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Articles by J Xiao
Total Records ( 5 ) for J Xiao
  J Xiao , S Yin , Y Li , S Xie , D Nie , L Ma , X Wang , Y Wu and J. Feng
 

S-phase kinase-associated protein 2 (SKP2) gene is a tumor suppressor gene, and is involved in the ubiquitin-mediated degradation of P27kip1. SKP2 and P27kip1 affect the proceeding and prognosis of leukemia through regulating the proliferation, apoptosis and differentiation of leukemia cells. In this study, we explored the mechanism of reversing of HL-60/A drug resistance through SKP2 down-regulation. HL-60/A cells were nucleofected by Amaxa Nucleofector System with SKP2 siRNA. The gene and protein expression levels of Skp2, P27kip1, and multi-drug resistance associated protein (MRP) were determined by reverse transcription-polymerase chain reaction and western blot analysis, respectively. The cell cycle was analyzed by flow cytometry. The 50% inhibitory concentration value was calculated using cytotoxic analysis according to the death rate of these two kinds of cells under different concentrations of chemotherapeutics to compare the sensitivity of the cells. HL-60/A cells showed multi-drug resistance phenotype characteristic by cross-resistance to adriamycin, daunorubicin, and arabinosylcytosine, due to the expression of MRP. We found that the expression of SKP2 was higher in HL-60/A cells than in HL-60 cells, but the expression of P27kip1 was lower. The expression of SKP2 in HL-60/A cells nucleofected by SKP2 siRNA was down-regulated whereas the protein level of P27kip1 was up-regulated. Compared with the MRP expression level in the control group (nucleofected by control siRNA), the mRNA and protein expression levels of MRP in HL-60/A cells nucleofected by SKP2 siRNA were lower, and the latter cells were more sensitive to adriamycin, daunorubicin, and arabinosylcytosine. Down-regulating the SKP2 expression and arresting cells in the G0/G1 phase improve drug sensitivity of leukemia cells with down-regulated MRP expression.

  Y Tan , Y Li , J Xiao , H Shao , C Ding , G. E Arteel , K. A Webster , J Yan , H Yu , L Cai and X. Li
  Aims

The effects on angiogenesis of a novel CXC chemokine receptor 4 (CXCR4) antagonist, SDF-1βP2G, derived from human stromal cell-derived factor-1β (SDF-1β), were examined in a model of hind limb ischaemia in mice.

Methods and results

The antagonistic activities of SDF-1βP2G against CXCR4 were evaluated in vitro and in vivo and compared with phosphate-buffered saline and AMD3100 (a small bicyclam antagonist of SDF-1). Angiogenesis, muscle regeneration and the expression of pro-angiogenic factors were evaluated in ischaemic gastrocnemius muscles. Distant toxic effects of SDF-1βP2G were evaluated by inflammatory and apoptotic markers. SDF-1βP2G induced CXCR4 internalization and competitively inhibited the chemotaxis of SDF-1β but did not mediate migration, calcium influx, or the phosphorylation of Akt and extracellular signal-regulated kinase in cultured T-lymphoblastic leukaemia cells or H9C2 cells. SDF-1βP2G enhanced blood flow, angiogenesis, and muscle regeneration in ischaemic hind limbs, and the enhancement was significantly better than that of AMD3100. Markers of angiogenesis and progenitor cell migration, including phosphorylated Akt, vascular endothelial growth factor (VEGF), SDF-1 and CXCR4, were up-regulated by SDF-1βP2G and co-localized with CD31-positive cells. Neutralization of VEGF with its specific antibody abolished SDF-1βP2G-induced blood reperfusion and angiogenesis. No apparent inflammatory and apoptotic effects were found in heart, liver, kidneys, and testes after SDF-1βP2G administration.

Conclusion

Our findings indicate that the novel CXCR4 antagonist, SDF-1βP2G, can efficiently enhance ischaemic angiogenesis, blood flow restoration, and muscle regeneration without apparent adverse effects, most likely through a VEGF-dependent pathway.

  P Ferrari , J Xiao , A Ukich and A. Irish
 

Aim. The aim of this study was to analyse the association between chronic kidney disease (CKD) defined by an estimated glomerular filtration rate (eGFR) <60 ml/min/ 1.73 m2 and anaemia in older people.

Background. Guidelines focus on early identification and management of CKD to prevent CKD progression and cardiovascular disease. However, the significance of CKD classification using eGFR in older people is unclear.

Methods. Serum creatinine and haemoglobin from individuals attending non-nephrology outpatient clinics were extracted from the state pathology provider over a 4-month period. The associations between eGFR, gender, age and haemoglobin were explored.

Results. Serum creatinine in 9853 individual patients aged ≥15 years was available for analysis. Haemoglobin was simultaneously available in 8752 (88.8%) subjects. There was a negative relationship between age and median eGFR, and the slope of the regression line was –0.68 ml/min/year for males and –0.74 ml/min/year for females. Over 35% of individuals ≥65 years were classified as having CKD stage ≥3. Odds ratios for haemoglobin <100 g/l for an eGFR <15, 15–29 and 30–59 versus reference GFR ≥60 ml/ min/1.73 m2 in subjects 25–44 years were 34.2 (30.7–37.7), 23.4 (20.2–26.6) and 7.2 (5.3–9.1), respectively. In comparison, these were 8.9 (6.7–11.1), 5.6 (4.9–7.3) and 1.6 (1.1–2.1), respectively, in subjects ≥65 years. In subjects ≥65 years, odds ratios for haemoglobin <100 g/l for an eGFR 30–44 and 45–59 ml/min/1.73 m2 versus reference GFR ≥60 ml/min/1.73 m2 were 1.9 (1.3–2.5) and 1.2 (0.7–1.7), respectively.

Conclusions. An eGFR <60 ml/min/1.73 m2 is very common in older people. Only an eGFR <45 ml/min/1.73 m2 identified a smaller sub-group of older people with an increased prevalence of significant anaemia suggesting a clinically relevant disease. The benefits of identifying older people with an eGFR ≥45 ml/min/1.73 m2 need to be determined.

  J Xiao , J. C. K Leung , L. Y. Y Chan , H Guo and K. N. Lai
 

Background. We have previously demonstrated a glomerulo-tubular ‘crosstalk’ operating in the pathogenesis of tubulointerstitial injury in IgA nephropathy (IgAN). The present study aims to explore any possible beneficial effect of a peroxisome proliferator-activated receptor- (PPAR-) agonist in alleviating the tubulointerstitial inflammation in IgAN.

Methods. Human proximal tubular epithelial cells (PTEC) were pre-treated with increasing concentration of a PPAR- agonist rosiglitazone or troglitazone (0–5 µM) followed by further incubation with the conditioned medium (IgA-HMC) collected from human mesangial cells (HMC) incubated with polymeric IgA isolated from IgAN patients. Gene expression of interleukin-6 (IL-6) and angiotensin II type 1 receptor (ATR1) was detected by reverse transcription–polymerase chain reaction (RT–PCR); protein expression of IL-6 and ATR1 was determined by ELISA and western blot, respectively. The mitogen-activated protein kinase extracellular signal-related kinase 1/2 (ERK1/2) activation was examined by western blot.

Results. An IgA-HMC conditioned medium prepared from IgAN patients increased gene expression and protein synthesis of IL-6 and ATR1 in PTEC when compared with a conditioned medium prepared from healthy controls. The upregulated gene expression and protein synthesis of IL-6 and ATR1 in PTEC induced by the IgA-HMC conditioned medium were readily attenuated following pre-treatment with a PPAR- agonist, thiazolidinedione (TZD). The ATR1-downregulating effect exerted by the PPAR- agonist occurred through the inhibition of ERK1/2 activation. The PPAR- antagonist, GW9662, significantly attenuated the inhibitory action of rosiglitazone on the increased synthesis of IL-6 and ATR1 protein.

Conclusion. Our current findings suggest that the PPAR- agonist attenuates excessive inflammatory response in activated PTEC in IgAN through suppressing ATR1 expression. This ATR1-downregulating effect is likely through the inhibition of ERK1/2 activation and is found to be PPAR- dependent. TZDs may possibly be new therapeutic additives to established treatment regime for renin–angiotensin system (RAS) blockade in IgAN.

  J Xiao , N. l Wang , B Sun and G. p. Cai
 

Estrogen receptors (ERs) play a pivotal role in adipogenesis; therefore, compounds targeting ERs may also affect fat formation. Recent studies have shown that the Dioscorea plant (commonly called yam) exhibits an antiobesity effect on rodents. However, the active compounds and underlying mechanisms responsible for this effect are not yet fully understood. We evaluated the effects of pseudoprotodiocsin (PPD), a steroid saponin from Dioscorea nipponica Makino (a type of Dioscorea), on adipogenesis and the mechanisms underlying this effect. Treatment with PPD at the onset of adipogenic differentiation resulted in significantly decreased adipogenesis in both in vitro and in vivo experimental systems. An increased amount of ER mRNA, protein, and the accumulation of ER in the nucleus were also observed. However, the expression pattern of ERβ was not altered. Furthermore, the antiadipogenic effect of PPD was found to be ER dependent. It was also accompanied by the decreased expression of several genes involved in adipogenesis, including lipoprotein lipase (LPL), leptin, CCAAT/enhancer-binding-protein- (C/EBP), and peroxisome proliferator-activated receptor- (PPAR), as well as the increased expression of some negative factors of adipogenesis, including preadipocyte factor 1 (Pre-1), GATA-binding protein 2 (GATA-2), GC-induced leucine-zipper protein (GILZ), and C/EBP homologous protein (CHOP-10). In addition to its estrogenic action, PPD also abolished the p38 mitogen-activated protein kinase (p38 MAPK) activation. Our results suggest that PPD inhibits adipogenesis in an ER-dependent manner and induces the expression of ER. These findings may provide a lead toward a novel agent that can be used to treat obesity.

 
 
 
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