Publications by authors named "Jiangtao Hou"

6 Publications

  • Page 1 of 1

Spinster homolog 2 in cancers, its functions and mechanisms.

Cell Signal 2021 01 2;77:109821. Epub 2020 Nov 2.

School of Medicine, South China University of Technology, Guangzhou, Guandong, 510006, PR China. Electronic address:

Spinster homolog 2 (SPNS2) is a multi-transmembrane transporter, widely located in the cell membrane and organelle membranes. It transports sphingosine-1-phosphate (S1P) into the extracellular space and the circulatory system, thus alters the concentration and the distribution of S1P, sphingosine-1-phosphate receptor (S1PRs) and S1P related enzymes, meaning that it exerts its functions via S1P signaling pathways. Studies also show that ectopic SPNS2 mediates parts of the physiological process of the cells. As of now, SPNS2 has been reported to participate in physiological processes such as angiogenesis, embryonic development, immune response and metabolisms. It is also associated with the transformation from inflammation to cancer as well as the proliferation and metastasis of cancer cells. In this review, we summarize the functions and the mechanisms of SPNS2 in the pathogenesis of cancer to provide new insights for the diagnosis and the treatments of cancer.
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January 2021

Effective dispersion of multi-walled carbon nanotubes in aqueous solution using an ionic-gemini dispersant.

J Colloid Interface Sci 2018 Feb 31;512:750-757. Epub 2017 Oct 31.

College of Materials Science and Engineering, Beijing University of Technology, Beijing 100124, China.

A promising ionic-gemini molecule, 4, 4'-di (n-tetradecyl) diphenylmethane disulfate salt (DSDM), is reported for effective dispersion of multi-walled carbon nanotubes (MWCNTs) in aqueous medium in the present investigation. The dispersibility and stability of the DSDM-modified MWCNTs were characterized by UV-vis spectrophotometer, Raman spectroscopy, Fourier transform infrared spectroscopy, transmission electron microscopy and zeta potential measurements. The hydrophobic interaction between alky chains and carbon nanotubes as well as the π-π-stacking interaction between benzene rings and carboatomic rings in MWCNTs enables a successful modification of DSDM onto the MWCNT surface. The dispersed MWCNTs individually existed in dispersion with no structural damage, indicating a much better performance than the MWCNTs dispersed by the sodium dodecylbenzene sulfonate (SDBS), a frequently reported single-chain ionic dispersant. Surface potential measurements showed that the DSDM-modified MWCNTs were negatively charged, giving rise to electrostatic repulsion between the MWCNTs in aqueous solution. A better MWCNT dispersion effect was observed with the increase in MWCNT surface potential, and the dispersion with high MWCNT surface potential presents high dispersion stability with no agglomeration appeared for more than 5 months. The magnesium (Mg) matrix composite fabricated based on the DSDM-dispersed MWCNTs demonstrated excellent mechanical properties compared to pure Mg. Our research may provide an alternative way to improve the mechanical properties of composites.
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February 2018

miR-155 targets Est-1 and induces ulcerative colitis via the IL-23/17/6-mediated Th17 pathway.

Pathol Res Pract 2017 Oct 25;213(10):1289-1295. Epub 2017 Aug 25.

Department of Laboratory, the First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China. Electronic address:

Background: Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) affecting millions of people worldwide. miR-155 has been reported to be upregulated in various inflammatory diseases and is a positive regulator of the T-cell response. IL-17 secreting helper T (Th17) cells have been heavily implicated in tissue-specific immune pathology, including UC.

Methods And Results: Therefore, we targeted miR-155 and investigated its expression levels in a DSS-induced UC mouse model, revealing increased expression. Est-1 expression was found to have decreased, but the levels of IL-23/17/6 were raised significantly and Th17 had experienced an obvious increase. We overexpressed miR-155 using a lentiviral treatment. Increased miR-155 expression induced a more severe damage to colon tissues. In this case, the level of Est-1 decreased even further, thereby enhancing IL-23/17/6-mediated Th17 differentiation.

Conclusion: miR-155 seems to target Est-1 and induces UC via the IL-23/17/6-mediated Th17 pathway.
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October 2017

Adalimumab for Moderately to Severely Active Ulcerative Colitis: A Systematic Review and Meta-Analysis.

BioDrugs 2016 Jun;30(3):207-17

The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, China.

Background: Evidence-based studies are increasingly being focused on evaluating the efficacy and safety of adalimumab (ADA) for moderately to severely active ulcerative colitis (UC). However, the dosage pattern of ADA for UC management is still not clear.

Objective: A meta-analysis was conducted to evaluate the efficacy and safety of different ADA dosage regimens for moderately to severely active UC.

Methods: The Medline, EMBASE, ISI Web of Knowledge, and Cochrane databases were searched from their inception to January 2015. Randomized controlled trials (RCTs) comparing ADA with placebo were eligible for initial inclusion. The efficacy and side effects were evaluated for ADA 160/80 (ADA 160/80 mg at weeks 0/2 and then 40 mg at weeks 4 and 6), and ADA 80/40 (ADA 80/40 mg at weeks 0/2 and then 40 mg at weeks 4 and 6) induction therapy, with ADA 40 mg every other week (EOW) for maintenance therapy of 52 weeks. The pooled risk ratio (RR) and its 95 % confidence interval (CI) were calculated.

