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  • Wiley  (67)
  • Li, Jie  (67)
  • 1
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    Effect of metformin on human periodontal ligament stem cells cultured with polydopamine‐templated hydroxyapatite
    Wiley ; 2019
    In:  European Journal of Oral Sciences Vol. 127, No. 3 ( 2019-06), p. 210-221
    Details
    In: European Journal of Oral Sciences, Wiley, Vol. 127, No. 3 ( 2019-06), p. 210-221
    Abstract: Polydopamine‐templated hydroxyapatite ( tHA ) is a type of nano‐biomaterial that can promote osteogenesis in bone tissue engineering. However, high concentrations of tHA stimulate production of reactive oxygen species ( ROS ), resulting in cell injury and apoptosis. Metformin has been demonstrated to activate the adenosine monophosphate‐activated protein kinase ( AMPK ) signaling pathway, which induces autophagy and decreases ROS production to prevent apoptosis. The present study was performed to investigate the potential application of tHA in combination with metformin in periodontal bone tissue engineering. Human periodontal ligament stem cells ( hPDLSC s) were exposed to tHA in the presence or absence of metformin, and cytocompatibility and osteogenesis were detected by related assays. Additionally, the autophagy signaling pathway was analyzed by western blotting. Polydopamine‐templated hydroxyapatite, in combination with metformin, substantially reduced ROS production and apoptosis, and enhanced proliferation and osteogenic differentiation of hPDLSC s. Enhanced levels of microtubule‐associated protein 1 light chain 3 II and Beclin‐1 were observed after exposure to tHA plus metformin. Expression of phosphorylated AMPK was increased and that of phosphorylated mammalian target of rapamycin ( mTOR ) was decreased after exposure to tHA plus metformin. Taken together, our results demonstrate that tHA , combined with metformin, increases the viability of hPDLSC s via the AMPK / mTOR signaling pathway by regulating autophagy and further improving the osteogenic effect.
    Type of Medium: Online Resource
    ISSN: 0909-8836 , 1600-0722
    URL: Issue
    URL: Article
    DOI: 10.1111/eos.2019.127.issue-3
    DOI: 10.1111/eos.12616
    Language: English
    Publisher: Wiley
    Publication Date: 2019
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    detail.hit.zdb_id: 1224820-4
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  • 2
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    Roles of Akirin1 in early prediction and treatment of graft kidney ischemia‒reperfusion injury
    Wiley ; 2024
    In:  Smart Medicine Vol. 3, No. 2 ( 2024-06)
    Details
    In: Smart Medicine, Wiley, Vol. 3, No. 2 ( 2024-06)
    Abstract: Ferroptosis is a predominant contributor to graft kidney ischemia‒reperfusion injury (IRI), resulting in delayed graft function (DGF). However, much less is known about the early predicting biomarkers and therapeutic targets of DGF, especially aiming at ferroptosis. Here, we propose a precise predicting model for DGF, relying on the Akirin1 level in extracellular vesicles (EVs) derived from recipient urine 48 h after kidney transplant. In addition, we decipher a new molecular mechanism whereby Akirin1 induces ferroptosis by strengthening TP53‐mediated suppression of SLC7A11 during the graft kidney IRI process, that is, Akirin1 activates the EGR1/TP53 axis and inhibits MDM2‐mediated TP53 ubiquitination, accordingly upregulating TP53 in two ways. Meanwhile, we present the first evidence that miR‐136‐5p enriched in EVs secreted by human umbilical cord mesenchymal stem cells (UM‐EVs) confers robust protection against ferroptosis and graft kidney IRI by targeted inhibition of Akirin1 but knockout of miR‐136‐5p in UM sharply mitigates the protection of UM‐EVs. The functional and mechanistic regulation of Akirin1 is further corroborated in an allograft kidney transplant model in wild‐type and Akirin1‐knockout mice. In summary, these findings suggest that Akirin1, which prominently induces ferroptosis, is a pivotal biomarker and target for early diagnosis and treatment of graft kidney IRI and DGF after kidney transplant.
