Publications by authors named "Guolong Qi"

5 Publications

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Role of Slit2 upregulation in recurrent miscarriage through regulation of stromal decidualization.

Placenta 2021 01 9;103:1-9. Epub 2020 Oct 9.

Department of Pathology, Jinan University School of Medicine, Guangzhou, 510632, China. Electronic address:

Introduction: Knockout mouse model has shown a relationship between Slit2/Robo1 signalling and altered fertility. Altered expression by endometrial epithelium and trophoblast and is associated with the pathogenesis of pregnancy complications but few studies have investigated the expression of decidual Slit2 in miscarriage.

Methods: Expression profiles of Slit2 and Robo1 were measured in human endometrial tissues during the menstrual cycle phases (n = 30), in decidua tissues from recurrent miscarriage (n = 20) and healthy control (n = 20) at 6-8 weeks of gestation. The hormonal regulation of Slit2/Robo1 expression and the role of Slit2/Robo1 signalling in decidualization was investigated in vitro, along with its effects on β-catenin and MET expression.

Results: In human endometrium, Slit2 and Robo1 protein expression in stromal cells were decreased between the late-proliferative and early-secretory phase. In recurrent miscarriage patients, decidual expression Slit2 was increased and associated with lower expression of E-cadherin and higher level vimentin compared to controls. In vitro, the expression of Slit2 was downregulated by cAMP and progesterone in hESCs. Upregulation of Slit2 resulted in inhibition of cell decidualization and β-catenin translocation to nucleus.

Discussion: This study indicates a functional role for Slit2 in endometrial stromal cell decidualization and the pathogenesis of recurrent miscarriage. Aberrant Increase in Slit2 expression may impairs decidualization of endometrial stromal cells leading to recurrent in recurrent miscarriage.
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http://dx.doi.org/10.1016/j.placenta.2020.10.008DOI Listing
January 2021

Baicalin rescues hyperglycemia-induced neural tube defects via targeting on retinoic acid signaling.

Am J Transl Res 2020 15;12(7):3311-3328. Epub 2020 Jul 15.

Division of Histology and Embryology, International Joint Laboratory for Embryonic Development & Prenatal Medicine, Medical College, Jinan University Guangzhou 510632, China.

We, in this study, studied whether or not antioxidant activities of Baicalin could reduce the incidence of neural tube defects (NTDs) in the presence of hyperglycemia. Using early chick embryos, we demonstrated that Baicalin at 6 μM dramatically reduced NTDs rate and impaired neurogenesis in E4.5-day and HH10 chick embryo neural tubes induced by high glucose (HG). Likewise, immunofluorescent staining showed that Baicalin mitigated the HG-induced regression of Pax7 expression in neural tubes of both HH10 and E4.5-day chick embryos. Additionally, PHIS3 immunofluorescent staining in neural tubes of both HH10 and E4.5-day chick embryos manifested that cell proliferation inhibited by HG was significantly reversed by the administration of Baicalin, and similar result could also be observed in neurosphere assay . c-Caspase3 or γH2AX immunofluorescent staining and quantitative PCR showed that Baicalin administration alleviated HG-induced cell apoptosis and DNA damage. Bioinformatics results indicated that retinoic acid (RA) was likely to be the signaling pathway that Baicalin targeted on, and this was confirmed by whole-mount RALDH2 hybridization and quantitative PCR of HH10 chick embryos in the absence/presence of Baicalin. In addition, blocking RA with an inhibitor abolished Baicalin's protective role in HG-induced NTDs, suppression of neurogenesis and cell proliferation, and induction of apoptosis, which further verified the centrality of RA in the process of Baicalin confronting HG-induced abnormal neurodevelopment.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7407732PMC
July 2020

Toxoplasma gondii Cathepsin C1 inhibits NF-κB signalling through the positive regulation of the HIF-1α/EPO axis.

Acta Trop 2019 Jul 17;195:35-43. Epub 2019 Apr 17.

