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  1. Article ; Online: Foxq1 Promotes Alveolar Epithelial Cell Death through Tle1-mediated Inhibition of the NFκB Signaling Pathway.

    Zhu, Xi / Hua, Ershi / Tu, Qifeng / Liu, Mei / Xu, Liqin / Feng, Jian

    American journal of respiratory cell and molecular biology

    2024  

    Abstract: Acute lung injury is a common respiratory disease characterized by diffuse alveolar injury and interstitial edema, as well as a hyperinflammatory response, lung cell damage and oxidative stress. Foxq1, a member of the FOX family of transcription factors, ...

    Abstract Acute lung injury is a common respiratory disease characterized by diffuse alveolar injury and interstitial edema, as well as a hyperinflammatory response, lung cell damage and oxidative stress. Foxq1, a member of the FOX family of transcription factors, is expressed in various tissues, such as the lungs, liver, and kidneys, and contributes to various biological processes, such as stress, metabolism, cell cycle arrest, and aging-related apoptosis. However, the role of Foxq1 in acute lung injury is unknown. We constructed ex vivo and in vivo acute lung injury models by lipopolysaccharide tracheal perfusion of ICR mice and conditioned medium stimulation of injured MLE-12 cells. Foxq1 expression was increased, and its localization was altered in our acute lung injury model. In normal or injured MLE-12 cells, knockdown of Foxq1 promoted cell survival, and overexpression had the opposite effect. This regulatory effect was likely mediated by Tle1 and the NFκB/Bcl2/Bax signaling pathway. These data suggest a potential link between Foxq1 and acute lung injury, indicating that Foxq1 can be used as a biomarker for the diagnosis of acute lung injury. Targeted inhibition of Foxq1 expression could promote alveolar epithelial cell survival and may provide a strategy for mitigating acute lung injury.
    Language English
    Publishing date 2024-04-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2023-0317OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
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  2. Article ; Online: Promising application of a novel biomaterial, light chain of silk fibroin combined with NT3, in repairment of rat sciatic nerve defect injury

    Yan, Yingying / Zhang, Wenxue / Wu, Ronghua / Guan, Tuchen / Li, Zhen / Tu, Qifeng / Liu, Yan / Gu, Xiaosong / Liu, Mei

    International Journal of Biological Macromolecules. 2023 June, v. 240 p.124447-

    2023  

    Abstract: Autologous nerve transplantation is the gold standard for treating peripheral nerve defects, but it is associated with defects such as insufficient donor and secondary injury. Artificial nerve guidance conduits (NGCs) are now considered promising ... ...

    Abstract Autologous nerve transplantation is the gold standard for treating peripheral nerve defects, but it is associated with defects such as insufficient donor and secondary injury. Artificial nerve guidance conduits (NGCs) are now considered promising alternatives for bridging long nerve gaps, although exploring new biomaterials to construct NGCs remains challenging. Silk fibroin (SF) has good biocompatibility and can self-assemble in aqueous solutions. However, the lack of proximal neurotrophic factors after nerve injury is a major concern, leading to incomplete nerve regeneration. In this study, NT-3, a neurotrophin that promotes neuronal survival and differentiation, was bound to the light chain of silk fibroin (FIBL) in two ways: one was directly bound to FIBL (FIBL-NT3) and the other was a polypeptides-linker (FIBL-Linker-NT3). The design aimed to take advantage of silk fiber's character of self-assembly of heavy-light chains and test whether a flexible linker with NT3 molecule is easy to be a NT3 dimer, the active form. In vitro studies indicated that FIBL-Linker-NT3 combined with SF membranes promoted axon growth in adult rat dorsal root ganglion (DRG) neurons. Then we tested if FIBL-Linker-NT3 could self-assemble with the SF heavy chain (SFH). DTT (Dithiothreitol) was used to break the disulfide bonds between the SF light and heavy chains, and the light-chain protein was removed via dialysis. SFH was assembled using FIBL-Linker-NT3, as evidenced by the western blotting results that showed a high molecular band corresponding to SFH-FIBL-Linker-NT3. Chitosan scaffolds have been identified to provide a suitable microenvironment, so a chitosan/SF-FIBL-Linker-NT3 conduit was also constructed. Nerve transplantation of this conduit was evaluated in vivo in a rat sciatic nerve defect model. Immunohistochemical assays showed that the chitosan/SF-FIBL-Linker-NT3 group was superior to the chitosan/PBS, SF, PBS + FIBL-Linker-NT3 groups in nerve regeneration. In addition, the chitosan/SF-FIBL-Linker-NT3 conduit-transplanted group exhibited better recovery in terms of neurite length, sciatic functional index value, sensitivity to heat, time on the rotarod, wet weight ratio, cross-sectional area, compound muscle action potential, number of myelin layers, and myelin thickness in the nerve. Taking together, our study identified that FIBL-Linker-NT3 could promote axonal growth and regeneration in vivo and in vitro and is a promising candidate biomaterial for artificial NGCs.
    Keywords action potentials ; adults ; biocompatibility ; biocompatible materials ; chitosan ; dialysis ; disulfides ; dithiothreitol ; fibroins ; ganglia ; heat ; immunohistochemistry ; models ; muscles ; myelin sheath ; nerve regeneration ; nerve tissue ; neurites ; rats ; silk ; Artificial nerve guidance conduit ; Peripheral nerve injury ; Neurotrophic factor 3 ; Silk fibroin light chain ; Self-assembly
    Language English
    Dates of publication 2023-06
    Publishing place Elsevier B.V.
    Document type Article ; Online
    ZDB-ID 282732-3
    ISSN 1879-0003 ; 0141-8130
    ISSN (online) 1879-0003
    ISSN 0141-8130
    DOI 10.1016/j.ijbiomac.2023.124447
    Database NAL-Catalogue (AGRICOLA)