    Type of Medium: Online Resource
    ISSN: 2751-1871 , 2751-1871
    URL: Issue
    URL: Article
    DOI: 10.1002/smmd.v3.2
    DOI: 10.1002/SMMD.20230043
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 3117049-3
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  • 3
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    Deep‐targeted gene sequencing reveals ARID1A mutation as an important driver of glioblastoma
    Wiley ; 2024
    In:  CNS Neuroscience & Therapeutics Vol. 30, No. 4 ( 2024-04)
    Details
    In: CNS Neuroscience & Therapeutics, Wiley, Vol. 30, No. 4 ( 2024-04)
    Abstract: To investigate the key factors influencing glioma progression and the emergence of treatment resistance by examining the intrinsic connection between mutations in DNA damage and repair‐related genes and the development of chemoresistance in gliomas. Methods We conducted a comprehensive analysis of deep‐targeted gene sequencing data from 228 glioma samples. This involved identifying differentially mutated genes across various glioma grades, assessing their functions, and employing I‐TASSER for homology modeling. We elucidated the functional changes induced by high‐frequency site mutations in these genes and investigated their impact on glioma progression. Results The analysis of sequencing mutation results of deep targeted genes in integration revealed that ARID1A gene mutation occurs frequently in glioblastoma and alteration of ARID1A could affect the tolerance of glioma cells to temozolomide treatment. The deletion of proline at position 16 in the ARID1A protein affected the stability of binding of the SWI/SNF core subunit BRG1, which in turn affected the stability of the SWI/SNF complex and led to altered histone modifications in the CDKN1A promoter region, thereby affecting the biological activity of glioma cells, as inferred from modeling and protein interaction analysis. Conclusion The ARID1A gene is a critical predictive biomarker for glioma. Mutations at the ARID1A locus alter the stability of the SWI/SNF complex, leading to changes in transcriptional regulation in glioma cells. This contributes to an increased malignant phenotype of GBM and plays a pivotal role in mediating chemoresistance.
    Type of Medium: Online Resource
    ISSN: 1755-5930 , 1755-5949
    URL: Article
    DOI: 10.1111/cns.14698
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 2423467-9
    detail.hit.zdb_id: 2423461-8
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  • 4
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    The Novel Compound Heterozygous Mutations of ECEL1 Identified in a Family with Distal Arthrogryposis Type 5D
    Wiley ; 2020
    In:  BioMed Research International Vol. 2020 ( 2020-05-27), p. 1-6
    Details
    In: BioMed Research International, Wiley, Vol. 2020 ( 2020-05-27), p. 1-6
    Abstract: Introduction . Distal arthrogryposis type 5D (DA5D) is an autosomal recessive disease. The clinical symptoms include contractures of the joints of limbs, especially camptodactyly of the hands and/or feet, unilateral ptosis, a round-shaped face, arched eyebrows, and micrognathia, without ophthalmoplegia. ECEL1 is a DA5D causative gene that encodes a membrane-bound metalloprotease. ECEL1 plays important roles in the final axonal arborization of motor nerves in limb skeletal muscles and neuromuscular junction formation during prenatal development. Methods . A DA5D family with webbing of the elbows and fingers was recruited. We performed whole-exome sequencing (WES) and filtered mutations by disease-causing genes of arthrogryposis multiplex congenita (AMC). Mutational analysis and cosegregation confirmation were then performed. Results . We identified novel compound heterozygous mutations of ECEL1 (NM_004826: c.69C 〉 A, p.C23 ∗ and c.1810G 〉 A, p.G604R) in the proband. Conclusions . We detected causative mutations in a DA5D family, expanding the spectrum of known ECEL1 mutations and contributing to the clinical diagnosis of DA5D.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2020/2149342
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2698540-8
    detail.hit.zdb_id: 2705584-X
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  • 5
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    Alleviated symptoms of SARS‐CoV‐2 Omicron variant infection in chronic hepatitis B patients with immune control
