Publications by authors named "Yuqing Mo"

9 Publications

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SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells.

Respir Res 2021 Jun 14;22(1):178. Epub 2021 Jun 14.

Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Xuhui District, Shanghai, 200032, China.

Background: Serine peptidase inhibitor, clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma. However, its role in the T-helper type 2 (Th2) response of allergic asthma is not known. The goal of this study was to unveil the function of SERPINB10 in the Th2 response of allergic asthma and the mechanism by which SERPINB10 affects the viability of Th2 cells.

Methods: Th2 cytokines and serum levels of house dust mite (HDM)-specific IgE in bronchoalveolar lavage fluid were examined by ELISA in an HDM-induced asthma model. The number and apoptosis of Th1 and Th2 cells in mouse lungs were measured by flow cytometry. Naïve CD4 T cells from patients with asthma were cultured under appropriate polarizing conditions to generate Th1 and Th2 cells. SERPINB10 expression in polarized Th1 and Th2 cells was quantified by real-time reverse transcription-quantitative polymerase chain reaction. SERPINB10 expression was knocked down in human CD4 T cells with lentivirus.

Results: Knockdown of SERPINB10 expression significantly diminished HDM-induced Th2 cytokine secretion and level of HDM-specific IgE. After HDM exposure, SERPINB10-knockdown mice had diminished numbers of Th2 cells, but similar numbers of Th1 cells, compared with those in negative-control mice. Th2 cells of SERPINB10-knockdown mice were more susceptible to apoptosis than that of control mice. Stimulating T-cell receptors (TCRs) with anti-CD3 antibody caused upregulation of SERPINB10 expression in polarized Th2 cells, but not polarized Th1 cells. Knockdown of SERPINB10 expression resulted in fewer numbers and greater apoptosis of polarized Th2 cells.

Conclusion: Our results suggest that SERPINB10 may contribute to allergic inflammation and the Th2 response of asthma by inhibiting the apoptosis of Th2 cells.
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http://dx.doi.org/10.1186/s12931-021-01757-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8201873PMC
June 2021

Proteomic Analysis of Serum Differentially Expressed Proteins Between Allergic Bronchopulmonary Aspergillosis and Asthma.

Mycopathologia 2021 Mar 12;186(1):1-13. Epub 2020 Nov 12.

Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, No. 180 Fenglin Road, Xuhui District, Shanghai, 200032, China.

Background: Allergic bronchopulmonary aspergillosis (ABPA) constantly develops in asthmatics, which has not been fully investigated.

Objectives: This study aimed to investigate serum differentially expressed proteins (DEPs) between ABPA and asthma using the new approach isobaric tags by relative and absolute quantitation (iTRAQ).

Methods: Each 16 serum samples from ABPA or asthmatic subjects were pooled and screened using iTRAQ. After bioinformatic analysis, five candidate DEPs were validated in the enlarged serum samples from additional 21 ABPA, 31 asthmatic and 20 healthy subjects using ELISA. A receiver operating characteristic (ROC) curve was used to estimate the diagnostic power of carnosine dipeptidase 1 (CNDP1).

Results: A total of 29 DEPs were screened out between ABPA and asthmatic groups. Over half of them were enriched in proteolysis and regulation of protein metabolic process. Further verification showed serum levels of immunoglobulin heavy constant gamma 1, α-1-acid glycoprotein 1, corticosteroid-binding globulin and vitronectin were neither differentially altered between ABPA and asthma nor consistent with the proteomic analysis. Only serum CNDP1 was significantly decreased in ABPA patients, compared with asthmatics and healthy controls (P < 0.01 and P < 0.05). The ROC analysis determined 10.73 ng/mL as the cutoff value of CNDP1, which could distinguish ABPA among asthmatics (AUC 0.770, 95%CI 0.632-0.875, P < 0.001).

Conclusions: This study firstly identified serological DEPs between ABPA and asthma using the new technique iTRAQ. Serum CNDP1 might assist the differential diagnosis of ABPA from asthma and serve as a new pathogenetic factor in fungal colonization and sensitization.
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http://dx.doi.org/10.1007/s11046-020-00506-0DOI Listing
March 2021

CircRNAs and LncRNAs in Osteoporosis.

Differentiation 2020 Nov - Dec;116:16-25. Epub 2020 Oct 28.

Jiangxi University of Science and Technology, Ganzhou, 341000, China; State Key Laboratory of High Performance Complex Manufacturing, Central South University, Changsha, 410083, China. Electronic address:

Osteoporosis is a systemic bone disease with bone fragility and increased fracture risk. The non-coding RNAs (ncRNAs) have appeared as important regulators of cellular signaling and pertinent human diseases. Studies have demonstrated that circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs) are involved in the progression of osteoporosis through a variety of pathways, and are considered as targets for the prophylaxis and treatment of osteoporosis. Based on an in-depth understanding of their roles and mechanisms in osteoporosis, we summarize the functions and molecular mechanisms of circRNAs and lncRNAs involved in the progression of osteoporosis and provide some new insights for the prognosis, diagnosis and treatment of osteoporosis.
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http://dx.doi.org/10.1016/j.diff.2020.10.002DOI Listing
October 2020

Possible Novel Therapeutic Targets in Lymphangioleiomyomatosis Treatment.

Front Med (Lausanne) 2020 24;7:554134. Epub 2020 Sep 24.

Department of Pulmonary and Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.

Lymphangioleiomyomatosis (LAM) is a rare systemic neoplastic disease that exclusively happens in women. Studies focusing on LAM and tuberous sclerosis complex (TSC) have made great progress in understanding the pathogenesis and searching for treatment. The inactive mutation of TSC1 or TSC2 is found in patients with LAM to activate the crucial mammalian target of rapamycin (mTOR) signaling pathway and result in enhanced cell proliferation and migration. However, it does not explain every step of tumorigenesis in LAM. Because cessation of rapamycin would break the stabilization of lung function or improved quality of life and lead to disease recurrent, continued studies on the pathogenesis of LAM are necessary to identify novel targets and new treatment. Researchers have found several aberrant regulations that affect the mTOR pathway such as its upstream or downstream molecules and compensatory pathways in LAM. Some therapeutic targets have been under study in clinical trials. New methods like genome-wide association studies have located a novel gene related to LAM. Herein, we review the current knowledge regarding pathogenesis and treatment of LAM and summarize novel targets of therapeutic potential recently.
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http://dx.doi.org/10.3389/fmed.2020.554134DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7542236PMC
September 2020

Lin28A Regulates Stem-like Properties of Ovarian Cancer Cells by Enriching RAN and HSBP1 mRNA and Up-regulating its Protein Expression.

Int J Biol Sci 2020 15;16(11):1941-1953. Epub 2020 Apr 15.

NHC Key Laboratory of Carcinogenesis of Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine; School of basic Medical Science, Central South University, Changsha, Hunan 410013, China.

Ovarian cancer (OC) is one of the malignant tumors that seriously threaten women's health, with the highest mortality rate in gynecological malignancies. The prognosis of patients with advanced OC is still poor, and the 5-year survival rate is only 20-30%. Therefore, how to improve the early diagnosis rate and therapeutic effect are urgent for patients with OC. In this research, we found that Lin28A can promote the expression of stem cell marker molecules CD133, CD44, OCT4 and Nanog. We later confirmed that Lin28A can enrich the mRNA of ras-related nuclear protein (RAN) and heat shock factor binding protein 1 (HSBP1) through RIP assay, and that Lin28A can regulate their protein expression. We also identified that RAN and HSBP1 are highly expressed in OC tissues, and that they are significantly positively correlated with the expression of Lin28A and negatively correlated with the survival prognosis of OC patients. After stable knockdown of RAN or HSBP1 in OC cells with high expression of Lin28A, the expression of the stem cell marker molecules such as OCT4, CD44 and Nanog are reduced. And after knocking down of RAN or HSBP1 in Lin28A highly expressed OC cells, the survival and invasion of OC cells and tumor size of OC xenograft in nude mice were markedly inhibited and apoptosis was increased. Our data also showed that knock down of RAN or HSBP1 can inhibit the invasion ability of OC cells by decreasing the expression of N-cadherin, Vimentin and promoting the expression of E-cadherin. Meanwhile, knockdown of RAN or HSBP1 induced cell apoptosis by inhibiting the expression of PARP. Our results indicated that Lin28A could regulate the biological behaviors in OC cells through RAN/HSBP1. These findings suggest that Lin28A/RAN/HSBP1 can be used as a marker for diagnosis and prognosis of OC patients, and RAN/HSBP1 may be a potential new target for gene therapy of OC.
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http://dx.doi.org/10.7150/ijbs.43504DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7211169PMC
April 2020

Linc02349 promotes osteogenesis of human umbilical cord-derived stem cells by acting as a competing endogenous RNA for miR-25-3p and miR-33b-5p.

