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4. Mitophagy deficiency increases NLRP3 to induce brown fat dysfunction in mice

Author

Ko, Myoung Seok, Yun, Ji Young, Baek, In-Jeoung, Jang, Jung Eun, Hwang, Jung Jin, Lee, Seung Eun, Heo, Seung-Ho, Bader, David A, Lee, Chul-Ho, Han, Jaeseok, Moon, Jong-Seok, Lee, Jae Man, Hong, Eun-Gyoung, Lee, In-Kyu, Kim, Seong Who, Park, Joong Yeol, Hartig, Sean M, Kang, Un Jung, Moore, David D, Koh, Eun Hee, and Lee, Ki-up

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, Nutrition, Obesity, Aetiology, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Underpinning research, Metabolic and endocrine, Cardiovascular, Adipocytes, Adipose Tissue, Brown, Animals, Autophagy, Energy Metabolism, Inflammasomes, Mice, Knockout, Mitochondria, Mitophagy, NLR Family, Pyrin Domain-Containing 3 Protein, Reactive Oxygen Species, Brown adipocyte, inflammasome, pink1, transcriptional activation, white adipocyte, Biochemistry & Molecular Biology, Biochemistry and cell biology
Abstract

Although macroautophagy/autophagy deficiency causes degenerative diseases, the deletion of essential autophagy genes in adipocytes paradoxically reduces body weight. Brown adipose tissue (BAT) plays an important role in body weight regulation and metabolic control. However, the key cellular mechanisms that maintain BAT function remain poorly understood. in this study, we showed that global or brown adipocyte-specific deletion of pink1, a Parkinson disease-related gene involved in selective mitochondrial autophagy (mitophagy), induced BAT dysfunction, and obesity-prone type in mice. Defective mitochondrial function is among the upstream signals that activate the NLRP3 inflammasome. NLRP3 was induced in brown adipocyte precursors (BAPs) from pink1 knockout (KO) mice. Unexpectedly, NLRP3 induction did not induce canonical inflammasome activity. Instead, NLRP3 induction led to the differentiation of pink1 KO BAPs into white-like adipocytes by increasing the expression of white adipocyte-specific genes and repressing the expression of brown adipocyte-specific genes. nlrp3 deletion in pink1 knockout mice reversed BAT dysfunction. Conversely, adipose tissue-specific atg7 KO mice showed significantly lower expression of Nlrp3 in their BAT. Overall, our data suggest that the role of mitophagy is different from general autophagy in regulating adipose tissue and whole-body energy metabolism. Our results uncovered a new mitochondria-NLRP3 pathway that induces BAT dysfunction. The ability of the nlrp3 knockouts to rescue BAT dysfunction suggests the transcriptional function of NLRP3 as an unexpected, but a quite specific therapeutic target for obesity-related metabolic diseases.Abbreviations: ACTB: actin, beta; BAPs: brown adipocyte precursors; BAT: brown adipose tissue; BMDMs: bone marrow-derived macrophages; CASP1: caspase 1; CEBPA: CCAAT/enhancer binding protein (C/EBP), alpha; ChIP: chromatin immunoprecipitation; EE: energy expenditure; HFD: high-fat diet; IL1B: interleukin 1 beta; ITT: insulin tolerance test; KO: knockout; LPS: lipopolysaccharide; NLRP3: NLR family, pyrin domain containing 3; PINK1: PTEN induced putative kinase 1; PRKN: parkin RBR E3 ubiquitin protein ligase; RD: regular diet; ROS: reactive oxygen species; RT: room temperature; UCP1: uncoupling protein 1 (mitochondrial, proton carrier); WT: wild-type.

Published
2021

11. Integrative analysis of microRNA-mediated mitochondrial dysfunction in hippocampal neural progenitor cell death in relation with Alzheimer’s disease

Author

Han, A Reum, primary, Moon, Tae Kwon, additional, Kang, Im Kyeung, additional, Yu, Dae Bong, additional, Kim, Yechan, additional, Byon, Cheolhwan, additional, Park, Sujeong, additional, Kim, Hae Lin, additional, Lee, Kyoung Jin, additional, Lee, Heuiran, additional, Woo, Ha-Na, additional, and Kim, Seong Who, additional

Published
2024
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22. Letter-to-editor, “Feedback amplification of senolysis using caspase-cleavable peptide-doxorubicin conjugate and 2DG” [Journal of Controlled Release, Volume 346, pp. 158-168, (2022), doi: 10.1016/j.jconrel.2022.04.012].

Author

Lee, Jong Cheol, primary, Kim, Gui Chul, additional, Kim, Seong Who, additional, Lee, Na Kyeong, additional, Cho, Young Seok, additional, Chung, Seung Woo, additional, Lee, Yoon Se, additional, Han, Myung Woul, additional, Chang, Hyo Won, additional, Byun, Youngro, additional, and Kim, Sang Yoon, additional

Published
2023
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23. Supplementary Methods from Radioresistant Cancer Cells Can Be Conditioned to Enter Senescence by mTOR Inhibition

Author

Nam, Hae Yun, primary, Han, Myung Woul, primary, Chang, Hyo Won, primary, Lee, Yoon Sun, primary, Lee, Myungjin, primary, Lee, Hyang Ju, primary, Lee, Byoung Wook, primary, Lee, Hee Jin, primary, Lee, Kyung Eun, primary, Jung, Min Kyo, primary, Jeon, Hyesung, primary, Choi, Seung-Ho, primary, Park, Neung Hwa, primary, Kim, Sang Yoon, primary, and Kim, Seong Who, primary

Published
2023
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24. Supplementary Figure S1 from Radioresistant Cancer Cells Can Be Conditioned to Enter Senescence by mTOR Inhibition

Author

Nam, Hae Yun, primary, Han, Myung Woul, primary, Chang, Hyo Won, primary, Lee, Yoon Sun, primary, Lee, Myungjin, primary, Lee, Hyang Ju, primary, Lee, Byoung Wook, primary, Lee, Hee Jin, primary, Lee, Kyung Eun, primary, Jung, Min Kyo, primary, Jeon, Hyesung, primary, Choi, Seung-Ho, primary, Park, Neung Hwa, primary, Kim, Sang Yoon, primary, and Kim, Seong Who, primary

Published
2023
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25. Data from Radioresistant Cancer Cells Can Be Conditioned to Enter Senescence by mTOR Inhibition

Author

Nam, Hae Yun, primary, Han, Myung Woul, primary, Chang, Hyo Won, primary, Lee, Yoon Sun, primary, Lee, Myungjin, primary, Lee, Hyang Ju, primary, Lee, Byoung Wook, primary, Lee, Hee Jin, primary, Lee, Kyung Eun, primary, Jung, Min Kyo, primary, Jeon, Hyesung, primary, Choi, Seung-Ho, primary, Park, Neung Hwa, primary, Kim, Sang Yoon, primary, and Kim, Seong Who, primary

Published
2023
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26. Supplementary Figure Legends from Radioresistant Cancer Cells Can Be Conditioned to Enter Senescence by mTOR Inhibition

Author

Nam, Hae Yun, primary, Han, Myung Woul, primary, Chang, Hyo Won, primary, Lee, Yoon Sun, primary, Lee, Myungjin, primary, Lee, Hyang Ju, primary, Lee, Byoung Wook, primary, Lee, Hee Jin, primary, Lee, Kyung Eun, primary, Jung, Min Kyo, primary, Jeon, Hyesung, primary, Choi, Seung-Ho, primary, Park, Neung Hwa, primary, Kim, Sang Yoon, primary, and Kim, Seong Who, primary

Published
2023
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32. Targeting prion-like protein doppel selectively suppresses tumor angiogenesis

Author

Hilal, Taslim A. Al-, Chung, Seung Woo, Choi, Jeong Uk, Alam, Farzana, Park, Jooho, Kim, Seong Who, Kim, Sang Yoon, Ahsan, Fakhrul, Kim, In-San, and Byun, Youngro

Subjects
Neovascularization -- Genetic aspects -- Health aspects, Carcinogenesis -- Genetic aspects -- Prevention, Prions -- Properties, Health care industry
Abstract

