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4. Additional file 1 of Hesperetin promotes longevity and delays aging via activation of Cisd2 in naturally aged mice

Author

Yeh, Chi-Hsiao, Shen, Zhao-Qing, Wang, Tai-Wen, Kao, Cheng-Heng, Teng, Yuan-Chi, Yeh, Teng-Kuang, Lu, Chung-Kuang, and Tsai, Ting-Fen

Abstract

Additional file 1: Table S1. The 60 noble herbs used to establish the compound library. Table S2. Diet composition of mouse food. Fig. S1. CISD2 reporter assay for hesperetin and its structural analogs. Fig. S2. Serum biochemical analyses revealed that hesperetin has no detectable in vivo toxicity after 6 months of treatment in the old WT mice. Fig. S3. Complete blood count (CBC) analyses revealed that hesperetin has no detectable toxicity on hematological parameters after 7 months of treatment in the old WT mice. Fig. S4. Compound concentrations of hesperetin, and two of the major conjugated metabolites, namely hesperetin-7-O-beta-d-glucuronide (H7G) and hesperetin-7-O-sulfate (H7S), in the dietary hesperetin-treated mice, as well as their bioactivity to enhance CISD2 expression in the HEK293-CISD2 reporter cells. Fig. S5. Comparison of whole body metabolic rate after hesperetin treatment for 1.5 and 6 months in old WT mice. Fig. S6. No significant difference in the glucose tolerance test (GTT) and insulin tolerance test (ITT) between the Veh-treated and Hes-treated old mice. Fig. S7. Hesperetin shifts the expression patterns of several insulin signaling-related differential expression genes (DEGs) in the aged livers toward the patterns of young mice. Fig. S8. Hesperetin delays skeletal muscle aging in a Cisd2-dependent manner. Fig. S9. Hesperetin delays cardiac aging in a Cisd2-dependent manner. Fig. S10. Subgroups of metabolism-related DEGs in the hearts and skeletal muscles. Fig. S11. Subgroups of proteostasis-related DEGs in the hearts and skeletal muscles. Fig. S12. Hesperetin decreases the levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS), and shifts the expression patterns of several ROS-related DEGs in the aged hearts and skeletal muscles toward the patterns of young mice.

Published
2022
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9. CISD2 maintains cellular homeostasis

Author

Shen, Zhao-Qing, primary, Huang, Yi-Long, additional, Teng, Yuan-Chi, additional, Wang, Tai-Wen, additional, Kao, Cheng-Heng, additional, Yeh, Chi-Hsiao, additional, and Tsai, Ting-Fen, additional

Published
2021
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23. CISD2 Haploinsufficiency Disrupts Calcium Homeostasis, Causes Nonalcoholic Fatty Liver Disease, and Promotes Hepatocellular Carcinoma

Author

Shen, Zhao-Qing, primary, Chen, Yi-Fan, additional, Chen, Jim-Ray, additional, Jou, Yuh-Shan, additional, Wu, Pei-Chun, additional, Kao, Cheng-Heng, additional, Wang, Chih-Hao, additional, Huang, Yi-Long, additional, Chen, Chian-Feng, additional, Huang, Ting-Shuo, additional, Shyu, Yu-Chiau, additional, Tsai, Shih-Feng, additional, Kao, Lung-Sen, additional, and Tsai, Ting-Fen, additional

Published
2017
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24. Comparative proteomic profiling reveals a role for Cisd2 in skeletal muscle aging.

Author

Huang, Yi‐Long, Shen, Zhao‐Qing, Wu, Chia‐Yu, Teng, Yuan‐Chi, Liao, Chen‐Chung, Kao, Cheng‐Heng, Chen, Liang‐Kung, Lin, Chao‐Hsiung, and Tsai, Ting‐Fen

Subjects
SKELETAL muscle, MUSCLE aging, SKELETAL muscle physiology, PROTEOMICS, ANIMAL models in research
Abstract

