Yingjie Wang

Nantong University, Tungchow, Jiangsu Sheng, China

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Publications (6)23.04 Total impact

  • Nature Communications 11/2015; 6:10033. DOI:10.1038/ncomms10033 · 11.47 Impact Factor
  • Xue Bai · Yingjie Wang · Lili Man · Qing Zhang · Cheng Sun · Wen Hu · Yan Liu · Mei Liu · Xiaosong Gu · Yongjun Wang ·
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    ABSTRACT: The regeneration-competent adult animals have ability to regenerate their lost complex appendages with a near-perfect replica, owing to the positional identity acquired by the progenitor cells in the blastema, i.e. the blastemal cells. CD59, a CD59/Ly6 family member, has been identified as a regulator of positional identity in the tail blastemal cells of Gekko japonicus. To determine whether this function of CD59 is unique to the regenerative amniote(s) and how CD59 mediates PD axis patterning during tail regeneration, we examined its protective role on the complement-mediated cell lysis and intervened CD59 expression in the tail blastemal cells using an in vivo model of adenovirus transfection. Our data revealed that gecko CD59 was able to inhibit complement-mediated cell lysis. Meanwhile, CD59 functioned on positional identity through expression in cartilage precursor cells. Intervening positional identity by overexpression or siRNA knockdown of CD59 resulted in abnormal cartilaginous cone patterning due to the decreased differentiation of blastemal cells to cartilage precursor cells. The cartilage formation-related genes were found to be under the regulation of CD59. These results indicate that CD59, an evolutionarily transitional molecule linking immune and regenerative regulation, affects tail regeneration by mediating cartilage patterning.
    Scientific Reports 08/2015; 5:12798. DOI:10.1038/srep12798 · 5.58 Impact Factor
  • Honghua Song · Lili Man · Yingjie Wang · Xue Bai · Sumei Wei · Yan Liu · Mei Liu · Xiaosong Gu · Yongjun Wang ·
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    ABSTRACT: The Wingless/Integrated (Wnt) signaling pathway plays important roles in central nervous system (CNS) development and regeneration, and β-catenin, the central component, has been considered in association with adult neurogenesis. To decipher its roles on spontaneous spinal cord regeneration, we cloned β-catenin from Gekko japonicus and examined its function in regenerating spinal cord. The protein was localized in the neurons and oligodendrocytes and maintained a stable expression levels during the spinal cord regeneration. The temporal pattern of expression has been found to be completely distinct with those of glycogen synthase kinase 3β (GSK3β). Experiments of gain-of-function by overexpression of full length β-catenin or stabilized ΔN90-β-catenin revealed that the accumulated protein attenuates the elongation of neurites and oligodendrocyte process. Knockdown of endogenous β-catenin, however, decreased proliferation of oligodendrocytes by affecting expression of downstream lef1 and c-jun. The upregulated extracellular matrix fibronectin in injured cord was found to be inefficient in regulation of β-catenin expression. Our results suggest that a tightly regulated stable expression of β-catenin is required for the spontaneous spinal cord regeneration.
    Journal of Molecular Neuroscience 09/2014; 55(3). DOI:10.1007/s12031-014-0405-5 · 2.34 Impact Factor
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    ABSTRACT: Uncontrolled, excessive inflammation contributes to the secondary tissue damage of traumatic spinal cord, and HMGB1 is highlighted for initiation of a vicious self-propagating inflammatory circle by release from necrotic cells or immune cells. Several regenerative-competent vertebrates have evolved to circumvent the second damages during the spontaneous spinal cord regeneration with an unknown HMGB1 regulatory mechanism. By genomic surveys, we have revealed that HMGB1 two paralogs are broadly retained from fish onwards in the phylogeny. However, their spatial-temporal expression and effects, as shown in lowest amniote gecko, were tightly controlled in order that limited inflammation was produced in spontaneous regeneration. Gecko HMGB1 (gHMGB1) two paralogs yielded distinct injury and infectious responses, with gHMGB1b significantly upregulated in the injured cord. The intracellular gHMGB1b induced less release of inflammatory cytokines than gHMGB1a in macrophages, and the effects could be shifted by exchanging one amino acid in the inflammatory domain. Both intracellular proteins were able to mediate neuronal programmed apoptosis, which has been indicated to produce negligible inflammatory responses. In vivo studies demonstrated that the extracellular proteins could not trigger a cascade of the inflammatory cytokines in the injured spinal cord. Signal transduction analysis found that the recombinant proteins could not bind with cell surface receptors TLR2 and TLR4 to activate inflammatory signaling pathway. However they were able to interact with RAGE to potentiate oligodendrocytes migration by activation of both NFκB and Rac1/Cdc42 signaling. Our results reveal that HMGB1 does not mediate the inflammatory response in spontaneous spinal cord regeneration, but promotes CNS regeneration.
    Journal of Biological Chemistry 05/2013; 288(25). DOI:10.1074/jbc.M113.463810 · 4.57 Impact Factor