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    Zs.B 2374: Show issues Location:
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  3. Article ; Online: Promising application of a novel biomaterial, light chain of silk fibroin combined with NT3, in repairment of rat sciatic nerve defect injury.

    Yan, Yingying / Zhang, Wenxue / Wu, Ronghua / Guan, Tuchen / Li, Zhen / Tu, Qifeng / Liu, Yan / Gu, Xiaosong / Liu, Mei

    International journal of biological macromolecules

    2023  Volume 240, Page(s) 124447

    Abstract: Autologous nerve transplantation is the gold standard for treating peripheral nerve defects, but it is associated with defects such as insufficient donor and secondary injury. Artificial nerve guidance conduits (NGCs) are now considered promising ... ...

    Abstract Autologous nerve transplantation is the gold standard for treating peripheral nerve defects, but it is associated with defects such as insufficient donor and secondary injury. Artificial nerve guidance conduits (NGCs) are now considered promising alternatives for bridging long nerve gaps, although exploring new biomaterials to construct NGCs remains challenging. Silk fibroin (SF) has good biocompatibility and can self-assemble in aqueous solutions. However, the lack of proximal neurotrophic factors after nerve injury is a major concern, leading to incomplete nerve regeneration. In this study, NT-3, a neurotrophin that promotes neuronal survival and differentiation, was bound to the light chain of silk fibroin (FIBL) in two ways: one was directly bound to FIBL (FIBL-NT3) and the other was a polypeptides-linker (FIBL-Linker-NT3). The design aimed to take advantage of silk fiber's character of self-assembly of heavy-light chains and test whether a flexible linker with NT3 molecule is easy to be a NT3 dimer, the active form. In vitro studies indicated that FIBL-Linker-NT3 combined with SF membranes promoted axon growth in adult rat dorsal root ganglion (DRG) neurons. Then we tested if FIBL-Linker-NT3 could self-assemble with the SF heavy chain (SFH). DTT (Dithiothreitol) was used to break the disulfide bonds between the SF light and heavy chains, and the light-chain protein was removed via dialysis. SFH was assembled using FIBL-Linker-NT3, as evidenced by the western blotting results that showed a high molecular band corresponding to SFH-FIBL-Linker-NT3. Chitosan scaffolds have been identified to provide a suitable microenvironment, so a chitosan/SF-FIBL-Linker-NT3 conduit was also constructed. Nerve transplantation of this conduit was evaluated in vivo in a rat sciatic nerve defect model. Immunohistochemical assays showed that the chitosan/SF-FIBL-Linker-NT3 group was superior to the chitosan/PBS, SF, PBS + FIBL-Linker-NT3 groups in nerve regeneration. In addition, the chitosan/SF-FIBL-Linker-NT3 conduit-transplanted group exhibited better recovery in terms of neurite length, sciatic functional index value, sensitivity to heat, time on the rotarod, wet weight ratio, cross-sectional area, compound muscle action potential, number of myelin layers, and myelin thickness in the nerve. Taking together, our study identified that FIBL-Linker-NT3 could promote axonal growth and regeneration in vivo and in vitro and is a promising candidate biomaterial for artificial NGCs.
    MeSH term(s) Rats ; Animals ; Fibroins/pharmacology ; Fibroins/chemistry ; Biocompatible Materials/pharmacology ; Biocompatible Materials/therapeutic use ; Chitosan/chemistry ; Renal Dialysis ; Silk/chemistry ; Sciatic Nerve/physiology ; Nerve Regeneration ; Tissue Scaffolds/chemistry
    Chemical Substances Fibroins (9007-76-5) ; Biocompatible Materials ; Chitosan (9012-76-4) ; Silk
    Language English
    Publishing date 2023-04-18
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 282732-3
    ISSN 1879-0003 ; 0141-8130
    ISSN (online) 1879-0003
    ISSN 0141-8130
    DOI 10.1016/j.ijbiomac.2023.124447
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Deficiency of Kif15 gene inhibits tumor growth due to host CD8

