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3. Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss.

Author

Tian, Jingwen, Moon, Ji Sun, Nga, Ha Thi, Lee, Ho Yeop, Nguyen, Thi Linh, Jang, Hyo Ju, Setoyama, Daiki, Shong, Minho, Lee, Ju Hee, and Yi, Hyon-Seung

Subjects
BONE density, PHYSIOLOGICAL effects of cold temperatures, BONE health, BROWN adipose tissue, BONE metabolism, BONE remodeling, BONE marrow
Abstract

This study examines the interplay between ambient temperature, brown adipose tissue (BAT) function, and bone metabolism, emphasizing the effects of cold exposure and BAT mitochondrial activity on bone health. Utilizing ovariectomized (OVX) mice to model primary osteoporosis and BAT-specific mitochondrial dysfunction (BKO) mice, we evaluated the impact of housing temperature on bone density, immune modulation in bone marrow, and the protective role of BAT against bone loss. Cold exposure was found to universally reduce bone mass, enhance osteoclastogenesis, and alter bone marrow T-cell populations, implicating the immune system in bone remodeling under cold stress. The thermogenic function of BAT, driven by mitochondrial oxidative phosphorylation, was crucial in protecting against bone loss. Impaired BAT function, through surgical removal or mitochondrial dysfunction, exacerbated bone loss in cold environments, highlighting BAT's metabolic role in maintaining bone health. Furthermore, cold-induced changes in BAT function led to systemic metabolic shifts, including elevated long-chain fatty acids, which influenced osteoclast differentiation and activity. These findings suggest a systemic mechanism connecting environmental temperature and BAT metabolism with bone physiology, providing new insights into the metabolic and environmental determinants of bone health. Future research could lead to novel bone disease therapies targeting these pathways. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Mitoribosomal defects aggravate liver cancer via aberrant glycolytic flux and T cell exhaustion

Author

Song, Byong-Sop, Moon, Ji Sun, Tian, Jingwen, Lee, Ho Yeop, Sim, Byeong Chang, Kim, Seok-Hwan, Kang, Seul Gi, Kim, Jung Tae, Ha, Thi, Benfeitas, Rui, Kim, Yeongmin, Park, Sanghee, Wolfe, Robert R., Eun, Hyuk Soo, Shong, Minho, Lee, Sunjae, Kim, Il-Young, Yi, Hyon-Seung, Song, Byong-Sop, Moon, Ji Sun, Tian, Jingwen, Lee, Ho Yeop, Sim, Byeong Chang, Kim, Seok-Hwan, Kang, Seul Gi, Kim, Jung Tae, Ha, Thi, Benfeitas, Rui, Kim, Yeongmin, Park, Sanghee, Wolfe, Robert R., Eun, Hyuk Soo, Shong, Minho, Lee, Sunjae, Kim, Il-Young, and Yi, Hyon-Seung

Abstract

Background Mitochondria are involved in cancer energy metabolism, although the mechanisms underlying the involvement of mitoribosomal dysfunction in hepatocellular carcinoma (HCC) remain poorly understood. Here, we investigated the effects of mitoribosomal impairment-mediated alterations on the immunometabolic characteristics of liver cancer. Methods We used a mouse model of HCC, liver tissues from patients with HCC, and datasets from The Cancer Genome Atlas (TCGA) to elucidate the relationship between mitoribosomal proteins (MRPs) and HCC. In a mouse model, we selectively disrupted expression of the mitochondrial ribosomal protein CR6-interacting factor 1 (CRIF1) in hepatocytes to determine the impact of hepatocyte-specific impairment of mitoribosomal function on liver cancer progression. The metabolism and immunophenotype of liver cancer was assessed by glucose flux assays and flow cytometry, respectively. Results Single-cell RNA-seq analysis of tumor tissue and TCGA HCC transcriptome analysis identified mitochondrial defects associated with high-MRP expression and poor survival outcomes. In the mouse model, hepatocyte-specific disruption of the mitochondrial ribosomal protein CRIF1 revealed the impact of mitoribosomal dysfunction on liver cancer progression. Crif1 deficiency promoted programmed cell death protein 1 expression by immune cells in the hepatic tumor microenvironment. A [U-13C6]-glucose tracer demonstrated enhanced glucose entry into the tricarboxylic acid cycle and lactate production in mice with mitoribosomal defects during cancer progression. Mice with hepatic mitoribosomal defects also exhibited enhanced progression of liver cancer accompanied by highly exhausted tumor-infiltrating T cells. Crif1 deficiency induced an environment unfavorable to T cells, leading to exhaustion of T cells via elevation of reactive oxygen species and lactate production. Conclusions Hepatic mitoribosomal defects promote glucose partitioning toward glycolytic flux and l

Published
2022
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7. Mitoribosomal defects aggravate liver cancer via aberrant glycolytic flux and T cell exhaustion

Author

Song, Byong-Sop, primary, Moon, Ji Sun, additional, Tian, Jingwen, additional, Lee, Ho Yeop, additional, Sim, Byeong Chang, additional, Kim, Seok-Hwan, additional, Kang, Seul Gi, additional, Kim, Jung Tae, additional, Nga, Ha Thi, additional, Benfeitas, Rui, additional, Kim, Yeongmin, additional, Park, Sanghee, additional, Wolfe, Robert R., additional, Eun, Hyuk Soo, additional, Shong, Minho, additional, Lee, Sunjae, additional, Kim, Il-Young, additional, and Yi, Hyon-Seung, additional

Published
2022
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8. Skeletal muscle mitoribosomal defects are linked to low bone mass caused by bone marrow inflammation in male mice

Author

Tian, Jingwen, primary, Chung, Hyo Kyun, additional, Moon, Ji Sun, additional, Nga, Ha Thi, additional, Lee, Ho Yeop, additional, Kim, Jung Tae, additional, Chang, Joon Young, additional, Kang, Seul Gi, additional, Ryu, Dongryeol, additional, Che, Xiangguo, additional, Choi, Je‐Yong, additional, Tsukasaki, Masayuki, additional, Sasako, Takayoshi, additional, Lee, Sang‐Hee, additional, Shong, Minho, additional, and Yi, Hyon‐Seung, additional

Published
2022
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13. Skeletal muscle mitochondrial dysfunction in mice is linked to bone loss via the bone marrow immune microenvironment

Author

Tian, Jingwen, primary, Moon, Ji Sun, additional, Nga, Ha Thi, additional, Chung, Hyo Kyun, additional, Lee, Ho Yeop, additional, Kim, Jung Tae, additional, Chang, Joon Young, additional, Kang, Seul Gi, additional, Ryu, Dongryeol, additional, Che, Xiangguo, additional, Choi, Je-Yong, additional, Tsukasaki, Masayuki, additional, Sasako, Takayoshi, additional, Lee, Sang-Hee, additional, Shong, Minho, additional, and Yi, Hyon-Seung, additional

Published
2020
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