Summary: Skeletal muscle has emerged as one of the most important tissues involved in regulating systemic metabolism. The gastrocnemius is a powerful skeletal muscle composed of predominantly glycolytic fast‐twitch fibers that are preferentially lost among old age. This decrease in gastrocnemius muscle mass is remarkable during aging; however, the underlying molecular mechanism is not fully understood. Strikingly, there is a ~70% decrease in Cisd2 protein, a key regulator of lifespan in mice and the disease gene for Wolfram syndrome 2 in humans, within the gastrocnemius after middle age among mice. A proteomics approach was used to investigate the gastrocnemius of naturally aged mice, and this was compared to the autonomous effect of Cisd2 on gastrocnemius aging using muscle‐specific Cisd2 knockout (mKO) mice as a premature aging model. Intriguingly, dysregulation of calcium signaling and activation of UPR/ER stress stand out as the top two pathways. Additionally, the activity of Serca1 was significantly impaired and this impairment is mainly attributable to irreversibly oxidative modifications of Serca. Our results reveal that the overall characteristics of the gastrocnemius are very similar when naturally aged mice and the Cisd2 mKO mice are compared in terms of pathological alterations, ultrastructural abnormalities, and proteomics profiling. This suggests that Cisd2 mKO mouse is a unique model for understanding the aging mechanism of skeletal muscle. Furthermore, this work substantiates the hypothesis that Cisd2 is crucial to the gastrocnemius muscle and suggests that Cisd2 is a potential therapeutic target for muscle aging. [ABSTRACT FROM AUTHOR]

Published
2018
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35. Progerin in muscle leads to thermogenic and metabolic defects via impaired calcium homeostasis.

Author

Wang, Wan‐Ping, Wang, Jing‐Ya, Lin, Wen‐Hsin, Kao, Cheng‐Heng, Hung, Ming‐Chun, Teng, Yuan‐Chi, Tsai, Ting‐Fen, and Chi, Ya‐Hui

Subjects
PROGERIN, SKELETAL muscle, PROGERIA, MUSCULAR dystrophy, CALCIUM, MUTANT proteins, ENDOPLASMIC reticulum
Abstract

Mutations in lamin A (LMNA) are responsible for a variety of human dystrophic and metabolic diseases. Here, we created a mouse model in which progerin, the lamin A mutant protein that causes Hutchinson–Gilford progeria syndrome (HGPS), can be inducibly overexpressed. Muscle‐specific overexpression of progerin was sufficient to induce muscular dystrophy and alter whole‐body energy expenditure, leading to premature death. Intriguingly, sarcolipin (Sln), an endoplasmic reticulum (ER)‐associated protein involved in heat production, is upregulated in progerin‐expressing and Lmna knockout (Lmna−/−) skeletal muscle. The depletion of Sln accelerated the early death of Lmna−/− mice. An examination at the molecular level revealed that progerin recruits Sln and Calnexin to the nuclear periphery. Furthermore, progerin‐expressing myoblasts presented enhanced store‐operated Ca2+ entry, as well as increased co‐localization of STIM1 and ORAI1. These findings suggest that progerin dysregulates calcium homeostasis through an interaction with a subset of ER‐associated proteins, resulting in thermogenic and metabolic abnormalities. [ABSTRACT FROM AUTHOR]

Published
2020
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36. Hepatocellular carcinoma mouse models: Hepatitis B virus-associated hepatocarcinogenesis and haploinsufficient tumor suppressor genes.

Author

Teng YC, Shen ZQ, Kao CH, and Tsai TF

Subjects
Animals, Carcinoma, Hepatocellular ultrastructure, Cocarcinogenesis, Haploinsufficiency, Hepatitis B virus genetics, Humans, Liver Neoplasms genetics, Liver Neoplasms virology, Liver Neoplasms, Experimental ultrastructure, Mice, Mice, Transgenic, Risk Factors, Signal Transduction genetics, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular virology, Genes, Tumor Suppressor, Hepatitis B virus pathogenicity, Liver Neoplasms, Experimental genetics, Liver Neoplasms, Experimental virology
Abstract

The multifactorial and multistage pathogenesis of hepatocellular carcinoma (HCC) has fascinated a wide spectrum of scientists for decades. While a number of major risk factors have been identified, their mechanistic roles in hepatocarcinogenesis still need to be elucidated. Many tumor suppressor genes (TSGs) have been identified as being involved in HCC. These TSGs can be classified into two groups depending on the situation with respect to allelic mutation/loss in the tumors: the recessive TSGs with two required mutated alleles and the haploinsufficient TSGs with one required mutated allele. Hepatitis B virus (HBV) is one of the most important risk factors associated with HCC. Although mice cannot be infected with HBV due to the narrow host range of HBV and the lack of a proper receptor, one advantage of mouse models for HBV/HCC research is the numerous and powerful genetic tools that help investigate the phenotypic effects of viral proteins and allow the dissection of the dose-dependent action of TSGs. Here, we mainly focus on the application of mouse models in relation to HBV-associated HCC and on TSGs that act either in a recessive or in a haploinsufficient manner. Discoveries obtained using mouse models will have a great impact on HCC translational medicine.

Published
2016
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