Zhaozong Fu

Nanfang Hospital, Shengcheng, Guangdong, China

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Publications (5)8.35 Total impact

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    ABSTRACT: The transcriptional cofactor CITED1 inhibits osteoblastic differentiation and blunts the stimulation of osteoblastic differentiation by parathyroid hormone (PTH). In the MC3T3-E1 osteoblastic cell line, we found that CITED1 was located predominantly in the cytoplasm and that hPTH(1-34) increased translocation of CITED1 from the cytoplasm to the nucleus. This response to hPTH(1-34) was not observed when all 9 serine residues within the 63-84 domain of CITED1 were mutated to alanines (CITED1 9S>A) or when a single serine to alanine mutation was made at position 79 (CITED1 S(79)>A). CITED1 containing mutations of these 9 serines to glutamic acid (9S>E) retained the same nuclear translocation response to PTH(1-34) as the wild type CITED1. ALP activity and formation of mineralized nodules were inhibited in cells transfected with pcDNA3-CFP-CITED1 or with pcDNA3-CFP-CITED1 9S>E with or without hPTH(1-34) treatment (all P<0.05); these changes were not observed using CITED1 9S>A. Cells exposed to intermittent treatment with hPTH(1-34) expressed more ALP2, Runx2 and osteocalcin than vehicle-treated cells. These effects of hPTH(1-34) were inhibited in cells transfected with pcDNA3-CFP-CITED1 or pcDNA3-CFP-CITED1 9S>E, but were slightly enhanced by the alanine mutants. PKC activator (TPA) increased nuclear translocation of CITED1, whereas a PKC inhibitor (Go6983) blunted the effect of hPTH(1-34) on the nuclear translocation of wildtype CITED1 but not of CITED1 S(79)>E. The data indicated that serine phosphorylation at position 79 in the 63-84 domain is associated with PKC activation, and is required for both CITED1 nuclear translocation induced by PTH and the negative effects of CITED1 on osteoblastic differentiation and mineralization.
    No preview · Article · Jul 2014 · Cellular Signalling
  • Peng Liu · Zhaozong Fu · Jianming Jiang · Liang Yuan · Zhen Lin
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    ABSTRACT: Medications compounded with isoniazid (INH) are usually applied to surgical sites at the completion of surgery to locally kill postoperative residual tubercle bacilli. However, the distribution and elimination of INH in the vertebrae in vivo are not known. In this study, isotope tracing was used in conjunction with high-pressure liquid chromatography (HPLC) to address this. INH and technetium-99 m-labeled INH were applied to the vertebrae of rabbits. After 2 and 6 h, osseous tissues containing INH, as determined by radionuclide imaging, were collected for detection with HPLC. The results showed that INH mainly stayed around the vertebrae 6 h after its application and did not permeate widely into the blood or other organs, except for the kidneys. The standard deviations of INH concentrations in the technetium-99 m-INH group were approximately four-fold smaller than those in the INH group. This method of coupling isotope tracing and HPLC can effectively limit experimental error during sample collection, allowing accurate and reliable identification of the concentration levels of INH in osseous tissues in vivo. Copyright © 2013 John Wiley & Sons, Ltd.
    No preview · Article · Sep 2013 · Biomedical Chromatography
  • Zhaozong Fu · Hai Lu · Jianming Jiang · Hui Jiang · Zhaofei Zhang
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    ABSTRACT: Oligodendrocyte-produced Nogo-A has been shown to inhibit axonal regeneration. Methylprednisolone plays an effective role in treating spinal cord injury, but the effect of methylprednisolone on Nogo-A in the injured spinal cord remains unknown. The present study established a rat model of acute spinal cord injury by the weight-drop method. Results showed that after injury, the motor behavior ability of rats was reduced and necrotic injury appeared in spinal cord tissues, which was accompanied by increased Nogo-A expression in these tissues. After intravenous injection of high-dose methylprednisolone, although the pathology of spinal cord tissue remained unchanged, Nogo-A expression was reduced, but the level was still higher than normal. These findings implicate that methylprednisolone could inhibit Nogo-A expression, which could be a mechanism by which early high dose methylprednisolone infusion helps preserve spinal cord function after spinal cord injury.