    Wiley ; 2023
    In:  Journal of Medical Virology Vol. 95, No. 10 ( 2023-10)
    Details
    In: Journal of Medical Virology, Wiley, Vol. 95, No. 10 ( 2023-10)
    Abstract: The impact of hepatitis B virus (HBV) infection on the progression of coronavirus disease 2019 (COVID‐19) disease remains controversial. We aimed to investigate whether pre‐existing chronic HBV (CHB) infection and therapy with anti‐HBV nucleos(t)ide analogs (NAs) influence the clinical presentation of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) Omicron variant infection. In this study, clinical information was collected via a questionnaire from patients with COVID‐19, and their clinical symptoms were quantitatively assessed for comparative analyses. Additionally, hepatitis B‐related laboratory data were collected for CHB patients. Propensity score matching (PSM) was used to minimize confounding biases. A total of 785 patients with COVID‐19 were included in the cohort, of which 387 were identified as being infected with CHB infection and they were categorized as being in the immune control or clearance phase. After PSM, the CHB group ( n  = 222) had a shorter duration of fever and disease course, milder clinical symptoms, and lower incidence of pneumonia than the non‐CHB group ( n  = 222) after Omicron variant infection ( p   〈  0.05). After the adjustment of confounding factors, CHB patients showed a lower risk of prolonged fever, severe clinical symptoms, and pneumonia ( p   〈  0.05). However, there were no statistically significant differences in the clinical symptoms and incidence of pneumonia between CHB patients who received and did not receive NAs, or CHB patients who received tenofovir disoproxil fumarate and entecavir ( p   〉  0.05). In conclusion, our findings suggest that the crosstalk of anti‐HBV immunity may contribute to the alleviated symptoms of SARS‐CoV‐2 Omicron variants infection in the CHB patients, independent of anti‐HBV NA therapy.
    Type of Medium: Online Resource
    ISSN: 0146-6615 , 1096-9071
    URL: Issue
    URL: Article
    DOI: 10.1002/jmv.v95.10
    DOI: 10.1002/jmv.29173
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 752392-0
    detail.hit.zdb_id: 1475090-9
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  • 6
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    Tribbles homolog 2 promotes hepatic fibrosis and hepatocarcinogenesis through phosphatase 1A‐Mediated stabilization of yes‐associated protein
    Wiley ; 2021
    In:  Liver International Vol. 41, No. 5 ( 2021-05), p. 1131-1147
    Details
    In: Liver International, Wiley, Vol. 41, No. 5 ( 2021-05), p. 1131-1147
    Abstract: Hepatic stellate cells (HSCs) play critical roles in liver fibrosis and hepatocellular carcinoma (HCC). Tribbles homolog 2 (TRIB2) is an oncogene implicated in a variety of cancers, including liver cancer. However, the biological function and regulatory mechanism of TRIB2 in HSCs are poorly understood. In addition, little is known about its role in liver fibrosis progression to HCC. Here, we revealed the clinical significance of TRIB2 in liver fibrosis and HCC development. Methods We investigated TRIB2 promoting liver fibrosis in vitro and in vivo. In mouse model of liver fibrosis and HCC, we measured hepatic fibrosis and HCC level through knockdown TRIB2 with shRNA. In addition, we performed western blotting, real‐time quantitative PCR, immunofluorescence and co‐immunoprecipitation assay to study TRIB2 function in LX‐2 cells. Results TRIB2 expression was strongly upregulated in human fibrotic liver tissues and HCC tissues. TRIB2 colocalized with α‐smooth muscle actin (α‐SMA) in fibrotic and HCC liver tissues. Knockdown of TRIB2 inhibited HSC activation and liver fibrosis in vitro and in vivo. TRIB2 promoted Yes‐associated protein (YAP) stabilization, nuclear localization, and subsequent fibrotic gene expression independent of the MST‐LATS phosphorylation cascade in HSCs. TRIB2 interacted with YAP to recruit phosphatase 1A (PP1A), promoting PP1A‐mediated YAP dephosphorylation. TRIB2 knockdown potently attenuated the development of fibrosis‐associated liver cancer. Conclusions TRIB2 is an attractive target for hepatic fibrosis and fibrosis‐associated liver cancer treatment.