Department of Pathogen Biology, School of Medicine, Jinan University, Guangzhou, China; Key Laboratory of environmental exposure and health in Guangzhou, Jinan University, Guangzhou, China; Guangzhou Key Laboratory of Environmental Exposure and Health in Guangzhou, Guangdong Key Laboratory of Environmental Pollution and Health, Jinan University, Guangzhou, Guangdong, China; The key laboratory for virology of Guangzhou, College of life science and technology, Jinan University, China. Electronic address:

Toxoplasma gondii has evolved many successful strategies for immune evasion. However, the parasite-derived effectors involved in modulating NF-κB signalling pathway are largely unknown. T. gondii Cathepsin C1 (CPC1) is widely conserved among T. gondii strains and is important for T. gondii intracellular growth and proliferation. Our study showed that CPC1 protein could abrogate NF-κB activation after screening dense granule proteins. CPC1 suppressed NF-κB activation at or downstream of p65 and decreased the production of IL-1, IL-8, IL-6, IL-12, and TNF-α. Western blot analysis revealed that CPC1 inhibited phospho-p65 and CPC1 proteins primarily settled in cytoplasm. RNA sequencing analysis revealed that overexpression of CPC1 significantly upregulated erythropoietin (EPO), which can be induced by the hypoxia-inducible factor -1α (HIF-1α) during hypoxia. Furthermore, dual-luciferase reporter assays confirmed that CPC1 upregulated HIF-1α. Finally, both the knockdown of EPO and restriction of HIF-1α partially eliminated the suppression impact of CPC1 on the NF-κB signalling pathway. Our study identified a previously unrecognized role of CPC1 in the negative regulation of NF-κB activation through positive regulation of the HIF-1α/EPO axis. For the first time, CPC1 was shown to play an important role in immune evasion during T. gondii infection.
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http://dx.doi.org/10.1016/j.actatropica.2019.04.018DOI Listing
July 2019

Heterogeneity of the biological properties and gene expression profiles of murine bone marrow stromal cells.

Int J Biochem Cell Biol 2013 Nov 30;45(11):2431-43. Epub 2013 Jul 30.

Center for Stem Cell Biology and Tissue Engineering, The Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Sun Yat-Sen University, Guangzhou, PR China.

Although mesenchymal stromal cells (MSCs) have demonstrated great therapeutic potential, the heterogeneity of MSCs may be responsible for the incongruent data obtained in MSC-based preclinical studies and clinical trials. Here, four mouse clonal MSC lines, termed MSC1, MSC2, MSC3, and MSC4, were isolated and extensively characterized. MSC4 cells grew most rapidly and formed colonies of the largest size, whereas MSC3 cells exhibited the slowest growth and formed only a few tiny clusters. MSC4 cells could differentiate into adipocytes, osteoblasts, and chondrocytes in vitro, and more importantly, establish hematopoietic microenvironment in vivo; whereas the other lines displayed uni-adipogenic, osteo-chondrogenic, or non-differentiation potential. All lines were positive for Sca-1, CD106, and CD44; MSC4 was also positive for CD90.2. In terms of immunosuppressive capacity, MSC2, MSC3, and MSC4 cells exerted clear inhibitory effects on lymphocyte proliferation, whereas MSC1 did not. Further investigation revealed that the NO and not the PGE2 pathway may play a role in the different immunomodulatory effects of the cell lines. To clarify the molecular basis of this heterogeneity, we employed RNA sequencing to compare the gene expression profiles of the four subtypes, revealing a relationship between gene expression and variability in subtype function. This study provides novel information about the heterogeneity of MSCs and insight into the selection of optimal cell sources for therapeutic applications.
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http://dx.doi.org/10.1016/j.biocel.2013.07.015DOI Listing
November 2013

Copy number increase of HER-2 in colorectal cancers.

Oncol Lett 2011 Mar 8;2(2):331-335. Epub 2010 Dec 8.

Biomedical Research Institute, Shenzhen-PKU-HKUST Medical Center, Guangdong.

HER-2 is involved in genetic instability and is overexpressed in a number of human carcinomas, including colorectal cancer (CRC). The choromosomal locus of HER-2, 17q21, is frequently amplified in breast cancer, but the correlation between copy-number variations and HER-2 overexpression in CRC has yet to be elucidated. The functional impact of such regions requires extensive investigation in large numbers of CRC samples. Case-matched tissues of colorectal adenocarcinomas and adjacent normal epithelia (n=134) were included in this study. Quantitative PCR was performed to examine the copy number and mRNA expression of HER-2 in CRC. The results showed that copy number gains of HER-2 were detected in a relatively high percentage of CRC samples (35.1%, 47 out of 134). A positive correlation was noted between the copy number increase of HER-2 and tumor progression. Furthermore, copy number gains of HER-2 showed a positive correlation with mRNA overexpression in CRC. However, the expression levels of HER-2 mRNA were also enhanced in the group of CRC samples with unaltered copy numbers. In conclusion, the findings suggest that a copy number increase of HER-2 is a potential diagnostic indicator for CRC; whether alone or in combination with other markers.
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http://dx.doi.org/10.3892/ol.2010.225DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3410603PMC
March 2011