    No preview · Article · Feb 2013 · Neural Regeneration Research
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    ABSTRACT: The major pathological changes of osteoarthritis (OA) include cartilage degeneration and synovial inflammation. Previous studies confirmed that interleukin-1 (IL-1) stimulates the secretion of multiple inflammatory factors in synoviocytes and chondrocytes. IL-18 is a member of the IL-1 superfamily. In this study, the pro-inflammatory effects of IL-18 on synoviocytes and chondrocytes in patients with OA were investigated. Knee synovial membrane and cartilage samples were obtained from OA patients, then primary cells were cultured. Synoviocytes and primary chondrocytes at different generations (primary, secondary and tertiary), were stimulated with IL-18, then inflammatory marker levels, including tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2) and cyclooxygenase-2 (COX-2), were measured using reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay. IL-1 receptor antagonist (IL-1Ra) was applied to interfere with the IL-18 stimulation of chondrocytes, and then the COX-2 expression in chondrocytes and the PGE2 levels in the medium were measured. The expression of IL-18 receptor α (IL-18Rα) and IL-18 receptor β (IL-18Rβ) in synoviocytes and chondrocytes was assessed, using RT-PCR. Our results showed that IL-18 stimulated the COX-2 and TNF-α expressions in primary synoviocytes, while increasing PGE2 and TNF-α levels in the supernatant (P<0.05) of the culture medium in primary synoviocytes. IL-18 also induced high PGE2 level production in second-generation synoviocytes (P<0.05). Moreover, IL-18 upregulated COX-2 and TNF-α mRNA in chondrocytes, while promoting PGE2 and TNF-α (P<0.05) secretions in a dose-dependent manner. The induced effects were not attenuated by the addition of IL-1Ra (P<0.05). IL-18Rα was expressed in the chondrocytes and synoviocytes of 4/8 patients, while IL-18Rβ was expressed in the chondrocytes of 4/8 patients and in the synoviocytes of 2/8 patients. We conclude that IL-18 induces inflammatory responses in synoviocytes and chondrocytes and that this effect was correlated with, although not entirely dependent on, IL-1β.
    Preview · Article · Jul 2012 · International Journal of Molecular Medicine
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    ABSTRACT: To study the effect of signal-selective parathyroid hormone (PTH) analogue peptide on Wnt signaling factors in osteoblasts isolated from neonatal mouse, and provide theoretical basis for the mechanism of PTH's function in bone metabolism. Osteoblasts were isolated from calvaria of 2-3-day-old C57BL neonatal mouse and identified by alkaline phosphatase (ALP) staining, and Alizarin red staining. The cells at passage 1 were divided into 4 groups: control group, PTH (1-34) group, G1R19 (1-34) group, and G1R19 (1-28) group. Then the medium was changed to a-MEM supplemented with 1% FBS. After 12 hours, trifluoroacetic acid or three peptides [(10 nmol/L PTH (1-34), 10 nmol/L G1R19 (1-34), and 100 nmol/L G1R19 (1-28)] were added into the culture medium. After 4 hours, the cells were washed gently with cold PBS 3 times before total RNA was isolated. The expressions of Wnt related genes were measured by quantitative real-time PCR. Most of the cells were polygonal and triangular; the cells were positive for ALP staining with blue cytoplasm at 14 days and the Alizarin red staining showed the formation of red mineralized nodules in the special mineralization induction medium at 28 days. The expressions of osteocalcin mRNA and Wnt5b mRNA in PTH (1-34) group, G1R19 (1-34) group, and G1R19 (1-28) group were significantly higher than those in control group (P < 0.05); the expression of Wnt2 mRNA was significantly lower than that in control group (P < 0.05); the expression of beta-catenin mRNA in PTH (1-34) group was significantly higher than that in control group (P < 0.05); the expression of Wnt7b mRNA in PTH (1-34) group and G1R19 (1-34) group was higher than that in control group, and the G1R19 (1-34) group was higher than PTH (1-34) group and G1R19 (1-28) group (P < 0.05). In the Wnt-related factors, PTH (1-34) and G1R19 (1-34) affect mainly canonical Wnt signal factors, but the G1R19 (1-28) chiefly acts on non-canonical Wnt signal factors.
    No preview · Article · Apr 2012 · Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery