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311 results on '"Tsang, Suk-Ying"'

17. Isogenic Human-Induced Pluripotent Stem-Cell-Derived Cardiomyocytes Reveal Activation of Wnt Signaling Pathways Underlying Intrinsic Cardiac Abnormalities in Rett Syndrome

Author

Ng, Kwong-Man, primary, Ding, Qianqian, additional, Tse, Yiu-Lam, additional, Chou, Oscar Hou-In, additional, Lai, Wing-Hon, additional, Au, Ka-Wing, additional, Lau, Yee-Man, additional, Ji, Yue, additional, Siu, Chung-Wah, additional, Tang, Clara Sze-Man, additional, Colman, Alan, additional, Tsang, Suk-Ying, additional, and Tse, Hung-Fat, additional

Published
2022
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30. Differential gene expressions in atrial and ventricular myocytes: insights into the road of applying embryonic stem cell-derived cardiomyocytes for future therapies

Author

Ng, Sze Ying, Wong, Chun Kit, and Tsang, Suk Ying

Subjects
Heart cells -- Physiological aspects, Heart cells -- Genetic aspects, Heart cells -- Research, Embryonic stem cells -- Physiological aspects, Embryonic stem cells -- Genetic aspects, Embryonic stem cells -- Research, Gene expression -- Physiological aspects, Gene expression -- Research, Biological sciences
Abstract

Myocardial infarction has been the leading cause of morbidity and mortality in developed countries over the past few decades. The transplantation of cardiomyocytes offers a potential method of treatment. However, cardiomyocytes are in high demand and their supply is extremely limited. Embryonic stem cells (ESCs), which have been isolated from the inner cell mass of blastocysts, can self-renew and are pluripotent, meaning they have the ability to develop into any type of cell, including cardiomyocytes. This suggests that ESCs could be a good source of genuine cardiomyocytes for future therapeutic purposes. However, problems with the yield and purity of ESC-derived cardiomyocytes, among other hurdles for the therapeutic application of ESC-derived cardiomyocytes (e.g., potential immunorejection and tumor formation problems), need to be overcome before these cells can be used effectively for cell replacement therapy. ESC-derived cardiomyocytes consist of nodal, atrial, and ventricular cardiomyocytes. Specifically, for treatment of myocardial infarction, transplantation of a sufficient quantity of ventricular cardiomyocytes, rather than nodal or atrial cardiomyocytes, is preferred. Hence, it is important to find ways of increasing the yield and purity of specific types of cardiomyocytes. Atrial and ventricular cardiomyocytes have differential expression of genes (transcription factors, structural proteins, ion channels, etc.) and are functionally distinct. This paper presents a thorough review of differential gene expression in atrial and ventricular myocytes, their expression throughout development, and their regulation. An understanding of the molecular and functional differences between atrial and ventricular myocytes allows discussion of potential strategies for preferentially directing ESCs to differentiate into chamber-specific cells, or for fine tuning the ESC-derived cardiomyocytes into specific electrical and contractile phenotypes resembling chamber-specific cells. atrial cardiomyocytes; ventricular cardiomyocytes; gene regulations; therapeutic application doi: 10.1152/ajpcell.00402.2009.

