Xiao Zhong

Third Military Medical University, Ch’ung-ch’ing-shih, Chongqing Shi, China

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Publications (8)21.21 Total impact

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    ABSTRACT: To investigate the regulation of intracellular store-operated calcium channels (SOCCs) in detrusor overactivity (DO) during detrusor function changes in Sprague-Dawley rats.
    Urology 06/2014; · 2.42 Impact Factor
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    ABSTRACT: Recent findings suggest that clinical hepatocellular carcinoma (HCC) progression is driven by hepatic cancer stem cells (HCSCs) through their capacity for self-renewal, generation of heterogeneous lineages of cancer cells, resistance to chemotherapy and their ability to divide limitlessly, which may contribute to the failure of existing therapies to consistently eradicate malignant tumors. Therefore, HCSC-directed therapeutic approaches might represent strategies to improve clinical HCC therapy. In previous studies, we showed that BC047440 was found to play a critical role in mediating HCC cell proliferation. The present study sought to determine whether BC047440 is involved in maintaining HCSC malignant behavior (including proliferation and differentiation). We demonstrated that BC047440 expression was markedly upregulated in HCSCs. Furthermore, we inhibited BC047440 in HCSCs using short hairpin RNA (shRNA). The effects of BC047440 on proliferation and differentiation were investigated. We also analyzed the involvement of critical molecular events known to regulate the proliferation and the differentiation machinery. Excluding apoptosis-related effects, we found that BC047440 inhibition resulted in enhanced cell proliferation through enhancing cytoplasmic accumulation of nuclear factor-κB (NF-κB) with a concomitant decrease in the nuclear fraction. BC047440 inhibition also resulted in inducing HCSC differentiation into hepatocytes. Furthermore, following downregulation of BC047440, the level of hepatocyte nuclear factor 4α (HNF4α) increased. Finally, tumorigenicity suppression following BC047440 depletion was confirmed in a nude mouse model. In conclusion, our findings indicate that BC047440 plays an important role in the proliferation and differentiation of HCSCs and may represent a novel therapeutic target for the treatment of HCC.
    Oncology Reports 02/2014; · 2.30 Impact Factor
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    ABSTRACT: OBJECTIVE: To investigate how the sodium/calcium exchanger subtype 3 (NCX3) and its reverse mode contribute to the function of interstitial cells of Cajal (ICCs) from the rat bladder. METHODS: The study used 20 female Wistar rats. We observed the expression of the NCX3 expression in the bladder using reverse transcriptase-polymerase chain reaction and Western blotting. The NCX3 in ICCs was also confirmed by double-labeled fluorescence. NCX3 functions in reverse mode of ICCs were observed using confocal microscopy with preload fluo-3AM, and its currents were evaluated using the whole-cell patch clamp technique, with or without the NCX3 inhibitor KB-R7943 (5 and 30μM), with an afterward identification of ICCs using single-cell polymerase chain reaction. RESULTS: NCX3 was confirmed in rat bladder ICCs. The time required for the intracellular calcium concentration [Ca(2+)]i of NCX3 was enhanced by KB-R7943 (5μM, P ≤.01). Moreover, KB-R7943 (5 and 30μM) significantly decreased the currents generated by the reverse mode of NCX3 from the ICCs (P <.05). CONCLUSION: NCX3 is expressed in rat bladder ICCs. The reverse mode of NCX3 can generate [Ca(2+)]i of the bladder ICCs.
    Urology 05/2013; · 2.42 Impact Factor
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    ABSTRACT: Cell therapy is the most promising therapy for end-stage liver diseases (ESLDs). Fetal liver stem/progenitor cells (FLSPCs) have the advantages of a high survival rate, high proliferation, small volume, and high safety, which make them one of the ideal cells for stem cell therapy for liver diseases. During the early phase of our study, we applied a three-step separation method to enrich FLSPCs and obtained a separation efficiency that was similar to the flow cell-sorting method. Additionally, using a fulminant hepatic failure rat model, we demonstrated that FLSPCs can contribute to the recovery of