    Zhang, Siming / Tu, Qifeng / Qian, Xiaowei / Wang, Junpei / Ma, Chao / Yang, Liu / Liu, Yan / Wu, Ronghua / Liu, Mei

    Biochemical and biophysical research communications

    2023  Volume 655, Page(s) 110–117

    Abstract: Kif15, also name kinesin-12, is a microtubule (MT) associate protein, which functions as a regulator of MT-dependent transport or spindle organization. Previous studies reported Kif15 increases in many tumors, however the effect of host Kif15 gene lack ... ...

    Abstract Kif15, also name kinesin-12, is a microtubule (MT) associate protein, which functions as a regulator of MT-dependent transport or spindle organization. Previous studies reported Kif15 increases in many tumors, however the effect of host Kif15 gene lack on tumor growth is not investigated. In this study, CRISPR/Cas9 mediated Kif15 gene knockout (Kif15
    MeSH term(s) Animals ; Mice ; CD8-Positive T-Lymphocytes/metabolism ; Kinesins/genetics ; Kinesins/metabolism ; Microtubules/metabolism ; Neoplasms/metabolism ; T-Lymphocytes/metabolism
    Chemical Substances Kinesins (EC 3.6.4.4) ; Kif15 protein, mouse
    Language English
    Publishing date 2023-03-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2023.03.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  5. Article: Fidgetin interacting with microtubule end binding protein EB3 affects axonal regrowth in spinal cord injury.

    Ma, Chao / Wang, Junpei / Tu, Qifeng / Bo, Weijuan / Hu, Zunlu / Zhuo, Run / Wu, Ronghua / Dong, Zhangji / Qiang, Liang / Liu, Yan / Liu, Mei

    Neural regeneration research

    2023  Volume 18, Issue 12, Page(s) 2727–2732

    Abstract: Fidgetin, a microtubule-severing enzyme, regulates neurite outgrowth, axonal regeneration, and cell migration by trimming off the labile domain of microtubule polymers. Because maintenance of the microtubule labile domain is essential for axon initiation, ...

    Abstract Fidgetin, a microtubule-severing enzyme, regulates neurite outgrowth, axonal regeneration, and cell migration by trimming off the labile domain of microtubule polymers. Because maintenance of the microtubule labile domain is essential for axon initiation, elongation, and navigation, it is of interest to determine whether augmenting the microtubule labile domain via depletion of fidgetin serves as a therapeutic approach to promote axonal regrowth in spinal cord injury. In this study, we constructed rat models of spinal cord injury and sciatic nerve injury. Compared with spinal cord injury, we found that expression level of tyrosinated microtubules in the labile portion of microtubules continuously increased, whereas fidgetin decreased after peripheral nerve injury. Depletion of fidgetin enhanced axon regeneration after spinal cord injury, whereas expression level of end binding protein 3 (EB3) markedly increased. Next, we performed RNA interference to knockdown EB3 or fidgetin. We found that deletion of EB3 did not change fidgetin expression. Conversely, deletion of fidgetin markedly increased expression of tyrosinated microtubules and EB3. Deletion of fidgetin increased the amount of EB3 at the end of neurites and thereby increased the level of tyrosinated microtubules. Finally, we deleted EB3 and overexpressed fidgetin. We found that fidgetin trimmed tyrosinated tubulins by interacting with EB3. When fidgetin was deleted, the labile portion of microtubules was elongated, and as a result the length of axons and number of axon branches were increased. These findings suggest that fidgetin can be used as a novel therapeutic target to promote axonal regeneration after spinal cord injury. Furthermore, they reveal an innovative mechanism by which fidgetin preferentially severs labile microtubules.
    Language English
    Publishing date 2023-07-14
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.373716
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Kif15 deficiency contributes to depression-like behavior in mice.