Cell Prolif 2020 May 29;53(5):e12814. Epub 2020 Apr 29.

Institute of Bioadditive Manufacturing, Jiangxi University of Science and Technology, Nanchang, China.

Objectives: Increasing evidences suggest that inducing mesenchymal stem cells to differentiate into osteoblasts has been as an especially important component in the prevention and therapy for degenerative bone disease. Here, we identify a novel lncRNA, linc02349, which increases significantly during osteogenic differentiation.

Materials And Methods: Human umbilical cord-derived stem cells (hUC-MSCs) and dental pulp mesenchymal stem cells were used. Overexpression and knockdown of linc02349 in cell lines were generated using lentiviral-mediated gene delivery method. Bioinformatics prediction, Ago2-RIP assay and dual-luciferase reporter system were employed to examine miRNA which interacts with linc02349. The RNA FISH assay was performed to identify the subcelluar location of linc02349. Alizarin Red S staining, ALP staining and qPCR were applied to identify the osteogenic differentiation. The potential linc02349-regulated genes, miR-25-3p and miR-33b-5p, were explored by ChIP, RIP and Western blotting assays. Micro-CT was used to measure the osteogenic content in bone formation assay in vivo.

Results: Linc02349 overexpression improves osteogenic differentiation by in vitro and in vivo analysis. Mechanistically, linc02349 acts as a molecular sponge for miR-25-3p and miR-33b-5p to control expression abundance of SMAD5 and Wnt10b, respectively, which eventually activated Dlx5/OSX pathway and hence promoted osteogenic differentiation. In addition, we revealed that STAT3 interacts with linc02349 promoter region and positively regulates the linc02349 transcriptional activity.

Conclusion: These findings identify that linc02349 modulates the osteogenic differentiation through acting as a sponge RNA of miR-25-3p and miR-33b-5p and regulating SMAD5 and Wnt10b, and proposed a new interaction between STAT3 and linc02349, which could be a potential target in the process the osteogenesis of hUC-MSCs for future clinical application.
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http://dx.doi.org/10.1111/cpr.12814DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260076PMC
May 2020

Salidroside suppresses group 2 innate lymphoid cell-mediated allergic airway inflammation by targeting IL-33/ST2 axis.

Int Immunopharmacol 2020 Apr 15;81:106243. Epub 2020 Feb 15.

Department of Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address:

Salidroside, an active component extracted from Rhodiola rosea, has been reported to inhibit allergic asthma. However, its mechanism has not been fully elucidated. Group 2 innate lymphoid cells (ILC2s) accumulate in the lung and cooperate with other cells to drive type 2 inflammation stimulated by inhaled allergens. The study aims to explore the suppressive effect of salidroside on ILC2s and IL-33/IL-33R (ST2) axis in allergic airway inflammation. The ovalbumin (OVA)-sensitized/challenged mice were established. Airway eosinophil recruitment, increased total IgE in the serum and type 2 cytokines IL-4, IL-5, and IL-13 in the bronchoalveolar lavage fluids and lung tissues were identified in the OVA-induced mice model, all of which were inhibited by pretreatment with different doses of salidroside. Moreover, salidroside suppressed lung total ILC2 and ST2-expressing ILC2 accumulation, lung IL-33 and ST2 expressions in mice. In vitro, OVA could induce IL-33 expression in BEAS-2B cells, which was also effectively inhibited by salidroside. This study firstly reveals salidroside as a potential therapeutic drug for allergic asthma by inhibiting ILC2-mediated airway inflammation via targeting IL-33/ST2 axis.
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http://dx.doi.org/10.1016/j.intimp.2020.106243DOI Listing
April 2020

Epithelial SERPINB10, a novel marker of airway eosinophilia in asthma, contributes to allergic airway inflammation.

