LncRNA-GAS5/miR-382-3p axis inhibits pulmonary artery remodeling and promotes autophagy in chronic thromboembolic pulmonary hypertension

Feng Xiaona,Wang Kaifeng,Yang Ting,Liu Yanhui,Wang Xiaodong 한국유전학회 2022 Genes & Genomics Vol.44 No.4

Background: We have clarified the role of miR-382-3p in chronic thromboembolic pulmonary hypertension (CTEPH), but what is less clear lies in its upstream regulatory mechanism. Objective: To explore the regulation mechanism of GAS5/miR-382-3p axis on CTEPH. Methods: In vitro, we constructed cell models by treating Pulmonary Artery Smooth Muscle Cells (PASMCs) with platelet-derived growth factor-BB (PDGF-BB). The effects of different concentrations of PDGF-BB on the activity of PASMCs were tested by cell counting kit-8 (CCK-8). The upstream lncRNA of miR-382-3p was screened and confirmed through bioinformatics analysis, RNA pull-down, quantitative reverse transcription polymerase chain reaction (qRT-PCR), dual luciferase reporter gene and RNA immunoprecipitation assays. The effects of GAS5/miR-382-3p axis on the viability, migration, and expressions of autophagy- and angiogenesis-related proteins were confirmed by rescue experiments (CCK-8, wound healing and western blot). In vivo, animal models by perfusing autologous blood vessels, the effects of GAS5 overexpression or silencing on the expressions of miR-382-3p, angiogenesis- and autophagy-related genes, mean pulmonary arterial pressure (mPAP) and pulmonary artery wall were determined by biological signal acquisition system, hematoxylin-eosin staining, qRT-PCR and western blot. Results: PDGF-BB dose-dependently promoted PASMCs viability. XIST and GAS5 expressions in PASMCs were affected by the concentration of PDGF-BB, but only GAS5 can be pulled down by miR-382-3p probe. GAS5 targeted miR-382-3p to inhibit the viability and migration of PAMSCs, mPAP in CTEPH rats, pulmonary artery wall thickening and angiogenesis, and promote autophagy. Conclusions: GAS5/miR-382-3p axis is involved in the regulation of pulmonary artery remodeling and autophagy in CTEPH.

The impaired redox status and activated nuclear factor-erythroid 2-related factor 2/antioxidant response element pathway in wooden breast myopathy in broiler chickens

Pan Xiaona,Zhang Lin,Xing Tong,Li Jiaolong,Gao Feng 아세아·태평양축산학회 2021 Animal Bioscience Vol.34 No.4

Objective: Wooden breast (WB) is a novel myopathy affecting modern broiler chickens, which causes substantial economic losses in the poultry industry. The objective of this study was to evaluate the effect of WB abnormality on meat quality, redox status, as well as the expression of genes of the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway. Methods: A total of 80 broilers (Ross 308, 42 days of age, about 2.6 kg body weight) raised at Jiujin farm (Suqian, Jiangsu, China) were used. Twelve unaffected (no detectable hardness of the breast area) and twelve WB-affected (diffuse remarkable hardness in the breast muscle) birds were selected from the commercial broiler farm according to the criteria proposed by previous studies. Results: The results indicated that WB showed histological lesions characterized by fiber degeneration and fibrosis, along with an increase of muscle fiber diameter (p<0.05). Moreover, higher pH value, lightness, yellowness, drip loss and cooking loss were observed in the WB group (p<0.05). Compared with the normal breast (NOR) group, the WB group showed higher formation of reactive oxygen species (p<0.05), increased level of oxidation products and antioxidant activities (p<0.05), accompanied with mitochondrial damages and lower mitochondrial membrane potential (p<0.05). Meanwhile, the relative mRNA expressions of Nrf2 and its downstream antioxidant genes including heme oxygenase‐1, NAD(P)H qui none dehydrogenase 1, glutathione peroxidase, superoxide dismutase, and glutamate-cysteine ligase were higher than those of the NOR group (p<0.05). Conclusion: In conclusion, WB myopathy impairs meat quality by causing oxidative damages and mitochondrial dysfunction in broilers, even though the activated Nrf2/antioxidant response element pathway provides protection for the birds. Objective: Wooden breast (WB) is a novel myopathy affecting modern broiler chickens, which causes substantial economic losses in the poultry industry. The objective of this study was to evaluate the effect of WB abnormality on meat quality, redox status, as well as the expression of genes of the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway.Methods: A total of 80 broilers (Ross 308, 42 days of age, about 2.6 kg body weight) raised at Jiujin farm (Suqian, Jiangsu, China) were used. Twelve unaffected (no detectable hardness of the breast area) and twelve WB-affected (diffuse remarkable hardness in the breast muscle) birds were selected from the commercial broiler farm according to the criteria proposed by previous studies.Results: The results indicated that WB showed histological lesions characterized by fiber degeneration and fibrosis, along with an increase of muscle fiber diameter (p<0.05). Moreover, higher pH value, lightness, yellowness, drip loss and cooking loss were observed in the WB group (p<0.05). Compared with the normal breast (NOR) group, the WB group showed higher formation of reactive oxygen species (p<0.05), increased level of oxidation products and antioxidant activities (p<0.05), accompanied with mitochondrial damages and lower mitochondrial membrane potential (p<0.05). Meanwhile, the relative mRNA expressions of Nrf2 and its downstream antioxidant genes including heme oxygenase‐1, NAD(P)H qui none dehydrogenase 1, glutathione peroxidase, superoxide dismutase, and glutamate-cysteine ligase were higher than those of the NOR group (p<0.05).Conclusion: In conclusion, WB myopathy impairs meat quality by causing oxidative damages and mitochondrial dysfunction in broilers, even though the activated Nrf2/antioxidant response element pathway provides protection for the birds.