    Wang, Junpei / Tu, Qifeng / Zhang, Siming / He, Xiaomei / Ma, Chao / Qian, Xiaowei / Wu, Ronghua / Shi, Xinyu / Yang, Zhangyi / Liu, Yan / Dong, Zhangji / Liu, Mei

    Metabolic brain disease

    2023  Volume 38, Issue 7, Page(s) 2369–2381

    Abstract: Neuropsychiatric disorders have a high incidence worldwide. Kinesins, a family of microtubule-based molecular motor proteins, play essential roles in intracellular and axonal transport. Variants of kinesins have been found to be related to many diseases, ...

    Abstract Neuropsychiatric disorders have a high incidence worldwide. Kinesins, a family of microtubule-based molecular motor proteins, play essential roles in intracellular and axonal transport. Variants of kinesins have been found to be related to many diseases, including neurodevelopmental/neurodegenerative disorders. Kinesin-12 (also known as Kif15) was previously found to affect the frequency of both directional microtubule transports. However, whether Kif15 deficiency impacts mood in mice is yet to be investigated. In this study, we used the CRISPR/Cas9 method to obtain Kif15
    MeSH term(s) Animals ; Female ; Mice ; Depression/genetics ; Kinesins/genetics ; Kinesins/metabolism ; Microtubules/metabolism ; Neurons/metabolism
    Chemical Substances Kinesins (EC 3.6.4.4) ; Kif15 protein, mouse
    Language English
    Publishing date 2023-05-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632824-6
    ISSN 1573-7365 ; 0885-7490
    ISSN (online) 1573-7365
    ISSN 0885-7490
    DOI 10.1007/s11011-023-01238-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2155: Show issues Location:
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  7. Article ; Online: Fidgetin impacts axonal growth and branching in a local mTOR signal dependent manner.

    Ma, Chao / Wang, Junpei / Tu, Qifeng / Wu, Ronghua / Lai, Xiaona / Lin, Ge / Dong, Zhangji / Guan, Tuchen / Qiang, Liang / Liu, Yan / Liu, Mei

    Experimental neurology

    2022  Volume 361, Page(s) 114315

    Abstract: Neurons require a constant increase in protein synthesis during axonal growth and regeneration. AKT-mTOR is a central pathway for mammalian cell survival and regeneration. Fidgetin (Fign) is an ATP-dependent microtubule (MT)-severing enzyme whose ... ...

    Abstract Neurons require a constant increase in protein synthesis during axonal growth and regeneration. AKT-mTOR is a central pathway for mammalian cell survival and regeneration. Fidgetin (Fign) is an ATP-dependent microtubule (MT)-severing enzyme whose functions are associated with neurite outgrowth, axon regeneration and cell migration. Although most previous studies have indicated that depletion of Fign is involved in those biological activities by increasing labile MT mass, it remains unknown whether mTOR activation contributes to this process. Here, we showed that depletion of Fign enhanced p-mTOR/p-S6K activation, and the mTOR inhibitor Rapamycin inhibited axon outgrowth and p-rpS6 activation. We then investigated the effects of neuronal-specific Fign deletion in a rat spinal cord hemisection model by injecting syn-GFP Fign shRNA virus. BBB values revealed an improvement in functional recovery. The p-mTOR was activated along with neuronal Fign depletion. The syn-mCherry virus showed more sprouting neurites entering the injury region, which was confirmed by immunostaining GAP43 protein. Further, we showed that Fign siRNA treatment promoted axon outgrowth and branching, whose underlying mechanism was firstly attributed to local activation of the mTOR pathway, and increased MT dynamicity. Finally, considering L-leucine, promotes axonal growth and neuronal survival, we applied L-leucine with Fign depletion after spinal cord injury or in chondroitin sulfate proteoglycan inhibitory molecules. The phenomenon of synergistically augmented axon regeneration was observed. In summary, our results indicated a novel local mTOR pathway for fidgetin to impact axon growth and provided a combined strategy in SCI.
    MeSH term(s) Rats ; Animals ; Axons/physiology ; Nerve Regeneration/physiology ; Leucine/metabolism ; Leucine/pharmacology ; Neurons/metabolism ; Spinal Cord Injuries ; TOR Serine-Threonine Kinases/metabolism ; Mammals
    Chemical Substances Leucine (GMW67QNF9C) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; mTOR protein, rat (EC 2.7.1.1)
    Language English
    Publishing date 2022-12-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 207148-4
    ISSN 1090-2430 ; 0014-4886
    ISSN (online) 1090-2430
    ISSN 0014-4886
    DOI 10.1016/j.expneurol.2022.114315
    Database MEDical Literature Analysis and Retrieval System OnLINE

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