Controlled and site-specific regulation of growth factor signaling remains a major challenge for current antiangiogenic therapies, as these antiangiogenic agents target normal vasculature as well tumor vasculature. In this article, we identified the prion-like protein doppel as a potential therapeutic target for tumor angiogenesis. We investigated the interactions between doppel and VEGFR2 and evaluated whether blocking the doppel/VEGFR2 axis suppresses the process of angiogenesis. We discovered that tumor endothelial cells (TECs), but not normal ECs, express doppel; tumors from patients and mouse xenografts expressed doppel in their vasculatures. Induced doppel overexpression in ECs enhanced vascularization, whereas doppel constitutively colocalized and complexed with VEGFR2 in TECs. Doppel inhibition depleted VEGFR2 from the cell membrane, subsequently inducing the internalization and degradation of VEGFR2 and thereby attenuating VEGFR2 signaling. We also synthesized an orally active glycosaminoglycan (LHbisD4) that specifically binds with doppel. We determined that LHbisD4 concentrates over the tumor site and that genetic loss of doppel in TECs decreases LHbisD4 binding and targeting both in vitro and in vivo. Moreover, LHbisD4 eliminated VEGFR2 from the cell membrane, prevented VEGF binding in TECs, and suppressed tumor growth. Together, our results demonstrate that blocking doppel can control VEGF signaling in TECs and selectively inhibit tumor angiogenesis., Introduction The process of angiogenesis drives the progression and development of many diseases. Tumors, for example, advance from the dormant stage to highly aggressive and metastatic cancers as a result [...]

Published
2016
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38. Additional file 2 of miR-3189-targeted GLUT3 repression by HDAC2 knockdown inhibits glioblastoma tumorigenesis through regulating glucose metabolism and proliferation

Author

Kwak, Sungmin, Park, Seung-Ho, Kim, Sung-Hak, Sung, Gi-Jun, Song, Ji-Hye, Jeong, Ji-Hoon, Kim, Hyunhee, Ha, Chang Hoon, Kim, Seong Who, and Choi, Kyung-Chul

Abstract

Additional file 2: Supplementary Table 1. List of primer for qRT-PCR. Supplementary Table 2. Complete list of materials and reagents for experimental.

Published
2022
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39. Additional file 1 of miR-3189-targeted GLUT3 repression by HDAC2 knockdown inhibits glioblastoma tumorigenesis through regulating glucose metabolism and proliferation

Author

Kwak, Sungmin, Park, Seung-Ho, Kim, Sung-Hak, Sung, Gi-Jun, Song, Ji-Hye, Jeong, Ji-Hoon, Kim, Hyunhee, Ha, Chang Hoon, Kim, Seong Who, and Choi, Kyung-Chul

Abstract

Additional file 1: Supplementary Fig. 1. A Expression of Class 1 HDAC Genes and Proteins in GBM cells. GBM cells were extracted in lysis buffer, and cell lysates were analyzed using western blot analysis with class I HDAC antibodies (HDAC1, 2, 3 and 8). B Quantification of protein level of class I HDAC expression. Densitometric quantification of protein signals was quantified by ImageJ (Java 1.8.0_112, NIH, Bethesda, MD, USA), and the level of protein expression was normalized to ��-actin. Data represent the means �� SD from three independent experiments. C Lentiviral infection of HDAC2 shRNA in GBM cells. A172 and U87MG cells were incubated for 6 days post-infection prior to measurement of cell viability by using MTT assay. All data are expressed as the mean �� SD for triplicates. D Class I HDAC siRNA was transfected into GBM cells. Cell lysates were analyzed by western blot using the indicated antibodies. E Class I HDAC siRNA was transfected into GBM and normal brain cells. SVGp12 and GBM cells were incubated for 48 h. Cell viability was measured via MTT assay. F qRT-PCR analysis and Immunoblot analysis of HDAC2 and GLUT3 expression in control GBM cells and HDAC2KD GBM cells upon doxycycline treatment. G IF in DOX-inducible shcontrol GBM cells and DOX-inducible shHDAC2 GBM cells upon doxycycline treatment (2.5 ��g/ml) (DAPI: blue and FITC-HDAC2: green). Scale bar: 100 ��m. H Luciferase reporter activities of DOX-inducible control and DOX-inducible shHDAC2 GBM cells (Upper: U87MG and Bottom: A172) with doxycycline. Cells were transiently transfected with reporter pGL3-Luc or pGL3-Puma-Luc plasmids. Dual luciferase activity was measured (420 nm) in cell lysates. Reporter activities were normalized relative to Renilla luciferase activities. I Cell viability of DOX-inducible shcontrol and DOX-inducible shHDAC2 GBM cells (Left: U87MG and Right: A172). GBM cells upon doxycycline treatment were measured in the presence or absence of Romidepsin by using WST-8 assay. All data are expressed as the mean �� SD from three independent experiments, each performed in triplicate. ***p

Published
2022
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