Published
2010

32. Additional file 1 of TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes

Author

Xianji Liu, Zhao, Rui, Qianqian Ding, Xiaoqiang Yao, and Tsang, Suk Ying

Abstract

Additional file 1: Supplementary Figure 1. TRPC7 was expressed in cardiomyocytes. A – B, Representative images showing immunostaining of nuclei (blue), TRPC7 (green) and (A) cTnT (red), (B) α-actinin (red) in mESC-CMs. C – D, Representative images showing immunostaining of nuclei (blue), TRPC7 (green) and (C) cTnT (red), (D) α-actinin (red) in NRVMs. The positive staining of cTnT and α-actinin suggested that these cells were cardiomyocytes, and the positive staining of TRPC7 indicated that the channel was expressed in cardiomyocytes. E, Representative images showing immunostaining of nuclei (blue), TRPC7 (green) and α-actinin (red) in NRVMs. In this experiment, the anti-TRPC7 was preincubated with its antigenic peptide to block its binding to TRPC7. The disappearance of TRPC7 staining signal suggested the specificity of the anti-TRPC7. Scale bars = 20 μm. Supplementary Figure2. TRPC7 was successfully knocked down and overexpressed in mESC-CMs. A – B, Overview of mESC-CMs infected by (A) TRPC7-knockdown adenovirus encoding GFP (Ad-CMV-GFP-U6-shTRPC7) and (B) TRPC7-overexpression adenovirus encoding BFP (Ad-CMV-TRPC7-CMV-BFP). Abundant GFP- and BFP-positive cells suggested that the infection efficiency of the adenoviruses was very high. C – D, Representative images showing immunostaining of α-actinin (yellow) and TRPC7 (red) in mESC-CMs infected by (C) knockdown-control and (D) TRPC7-knockdown adenoviruses. The positive signal of GFP (green) suggested that the cells were infected by adenoviruses. The intensity of TRPC7 signal decreased after infection with TRPC7-knockdown adenoviruses, suggesting the successful knockdown of TRPC7. E – F, Representative images showing immunostaining of HA (red) in mESC-CMs infected by (C) overexpression-control and (D) Tag-TRPC7-overexpression adenoviruses. The positive signal of BFP (blue) suggested that the cells were infected by adenoviruses. The intensity of HA signal increased after infection with Tag-TRPC7-overexpression adenoviruses, suggesting the successful overexpression of TRPC7. Supplementary Figure 3. The purity of cardiomyocyte was high in the NRVM preparation. A - B, Representative images showing immunostaining of nuclei (blue) and (A) cTnT (red), (B) α-actinin (red) in NRVM preparation. In the images, only two cells with an identity other than cardiomyocyte was found (indicated by arrows), while all others were cardiomyocytes (15 out of 17 were cardiomyocytes). The purity of cardiomyocyte estimated from these images was more than 85%. Scale bars = 20 μm.

Published
2021
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38. Remdesivir induces persistent mitochondrial and structural damage in human induced pluripotent stem cell-derived cardiomyocytes.

Author

Kwok, Maxwell, Lee, Carrie, Li, Hung Sing, Deng, Ruixia, Tsoi, Chantelle, Ding, Qianqian, Tsang, Suk Ying, Leung, Kam Tong, Yan, Bryan P, and Poon, Ellen N

Subjects
CORONAVIRUS disease treatment, REMDESIVIR, COVID-19, MITOCHONDRIA, ADENOSINE triphosphate, PRODRUGS
Abstract

Aims Remdesivir is a prodrug of an adenosine triphosphate analogue and is currently the only drug formally approved for the treatment of hospitalized coronavirus disease of 2019 (COVID-19) patients. Nucleoside/nucleotide analogues have been shown to induce mitochondrial damage and cardiotoxicity, and this may be exacerbated by hypoxia, which frequently occurs in severe COVID-19 patients. Although there have been few reports of adverse cardiovascular events associated with remdesivir, clinical data are limited. Here, we investigated whether remdesivir induced cardiotoxicity using an in vitro human cardiac model. Methods and results Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were exposed to remdesivir under normoxic and hypoxic conditions to simulate mild and severe COVID-19, respectively. Remdesivir induced mitochondrial fragmentation, reduced redox potential, and suppressed mitochondrial respiration at levels below the estimated plasma concentration under both normoxic and hypoxic conditions. Non-mitochondrial damage such as electrophysiological alterations and sarcomere disarray were also observed. Importantly, some of these changes persisted after the cessation of treatment, culminating in increased cell death. Mechanistically, we found that inhibition of DRP1, a regulator of mitochondrial fission, ameliorated the cardiotoxic effects of remdesivir, showing that remdesivir-induced cardiotoxicity was preventable and excessive mitochondrial fission might contribute to this phenotype. Conclusions Using an in vitro model, we demonstrated that remdesivir can induce cardiotoxicity in hiPSC-CMs at clinically relevant concentrations. These results reveal previously unknown potential side-effects of remdesivir and highlight the importance of further investigations with in vivo animal models and active clinical monitoring to prevent lasting cardiac damage to patients. [ABSTRACT FROM AUTHOR]

Published
2022
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42. Uptake, Accumulation, and Biomarkers of PM2.5-Associated Organophosphate Flame Retardants in C57BL/6 Mice after Chronic Exposure at Real Environmental Concentrations

Author

Chen, Min, primary, Liao, Xiaoliang, additional, Yan, Shi-chao, additional, Gao, Yanpeng, additional, Yang, Chun, additional, Song, Yuanyuan, additional, Liu, Yi, additional, Li, Weiquan, additional, Tsang, Suk-Ying, additional, Chen, Zhi-Feng, additional, Qi, Zenghua, additional, and Cai, Zongwei, additional

Published
2020
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48. RALOXIFENE, TAMOXIFEN AND VASCULAR TONE

Author

Leung, Fung Ping, Tsang, Suk Ying, Wong, Chi Ming, Yung, Lai Ming, Chan, Yau Chi, Leung, Hok Sum, Yao, Xiaoqiang, and Huang, Yu

Published
2007

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