Results: Three RCTs were included. All of the studies were considered to have a low risk of bias. ADA 160/80 was more effective than placebo for induction of clinical remission (RR 1.62, 95 % CI 1.15-2.29), clinical response (RR 1.37, 95 % CI 1.19-1.59), mucosal healing (RR 1.27, 95 % CI 1.08-1.50), and inflammatory bowel disease questionnaire (IBDQ) response (RR 1.22, 95 % CI 1.05-1.43) and did not increase adverse events (RR 1.10, 95 % CI 0.95-1.27). Compared with placebo, ADA 80/40 did not show significant differences for induction of clinical remission and clinical response and did not increase adverse events. ADA 40 mg EOW was superior to placebo in maintaining clinical remission (RR 2.38, 95 % CI 1.57-3.59), clinical response (RR 1.69, 95 % CI 1.29-2.21), mucosal healing (RR 1.69, 95 % CI 1.26-2.28), and IBDQ response (RR 1.73, 95 % CI 1.28-2.34). Compared with placebo, ADA 40 mg EOW increased adverse events (RR 1.28, 95 % CI 1.06-1.54).

Conclusion: ADA 160/80 was a safe and effective treatment for induction management of moderately to severely active UC, but the benefits of ADA 80/40 application were limited. ADA 40 mg EOW was effective for maintenance management of UC. Additional well designed RCTs are needed to confirm these results.
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June 2016

MiR-29a promotes intestinal epithelial apoptosis in ulcerative colitis by down-regulating Mcl-1.

Int J Clin Exp Pathol 2014 1;7(12):8542-52. Epub 2014 Dec 1.

First School of Clinic Medicine & First Affiliated Hospital of Guangzhou University of Chinese Medicine China.

Objective: While it's widely accepted that the etiology of ulcerative colitis (UC) involves both genetic and environmental factors, the pathogenesis of ulcerative colitis is still poorly understood. Intestinal epithelial apoptosis is one of the most common histopathological changes of UC and the expression of a number of apoptosis genes may contribute to the progression of UC. MicroRNAs have recently emerged as powerful regulators of diverse cellular processes and have been shown to be involved in many immune-mediated disorders such as psoriasis, rheumatoid arthritis, lupus, and asthma. A unique microRNA expression profile has been identified in UC, suggesting that, microRNAs play an important role in the pathogenesis of UC. We investigated the role of miR-29a in intestinal epithelial apoptosis in UC.

Methods: The expression of miR-29a and Mcl-1, an anti-apoptotic BCL-2 family member, was evaluated in both UC patients and UC mice model induced by dextran sodium sulfate (DSS). The apoptosis rate of intestinal epithelial cells was also evaluated.

Results: In UC patients and DSS-induced UC in mice, the expression of miR-29a and Mcl-1, were up-regulated and down-regulated, respectively. We identified a miR-29a binding site (7 nucleotides) on the 3'UTR of mcl-1 and mutation in this binding site on the 3'UTR of mcl-1 led to mis-match between miR-29a and mcl-1. Knockout of Mcl-1 caused apoptosis of the colonic epithelial HT29 cells. In addition, miR-29a regulated intestinal epithelial apoptosis by down-regulating the expression of Mcl-1.

Conclusion: miR-29a is involved in the pathogenesis of UC by regulating intestinal epithelial apoptosis via Mcl-1.
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October 2015

Association of interleukin-17F 7488 single nucleotide polymorphism and inflammatory bowel disease in the Chinese population.

Scand J Gastroenterol 2009 ;44(6):720-6

Department of Gastroenterology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, PR China.

Objective: The functional polymorphism of interleukin (IL)-17F 7488 A > G was found to be associated with autoimmune inflammatory diseases and also high IL-17F intestinal expression in inflammatory bowel disease (IBD) was detected. The purpose of this study was to investigate the association between the polymorphism and IBD in the Chinese population and to elucidate potential interactions between IL-17F genotypes and clinical phenotypes.

Material And Methods: DNA was extracted from peripheral blood cells of 148 ulcerative colitis (UC), 134 Crohn's disease (CD) patients and 373 age- and gender-matched healthy controls. The IL-17F 7488 A > G polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and sequencing.

Results: In UC patients, the homozygous GG genotype frequency was significantly lower than that in the controls (0.0% versus 3.8%, p=0.014); Compared to that of wild-type AA patients, the AG heterozygous carriers have a later onset (43.3+/-11.1 years versus 34.6+/-14.8 years, p = 0.012) and a significantly higher incidence of mild severity (94.1% versus 61.0%, p = 0.009, OR = 0.96, 95% CI = 0.94-0.96), respectively, indicating that subjects with the GG genotype have a slightly decreased risk of 0.96 times for UC compared with that of other genotypes. Further analysis also revealed that G carrier subjects were more likely to present mild severity and had 10.2 times higher incidence of getting mild severity than those with AA genotype (OR = 10.2, 95% CI = 1.3-81.0).

Conclusions: This study shows that IL-17F 7488 A > G polymorphism is associated with weak UC protection in the Chinese population. The clinical phenotypes of UC are also affected by this polymorphism.
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October 2009