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    URL: Article
    DOI: 10.1111/liv.v41.5
    DOI: 10.1111/liv.14782
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2102783-3
    detail.hit.zdb_id: 2124684-1
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  • 7
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    Correlation between ankle‐brachial index and subtle cognitive decline
    Wiley ; 2023
    In:  Brain and Behavior Vol. 13, No. 6 ( 2023-06)
    Details
    In: Brain and Behavior, Wiley, Vol. 13, No. 6 ( 2023-06)
    Abstract: Subtle cognitive decline (SCD) is considered the early stage of Alzheimer's disease (AD) and is of great clinical significance for the prevention and treatment of AD. The ankle‐brachial index (ABI) has been reported to be associated with cognitive impairment; however, there are few studies on the relationship between ABI and SCD. Methods From August 2019 to April 2021, subjects were recruited to participate in a cognitive function test at the Shanghai Sixth People's Hospital. Based on the test results, 217 patients with SCD were selected as the experimental group and 259 patients with normal cognitive function were selected as the control group. The data of the two groups were compared, and the correlation between the ABI and cognitive decline was analyzed. Results There were significant differences in age, sex, smoking status, hypertension, diabetes, triglycerides, serum creatinine, and ABI ( p   〈  .05)between the two groups. Logistic regression analysis showed that age, hypertension, diabetes, and ABI influenced cognitive decline( p   〈  .05). After correcting for other factors, ABI was independently related to cognitive decline. Pearson's correlation analysis showed that a low ABI ( 〈 0.9) had a significant effect on memory and visual space of the cognitive domain ( p   〈  . 05). Conclusions ABI is significantly associated with SCD and may be a critical tool to predict early cognitive decline.
    Type of Medium: Online Resource
    ISSN: 2162-3279 , 2162-3279
    URL: Issue
    URL: Article
    DOI: 10.1002/brb3.v13.6
    DOI: 10.1002/brb3.3019
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2623587-0
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  • 8
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    Protective role of α2‐macroglobulin against jaw osteoradionecrosis in a preclinical rat model
    Wiley ; 2019
    In:  Journal of Oral Pathology & Medicine Vol. 48, No. 2 ( 2019-02), p. 166-173
    Details
    In: Journal of Oral Pathology & Medicine, Wiley, Vol. 48, No. 2 ( 2019-02), p. 166-173
    Abstract: We have previously demonstrated the effect of alpha‐2‐macroglobulin (α2M) in the remediation of radiation‐induced cellular damage. Here, we investigated the protective effects of α2M in a preclinical rat model of jaw osteoradionecrosis ( ORN ). Methods Eighteen rats were divided randomly into three groups: the control group, the radiation therapy ( RT ) alone group, and the radiated mandibles pretreated with α2M (α2M + RT ) group. One month after radiation, all left molar teeth were extracted. After another 3 months, the animals were sacrificed and body weight, histopathology, microcomputed tomography and immunofluorescence were evaluated in all groups. Results The RT group showed serious alopecia, bone exposure, inflammation, necrosis, fibrosis, and the absence of new bone formation within the socket. The α2M + RT group exhibited less alopecia than the RT group and slight inflammation and fibrosis in the bone marrow cavity. The cortical bone was similar to normal bone tissue. Interestingly, compared with RT group, serum superoxide dismutase levels in the α2M + RT group increased at the 1th day ( P = 0.037), 14th day ( P = 0.012), while reactive oxygen species levels clearly decreased at the 1th day ( P 〈 0.001), 14th day ( P = 0.007), and 28th day ( P = 0.013). Conclusions A clinically translational model of jaw ORN was successfully established and the application of α2M prior to radiation protected the bone from being injured by the radiation, possibly related to oxidative stress.
