µl of coxsackievirus B3 (CVB3) diluted in Eagle's minimal essential medium (EMEM). Seven days after the treatment, serum, splenetic, and cardiac tissues were examined. The results showed that pre-exposure to PM2.5 aggravated the cardiac inflammation in the CVB3-infected mice along with an increase of Treg cells in the spleen. The mRNA expressions of interleukin-6 (IL-6), TNF-α, transforming growth factor-ß (TGF-ß), and Foxp3 were up-regulated in the PM2.5-pretreated mice than that in the CVB3-treated mice. Similar results were found in the sera. In addition, compared with the CVB3-treated mice, the cardiac protein expression of TGF-ß increased in the PM2.5-pretreated mice. These results demonstrated that preexposure to PM2.5 exacerbated virus-induced myocarditis possibly through the depression of the immune response and increase of inflammation in myocardium through the Treg responses.

Identification of plant cadmium resistance gene family in Brassica napus and functional analysis of BnPCR10.1 involved in cadmium and copper tolerance.

The plant cadmium resistance (PCR) family proteins play important roles in maintaining metal homeostasis and detoxification. However, few functional PCR genes have been well-characterized in plants. In this study, we identified and cloned 26 BnPCR genes from the rapeseed (Brassica napus) genome. They were divided into four groups (I-IV) based on their phylogenetic relationship. Yeast functional complementation experiments showed that BnPCRs can transport copper (Cu) and cadmium (Cd) in yeast. The expression levels of the BnPCRs were variable among different organs. Moreover, most of the genes were induced by Cu2+ and Cd2+ stress. Among these genes, BnPCR10.1 was highly expressed in various organs and induced by Cu2+ and Cd2+. Therefore, we studied the function of BnPCR10.1 in more detail. BnPCR10.1 was localized to the plasma membrane (PM), and expression in yeast enhanced yeast cells to export Cu and Cd. Furthermore, overexpression of BnPCR10.1 transgenic lines pro35S::BnPCR10.1;athma5 had lower concentration of Cu in roots than athma5 mutants. In addition, transgenic plants pro35S::BnPCR10.1;atpdr8 had lower concentration of Cd in shoots and roots than atpdr8 mutants. Net Cu2+ and Cd2+ efflux assay showed that there was decreased absorption of Cu2+ and Cd2+ in the transgenic Arabidopsis elongation zone of roots than in athma5 and atpdr8 mutants, respectively. These results provide new information on BnPCRs and their roles in response to heavy metals and reveal the mechanism used by BnPCR10.1 to detoxify Cu and Cd. Our findings facilitate a theoretical basis for the genetic improvement of Cu-Cd tolerance in rapeseed.

Preliminary study to explore gene-PM2.5 interactive effects on respiratory system in traffic policemen.

OBJECTIVES: Traffic-related particulate matter (PM) is one of the major sources of air pollution in metropolitan areas. This study is to observe the interactive effects of gene and fine particles (particles smaller than 2.5 µm - PM2.5) on the respiratory system and explore the mechanisms linking PM2.5 and pulmonary injury. MATERIAL AND METHODS: The participants include 110 traffic policemen and 101 common populations in Shanghai, China. Continuous 24 h individual-level PM2.5 is detected and the pulmonary function, high-sensitivity C-reactive protein (hs-CRP), Clara cell protein 16 (CC16) and the polymorphism in CXCL3, NME7 and C5 genes are determined. The multiple linear regression method is used to analyze the association between PM2.5 and health effects. Meanwhile, the interactive effects of gene and PM2.5 on lung function are analyzed. RESULTS: The individual PM2.5 exposure for traffic policemen was higher than that in the common population whereas the forced expiratory volume in 1 s (FEV1), the ratio of FEV1 to forced vital capacity (FEV1/FVC) and lymphocytes are lower. In contrast, the hs-CRP level is higher. In the adjusted analysis, PM2.5 exposure was associated with the decrease in lymphocytes and the increase in hs-CRP. The allele frequencies for NME7 and C5 have significant differences between FEV1/FVC ≤ 70% and FEV1/FVC > 70% participants. The results didn't find the interaction effects of gene and PM2.5 on FEV1/FVC in all the 3 genes. CONCLUSIONS: The results indicated that traffic exposure to high levels of PM2.5 was associated with systemic inflammatory response and respiratory injury. Traffic policemen represent a high risk group suffering from the respiratory injury.

Association between individual PM2.5 exposure and DNA damage in traffic policemen.

OBJECTIVE: The aim of this study was to explore the association between individual PM2.5 and DNA damage in traffic policemen. METHODS: The participants included 110 traffic policemen and 101 common populations. The continuous 24-hour individual PM2.5 measurement was performed in participants. BPDE (benzo[a]pyrene 7,8-diol-9,10-epoxide)-DNA adducts and 1-OHP were detected. RESULTS: The average concentration of 24-hour personal PM2.5 for traffic policemen was significantly higher than that in the control group. PM2.5 exposure is associated with a 1.1% increase in 1-OHP and 0.8% increase in BPDE-DNA adducts after adjusted for body mass index, educational time period, and alcohol intake. Exposure group has 2.04 times higher of 1-OHP and 1.25 times higher of BPDE-DNA adducts when compared to the control group. CONCLUSIONS: These results demonstrated that traffic policemen have been a high-risk group suffering DNA damage because of the high PM2.5 exposure.