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27 results on '"Weng, Xiong"'

19. Female Alms1-deficient mice develop echocardiographic features of adult but not infantile Alström syndrome cardiomyopathy

Author

McKay, Eleanor J., Luijten, Ineke, Broadway-Stringer, Sophie, Thomson, Adrian, Weng, Xiong, Gehmlich, Katya, Gray, Gillian A., and Semple, Robert K.

Abstract

Alström syndrome (AS), a multisystem disorder caused by biallelic ALMS1 mutations, features major early morbidity and mortality due to cardiac complications. The latter are biphasic, including infantile dilated cardiomyopathy and distinct adult-onset cardiomyopathy, and poorly understood. We assessed cardiac function of Alms1 knockout (KO) mice by echocardiography. Cardiac function was unaltered in Alms1 global KO mice of both sexes at postnatal day 15 (P15) and 8 weeks. At 23 weeks, female − but not male − KO mice showed increased left atrial area and decreased isovolumic relaxation time, consistent with early restrictive cardiomyopathy, as well as reduced ejection fraction. No histological or transcriptional changes were seen in myocardium of 23-week-old female Alms1 global KO mice. Female mice with Pdgfra-Cre-driven Alms1 deletion in cardiac fibroblasts and in a small proportion of cardiomyocytes did not recapitulate the phenotype of global KO at 23 weeks. In conclusion, only female Alms1-deficient adult mice show echocardiographic evidence of cardiac dysfunction, consistent with the cardiomyopathy of AS. The explanation for sexual dimorphism remains unclear but might involve metabolic or endocrine differences between sexes.

Published
2024
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20. Overexpression of IC53d promotes the proliferation of gastric cancer cells by activating the AKT/GSK3β/cyclin�D1 signaling pathway

Author

Lin, Jian‑Xian, primary, Xie, Xin‑Sheng, additional, Weng, Xiong‑Feng, additional, Qiu, Sheng‑Liang, additional, Xie, Jian‑Wei, additional, Wang, Jia‑Bin, additional, Lu, Jun, additional, Chen, Qi‑Yue, additional, Cao, Long‑Long, additional, Lin, Mi, additional, Tu, Ru‑Hong, additional, Li, Ping, additional, Huang, Chang‑Ming, additional, and Zheng, Chao‑Hui, additional

Published
2019
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26. Mesenchymal-specific Alms1 knockout in mice recapitulates key metabolic features of Alström Syndrome.

Author

McKay EJ, Luijten I, Weng X, Martinez de Morentin PB, De Frutos González E, Gao Z, Kolonin MG, Heisler LK, and Semple RK

Abstract

Background: Alström Syndrome (AS), a multi-system disease caused by mutations in the ALMS1 gene, includes obesity with disproportionately severe insulin resistant diabetes, dyslipidemia, and hepatosteatosis. How loss of ALMS1 causes this phenotype is poorly understood, but prior studies have circumstancially implicated impaired adipose tissue expandability. We set out to test this by comparing the metabolic effects of selective Alms1 knockout in mesenchymal cells including preadipocytes to those of global Alms1 knockout., Methods: Global Alms1 knockout (KO) mice were generated by crossing floxed Alms1 and CAG-Cre mice. A Pdgfrα -Cre driver was used to abrogate Alms1 function selectively in mesenchymal stem cells (MSCs) and their descendants, including preadipocytes. We combined metabolic phenotyping of global and Pdgfrα + Alms1 -KO mice on a 45% fat diet with measurements of body composition and food intake, and histological analysis of metabolic tissues., Results: Global Alms1 KO caused hyperphagia, obesity, insulin resistance, dyslipidaemia, and fatty liver. Pdgfrα - cre driven KO of Alms1 (MSC KO) recapitulated insulin resistance, fatty liver, and dyslipidaemia in both sexes. Other phenotypes were sexually dimorphic: increased fat mass was only present in female Alms1 MSC KO mice. Hyperphagia was not evident in male Alms1 MSC KO mice, but was found in MSC KO females, despite no neuronal Pdgfr α expression., Conclusions: Mesenchymal deletion of Alms1 recapitulates the metabolic features of AS, including severe fatty liver. This confirms a key role for Alms1 in the adipose lineage, where its loss is sufficient to cause systemic metabolic effects and damage to remote organs. AS should be regarded as a forme fruste of lipodystrophy. Therapies should prioritise targeting positive energy balance.

Published
2023
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27. [Artesunate inhibits proliferation of glioblastoma cells by arresting cell cycle].

Author

Weng X, Zhu SQ, and Cui HJ

Subjects
Apoptosis, Cell Line, Tumor, Cyclin B1 metabolism, Cyclin D1 metabolism, Cyclin-Dependent Kinase 2 metabolism, Cyclin-Dependent Kinase 4 metabolism, Glioblastoma drug therapy, Humans, Antineoplastic Agents pharmacology, Artesunate pharmacology, Cell Cycle Checkpoints drug effects, Cell Proliferation drug effects, Glioblastoma pathology
Abstract

Glioblastoma is a common brain tumor and the overall survival rate of the patients is very low, so it is an effective way to develop the potential chemotherapy or adjuvant chemotherapy drugs in glioblastoma treatment. As a well-known antimalarial drug, artesunate(ARTs) has clear side effects, and recently it has been reported to have antitumor effects, but rarely reported in glioblastoma. Different concentrations of ARTs were used to treat the glioblastoma cells, and then the inhibitory effect of ARTs on glioblastoma proliferation was detected by MTT assay; Ki67 immunofluorescence assay was used to detect the proliferation of cells; Soft agar experiment was used to explain the clonal formation abilities in vitro ; Flow Cytometry was used to detect the cell cycle; and Western blot assay was used to determine the expression of key cell cycle protein. MTT assay results indicated that ARTs-treated glioblastoma cell A172, U251, U87 were significantly inhibited in a time-and-dose dependent manner as compared to the control group(DMSO treatment group). Soft agar experiment showed that ARTs could significantly reduce the clonal formation ability of glioblastoma. Furthermore, Flow cytometry analysis showed that ARTs could obviously increase the cell proportion in G₀/G₁ phase and reduce the cell proportion in S phase. Western blot results showed that the expressions of cell cycle-related proteins CDK2, CDK4, cyclin D1 and cyclin B1 were all obviously down-regulated. Above all, ARTs may inhibit the proliferation of glioblastoma cells by arresting cell cycle in G₀/G₁ phase through down-regulating the expression of CDK2, CDK4, cyclin D1, cyclin B1. These results may not only provide a novel method for rediscovering and reusing ARTs but also provide a new potential drug for treating glioblastoma., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Chinese Pharmaceutical Association.)

Published
2018
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