    Type of Medium: Online Resource
    ISSN: 0904-2512 , 1600-0714
    URL: Issue
    URL: Article
    DOI: 10.1111/jop.2019.48.issue-2
    DOI: 10.1111/jop.12809
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1021270-X
    detail.hit.zdb_id: 2026385-5
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  • 9
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    Activatable Semiconducting Theranostics: Simultaneous Generation and Ratiometric Photoacoustic Imaging of Reactive Oxygen Species In Vivo
    Wiley ; 2018
    In:  Advanced Materials Vol. 30, No. 23 ( 2018-06)
    Details
    In: Advanced Materials, Wiley, Vol. 30, No. 23 ( 2018-06)
    Abstract: Enhancing the generation of reactive oxygen species (ROS) is an effective anticancer strategy. However, it is a great challenge to control the production and to image ROS in vivo, both of which are vital for improving the efficacy and accuracy of cancer therapy. Herein, an activatable semiconducting theranostic nanoparticle (NP) platform is developed that can simultaneously enhance ROS generation while self‐monitoring its levels through ratiometric photoacoustic (PA) imaging. The NP platform can further guide in vivo therapeutic effect in tumors. The theranostic NP platform is composed of: (i) cisplatin prodrug and ferric ion catalyst for ROS generation, a part of combination cancer therapy; and (ii) a ratiometric PA imaging nanoprobe consisting of inert semiconducting perylene‐diimide (PDI) and ROS activatable near‐infrared dye (IR790s), used in ratiometric PA imaging of ROS during cancer treatment. Ratiometric PA signals are measured at two near‐infrared excitation wavelengths: 680 and 790 nm for PDI and IR790s, respectively. The measurements show highly accurate visualization of • OH generation in vivo. This novel ROS responsive organic theranostic NP allows not only synergistic cancer chemotherapy but also real‐time monitoring of the therapeutic effect through ratiometric PA imaging.
    Type of Medium: Online Resource
    ISSN: 0935-9648 , 1521-4095
    URL: Issue
    URL: Article
    DOI: 10.1002/adma.v30.23
    DOI: 10.1002/adma.201707509
    RVK:
    UA 1538
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1012489-5
    detail.hit.zdb_id: 1474949-X
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  • 10
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    Emerging Approaches of Cell‐Based Nanosystems to Target Cancer Metastasis
    Wiley ; 2019
    In:  Advanced Functional Materials Vol. 29, No. 48 ( 2019-11)
    Details
    In: Advanced Functional Materials, Wiley, Vol. 29, No. 48 ( 2019-11)
    Abstract: Cancer metastasis accounts for the high mortality of cancer‐related deaths and the therapy is greatly challenged by the limited drug delivery efficiency. Inspired by the essential role of culprit cancer cells and versatile accessory cells during cancer metastasis, diverse cell‐based nanosystems (CBNs) are emerging as attractive and encouraging drug delivery platforms to target cancer metastasis. Herein, the authors focus on the emerging strategies of versatile CBNs that synergistically combine the merit of source cells and nanoparticles for antimetastasis therapy. CBNs are usually comprised of natural nanosized vesicles, cell membrane camouflaged nanoparticles, and bioengineered living cell vehicles. The authors discuss the rationality and advances of various CBNs in targeting different stages of cancer metastasis, including primary tumor, circulating tumor cells (CTCs), and distant metastasis as well as the tumor immune microenvironments (TIM). On this basis, this review provides some feasible perspectives on designing CBNs to enhance the drug delivery efficiency for treating cancer metastasis.
    Type of Medium: Online Resource
    ISSN: 1616-301X , 1616-3028
    URL: Issue
    URL: Article
    DOI: 10.1002/adfm.v29.48
    DOI: 10.1002/adfm.201903441
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2029061-5
    detail.hit.zdb_id: 2039420-2
    SSG: 11
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