Am J Physiol Lung Cell Mol Physiol 2019 01 1;316(1):L245-L254. Epub 2018 Nov 1.

Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan , China.

Serine peptidase inhibitor, clade B, member 10 (SERPINB10) expression is increased in IL-13-stimulated human bronchial epithelial cells and in a murine model of allergic airway inflammation. However, the role of SERPINB10 in asthma remains unknown. We examined the association between epithelial SERPINB10 expression and airway eosinophilia in subjects with asthma and the role of Serpinb10 in allergic airway inflammation in an animal model. Epithelial SERPINB10 mRNA and protein expression were markedly increased in subjects with asthma ( n = 60) compared with healthy controls ( n = 25). Epithelial SERPINB10 mRNA levels were significantly correlated with airway hyperresponsiveness (AHR) and three parameters reflecting airway eosinophilia including the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa, and fraction of exhaled nitric oxide in subjects with asthma. Moreover, epithelial SERPINB10 expression was strongly correlated with the epithelial gene signature ( CLCA1, POSTN, and SERPINB2) for type 2 status. In normal human bronchial epithelial cells cultured at air-liquid interface, knockdown of SERPINB10 suppressed IL-13-stimulated periostin (encoded by POSTN) and CCL26 (eotaxin-3) expression by inhibiting the activation of p38 MAPK. Epithelial CCL26 mRNA levels were correlated with SERPINB10 expression in subjects with asthma. Airway knockdown of Serpinb10 alleviated AHR, airway eosinophilia and the expression of periostin and Ccl26 in a murine model of allergic airway disease. Taken together, epithelial SERPINB10 is a novel marker for airway eosinophilia in asthma. Epithelial SERPINB10 contributes to allergic airway eosinophilic inflammation, at least in part, by regulating the expression of periostin and CCL26.
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http://dx.doi.org/10.1152/ajplung.00362.2017DOI Listing
January 2019

The association between CD209 gene polymorphisms and pulmonary tuberculosis susceptibility: a meta-analysis.

Int J Clin Exp Pathol 2015 1;8(10):12437-45. Epub 2015 Oct 1.

Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Wuhan, Hubei, China ; Key Laboratory of Respiratory Diseases, National Health and Family Planning Commission of The People's Republic of China China ; National Clinical Research Center for Respiratory Diseases China.

Aim: Three common polymorphisms in CD209 gene (-336A/G, -871A/G and -139G/A) have been reportedly associated with pulmonary tuberculosis risk. However, the findings from different studies were inconsistent. Therefore, we conducted a comprehensive meta-analysis to determine the association between CD209 gene polymorphisms and pulmonary tuberculosis susceptibility.

Methods: The PubMed, SCI and Elsevier were searched up to April 18, 2015 for studies on the association of CD209 gene polymorphisms and pulmonary tuberculosis. Pooled odds ratio (ORs) and 95% confidence intervals (95% CIs) were calculated in a fixed-effects or random-effects model.

Results: Twelve case-control studies with 3114 cases and 3088 controls were included. For -871A/G mutation, significant decreased pulmonary tuberculosis risk was observed in allele model (G vs. A: P = 0.009; OR = 0.70, 95% CI = 0.54-0.92), heterozygous model (AG vs. AA: P = 0.009; OR = 0.59, 95% CI = 0.40 to 0.88) and dominant model (AG+GG vs. AA: p =0.01; OR = 0.61, 95% CI = 0.42 to 0.89). For -336A/G polymorphism, no associations were found in all genetic models. In the subgroup analysis by ethnicity, statistical association was observed for Asians in GG vs. AA (P = 0.04; OR = 2.31, 95% CI = 1.05-5.09). No significant association was identified between -139G/A variation and pulmonary tuberculosis risk.

Conclusions: This meta-analysis provides evidences that CD209 gene -871A/G is associated with decreased susceptibility to pulmonary tuberculosis in overall population; -336A/G polymorphism is associated with increased susceptibility of pulmonary tuberculosis in Asians. However, the -139G/A polymorphism is not associated with susceptibility to pulmonary tuberculosis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4680375PMC
October 2016
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