Preparation and characterization of hydrophilic polydopamine-coated Fe3O4/oxide graphene imprinted nanocomposites for removal of bisphenol A in waters

Suyu Ren,Jing Tao,Ying Cui,Jinsuo Gao,Xiaona Li,Feng Tan 한국화학공학회 2018 Korean Journal of Chemical Engineering Vol.35 No.9

Bisphenol A (BPA), a known endocrine disruptor, is of global concern because it poses serious threats to the ecological environment and human health. In this work, hydrophilic polydopamine-coated Fe3O4/oxide graphene (IPDA@MGO) magnetic imprinted nanocomposites were prepared by the self-polymerization of dopamine on the surface of Fe3O4/GO in Tris-HCl buffer using BPA as a template for selective adsorption of BPA in water. IPDA@MGO showed specific recognition toward BPA with a high imprinting factor of 3.2 compared with nonimprinted polymer. The capacity of IPDA@MGO toward BPA was 41.2mg/g and the adsorption reached equilibrium within 30 min. The adsorption agreed well with the Freundlich and pseudo-second order kinetic models. The good adsorption performance was attributed to the abundant binding sites and good dispersibility of IPDA@MGO nanocomposites derived from its excellent hydrophilicity. The nanocomposites could be removed rapidly by an external magnet and regenerated for repeated adsorption of BPA in water. The proposed method has potential applications for efficient removal of BPA in environmental waters.

Dysfunction of Shh signaling activates autophagy to inhibit trophoblast motility in recurrent miscarriage

Pan Yibin,Yan Lili,Chen Qiaoqiao,Wei Cheng,Dai Yongdong,Tong Xiaomei,Zhu Haiyan,Lu Meifei,Zhang Yanling,Jin Xiaoying,Zhang Tai,Lin Xiaona,Zhou Feng,Zhang Songying 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-

In early pregnancy, the placenta anchors the conceptus and supports embryonic development and survival. This study aimed to investigate the underlying functions of Shh signaling in recurrent miscarriage (RM), a serious disorder of pregnancy. In the present study, Shh and Gli2 were mainly observed in cytotrophoblasts (CTBs), Ptch was mainly observed in syncytiotrophoblasts (STBs), and Smo and Gli3 were expressed in both CTBs and STBs. Shh signaling was significantly impaired in human placenta tissue from recurrent miscarriage patients compared to that of gestational age-matched normal controls. VEGF-A and CD31 protein levels were also significantly decreased in recurrent miscarriage patients. Furthermore, inhibition of Shh signaling impaired the motility of JAR cells by regulating the expression of Gli2 and Gli3. Intriguingly, inhibition of Shh signaling also triggered autophagy and autolysosome accumulation. Additionally, knockdown of BECN1 reversed Gant61-induced motility inhibition. In conclusion, our results showed that dysfunction of Shh signaling activated autophagy to inhibit trophoblast motility, which suggests the Shh pathway and autophagy as potential targets for RM therapy.