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    ABSTRACT: SNARE complex mediates cellular membrane fusion events essential for neurotransmitter release and synaptogenesis. SNAP25, a member of the SNARE proteins, plays critical roles during the development of the central nervous system via regulation by alternative splicing and protein kinase phosphorylation. To date, little information is available regarding the protein in the spinal cord regeneration, especially for the postnatal highly expressed isoform SNAP25b. In the present study, we characterized gecko SNAP25b, which shared high identity with those of other vertebrates. Expression of gecko SNAP25b was temporally upregulated in both neurons of spinal cord and forming ependymal tube following tail amputation, coinciding with the occurrence of regenerate re-innervation. Overexpression of gecko wild type SNAP25b in the SH-SY5Y and undifferentiated PC12 cells promoted the elongation and outgrowth of neurites, while mutant constructs at Serine(187) resulted in differential effects for which S187A had a promoting role. Knockdown of endogenous SNAP25b affected the formation of neurites, which could be rescued by overexpression of SNAP25b. FM1-43 staining revealed that transfection of S187E mutant construct reduced the recruitment of vesicles. In addition, transfection of gecko SNAP25b in the astrocyte, which is absent from neuronal specific VAMP2, was capable of enhancing process elongation, indicating a potential for various alternative protein combinations. Taken together, our data suggest that gecko SNAP25b is involved in spinal cord regeneration by promoting outgrowth and elongation of neurites in a more extensive protein binding manner.
    The international journal of biochemistry & cell biology 09/2012; 44(12):2288-2298. DOI:10.1016/j.biocel.2012.09.011 · 4.05 Impact Factor
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    ABSTRACT: GSK-3β signaling is involved in regulation of both neuronal and glial cell functions, and interference of the signaling affects central nervous system (CNS) development and regeneration. Thus, GSK-3β was proposed to be an important therapeutic target for promoting functional recovery of adult CNS injuries. To further clarify the regulatory function of the kinase on the CNS regeneration, we characterized gecko GSK-3β and determined the effects of GSK-3β inactivation on the neuronal and glial cell lines, as well as on the gecko tail (including spinal cord) regeneration. Gecko GSK-3β shares 91.7-96.7% identity with those of other vertebrates, and presented higher expression abundance in brain and spinal cord. The kinase strongly colocalized with the oligodendrocytes while less colocalized with neurons in the spinal cord. Phosphorylated GSK-3β (pGSK-3β) levels decreased gradually during the normally regenerating spinal cord ranging from L13 to the 6th caudal vertebra. Lithium injection increased the pGSK-3β levels of the corresponding spinal cord segments, and in vitro experiments on neurons and oligodendrocyte cell line revealed that the elevation of pGSK-3β promoted elongation of neurites and oligodendrocyte processes. In the normally regenerate tails, pGSK-3β kept stable in 2 weeks, whereas decreased at 4 weeks. Injection of lithium led to the elevation of pGSK-3β levels time-dependently, however destructed the regeneration of the tail including spinal cord. Bromodeoxyuridine (BrdU) staining demonstrated that inactivation of GSK-3β decreased the proliferation of blastemal cells. Our results suggested that species-specific regulation of GSK-3β was indispensable for the complete regeneration of CNS.
    Journal of Cellular Biochemistry 06/2012; 113(6):1842-51. DOI:10.1002/jcb.24053 · 3.26 Impact Factor
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    ABSTRACT: Several adult reptiles, such as Gekko japonicus, have the ability to precisely re-create a missing tail after amputation. To ascertain the associated acquisition of positional information from blastemal cells and the underlying molecular mechanism of tail regeneration, a candidate molecule CD59 was isolated from gecko. CD59 transcripts displayed a graded expression in the adult gecko spinal cord with the highest level in the anterior segment, with a stable expression along the normal tail. After tail amputation, CD59 transcripts in the spinal cord proximal to the injury sites increased markedly at 1 day and 2 weeks; whereas in the regenerating blastema, strong CD59 positive signals were detected in the blastemal cells anterior to the blastema, with a gradual decrease along the proximodistal (PD) axis. When treated with RA following amputation, CD59 transcripts in the blastema were up-regulated. PD confrontation assays revealed that the proximal blastema engulfed the distal one after in vitro culture, and rabbit-anti human CD59 antibody was able to block this PD engulfment. Overexpression of the CD59 during tail regeneration causes distal blastemal cells to translocate to a more proximal location. Our results suggest that position identity is not restricted to amphibian limb regeneration, but has already been established in tail blastema of reptiles. The CD59, a cell surface molecule, acted as a determinant of proximal-distal cell identity.
    PLoS ONE 03/2011; 6(3):e17878. DOI:10.1371/journal.pone.0017878 · 3.23 Impact Factor