hepatic morphogenesis and function. However, two problems remain to be resolved to explore the therapeutic potential of FLSPCs. First, how can FLSPCs be induced to accurately differentiate into hepatocytes and cholangiocytes? Second, how do FLSPCs maintain self-renewal? The Notch signaling plays a critical role in regulating the differentiation and self-renewal of many types of stem cells. Additionally, our previous findings have shown that the Notch signaling plays an important role in FLSPC differentiation into hepatocytes. Therefore, we hypothesized that the Notch signaling may be involved in the differentiation and self-renewal of FLSPCs. We began a study on the regulatory effects and relative molecular mechanisms of the Notch signaling on FLSPCs and found the corresponding interfering target, which may become an index for the clinical application of FLSPCs.
    Archives of medical research 10/2012; · 1.88 Impact Factor
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    ABSTRACT: OBJECTIVE: To investigate the expression and function of T-type calcium channels in the interstitial cells of Cajal in rat bladders. METHODS: Bladders were harvested from Sprague-Dawley rats. The expression of T-type calcium channels subtypes (α1G, α1H, and α1I) in interstitial cells of Cajal were identified by double-labeled immunofluorescence analysis and reverse transcription-polymerase chain reaction analysis in whole mount preparations of rat bladders. The function of T-type calcium channels in freshly isolated interstitial cells of Cajal was assessed by detecting the changes of intracellular calcium ([Ca(2+)](i)) with preloading fluo-3 AM, and by evaluating the changes of the phasic contractions of rat bladder strips after treating with mibefradil and glivec. RESULTS: Three T-type calcium channels subtypes, α1G, α1H, and α1I, colocalized with c-kit in bladder interstitial cells of Cajal by double-labeled immunofluorescence analysis, and this was confirmed using reverse transcription-polymerase chain reaction. The T-type calcium channels selective blocker, mibefradil (1 μM), significantly decreased the intracellular calcium concentration ([Ca(2+)](i)) in isolated interstitial cells of Cajal (P < .01) and inhibited the spontaneous phasic contraction of bladder strips (P < .01). Moreover, the c-kit receptor blocker, glivec, significantly decreased the [Ca(2+)](i) of interstitial cells of Cajal further (P < .01) and the spontaneous phasic contraction of bladder strips. CONCLUSION: T-type calcium channel subtypes were confirmed to colocalize in interstitial cells of Cajal in rats bladders, which might participate in the spontaneous activity of interstitial cells of Cajal and phasic contractions of bladder strips by modulating [Ca(2+)](i) in interstitial cells of Cajal.
    Urology 09/2012; · 2.42 Impact Factor
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    ABSTRACT: BACKGROUND: Although hypoxia is known to promote hepatoma cell invasion and migration, little is known regarding the molecular mechanisms of this process. Our previous research showed that loss of Tg737 is associated with hepatoma cell invasion and migration; therefore, we hypothesized that the Tg737 signal might be required for hypoxia-enhanced invasion and migration. METHODS: We established in vitro normoxic or hypoxic models to investigate the role of Tg737 in the hypoxia-enhanced invasion and migration of hepatoma cells. The hepatoma cell lines HepG2 and MHCC97-H were subjected to normoxic or hypoxic conditions, and the cell adhesion, invasion, and migration capabilities were tested. The expression of Tg737 under normoxia or hypoxia was detected using western blot assays; cell viability was determined using flow cytometry. Furthermore, we created HepG2 and MHCC97-H cells that over expressed Tg737 prior to incubation under hypoxia and investigated their metastatic characteristics. Finally, we analyzed the involvement of critical molecular events known to regulate invasion and migration. RESULTS: In this study, Tg737 expression was significantly inhibited in HepG2 and MHCC97-H cells following exposure to hypoxia. The down regulation of Tg737 expression corresponded to significantly decreased adhesion and increased invasion and migration. Hypoxia also decreased the expression/secretion of polycystin-1, increased the secretion of interleukin-8 (IL-8), and increased the levels of active and total transforming growth factor beta 1 (TGF-beta1), critical regulators of cell invasion and migration. Moreover, the decrease in adhesiveness and the increase in the invasive and migratory capacities of hypoxia-treated hepatoma cells were attenuated by pcDNA3.1-Tg737 transfection prior to hypoxia. Finally, following the up regulation of Tg737, the expression/secretion of polycystin-1 increased, and the secretion of IL-8 and the levels of active and total TGF-beta1 decreased correspondingly. CONCLUSIONS: These data provide evidence that Tg737 contributes to hypoxia-induced invasion and migration, partially through the polycystin-1, IL-8, and TGF-beta1 pathway. Taken together, this work suggests that Tg737 is involved in the invasion and migration of hepatoma cells under hypoxia, with the involvement of the polycystin-1, IL-8, and TGF-beta1 signaling pathway. Tg737 is a potential therapeutic target for inhibiting the high invasion and migration potential of hepatoma cells in hypoxic regions.
    Journal of Experimental & Clinical Cancer Research 09/2012; 31(1):75. · 3.07 Impact Factor
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    ABSTRACT: To investigate the distribution and effects of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel and its isoforms in bladder, especially in bladder interstitial cells of Cajal (ICC). Four HCN isoforms were detected in bladder tissue from rats using reverse transcription-polymerase chain reaction and Western blotting. The HCN1 subtype was observed in bladder ICCs by double-labeled fluorescence. The effect of the HCN blocker, ZD7288, was investigated using the bladder smooth muscle strip test. HCN1-4 isoforms were all identified in bladder ICCs using reverse transcription-polymerase chain reaction and Western blotting. Based on our semiquantitative analysis, HCN1 was found to be the most prominent isoform. The expression of HCN1 was confirmed in bladder ICCs by double-labeled fluorescence through colabeling of HCN1 and kit (CD117). ZD7288 significantly decreased the bladder excitation. All 4 HCN channel isoforms exist in the bladder, and they affect the bladder excitation, presumably via bladder ICCs.
    Urology 03/2012; 79(6):1411.e7-13. · 2.42 Impact Factor
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    ABSTRACT: Cancer stem/progenitor cells (CSPCs) may originate from the malignant transformation of normal stem cells. However, the mechanism by which normal stem cells undergo such transformation is not understood. Our previous studies provided evidence that Tg737 may play an important role in carcinogenesis of liver stem cells. In this study, we investigated the role of Tg737 in the malignant transformation of fetal liver stem/progenitor cells (FLSPCs). We inhibited Tg737 in FLSPCs using short hairpin RNA (shRNA). The microscopic observations of freshly purified Tg737 normal FLSPCs (nFLSPCs) and Tg737-silent FLSPCs (sFLSPCs), which showed high expression levels of stem cell markers, revealed no significant morphological changes in sFLSPCs. Following RNAi of Tg737, the mRNA and protein levels of sFLSPCs decreased by 81.81% and 80.10% as shown by PCR, Western blot and immunocytochemistry analyses. Excluding apoptosis-related effects, we found that silencing of Tg737 resulted in enhanced cell proliferation through promoting cell-cycle progression via upregulation of cyclin D1 and cyclin B expression (P < 0.05). Silencing of Tg737 also resulted in significant arrest of cell differentiation (P < 0.05), stable expression of both albumin (ALB) and alpha fetoprotein (AFP) (P > 0.05) and quiescent ultrastructure. Assessment of cell malignant traits by transwell migration assays and by growth of xenograft tumors in athymic mice showed that reduced expression of Tg737 greatly promoted cell invasion and hepatocarcinogenesis of FLSPCs (P < 0.05). This work shows that inactivation of Tg737 may play an important role in malignant transformation of FLSPCs.
    Molecular Carcinogenesis 08/2011; 51(8):659-73. · 4.27 Impact Factor

Publication Stats

10 Citations
21.21 Total Impact Points

Institutions

  • 2012–2014
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
  • 2011–2012
    • Fourth Military Medical University
      • Department of Hepatobiliary Surgery
      Xi’an, Liaoning, China
    • Xinqiao Hospital
      Ch’ung-ch’ing-shih, Chongqing Shi, China