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33 results on '"Son, Heehwa G."'

10. Rejection of benign melanocytic nevi by nevus-resident CD4 + T cells

Author

Schiferle, Erik B., primary, Cheon, Se Yun, additional, Ham, Seokjin, additional, Son, Heehwa G., additional, Messerschmidt, Jonathan L., additional, Lawrence, Donald P., additional, Cohen, Justine V., additional, Flaherty, Keith T., additional, Moon, James J., additional, Lian, Christine G., additional, Sullivan, Ryan J., additional, and Demehri, Shadmehr, additional

Published
2021
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12. Caenorhabditis elegans Lipin 1 moderates the lifespan‐shortening effects of dietary glucose by maintaining ω‐6 polyunsaturated fatty acids

Author

Jung, Yoonji, primary, Kwon, Sujeong, additional, Ham, Seokjin, additional, Lee, Dongyeop, additional, Park, Hae‐Eun H., additional, Yamaoka, Yasuyo, additional, Jeong, Dae‐Eun, additional, Artan, Murat, additional, Altintas, Ozlem, additional, Park, Sangsoon, additional, Hwang, Wooseon, additional, Lee, Yujin, additional, Son, Heehwa G., additional, An, Seon Woo A., additional, Kim, Eun Ji E., additional, Seo, Mihwa, additional, and Lee, Seung‐Jae V., additional

Published
2020
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13. KIN‐4/MAST kinase promotes PTEN‐mediated longevity of Caenorhabditis elegans via binding through a PDZ domain

Author

An, Seon Woo A., primary, Choi, Eun‐Seok, additional, Hwang, Wooseon, additional, Son, Heehwa G., additional, Yang, Jae‐Seong, additional, Seo, Keunhee, additional, Nam, Hyun‐Jun, additional, Nguyen, Nhung T. H., additional, Kim, Eun Ji E., additional, Suh, Bo Kyoung, additional, Kim, Youngran, additional, Nakano, Shunji, additional, Ryu, Youngjae, additional, Man Ha, Chang, additional, Mori, Ikue, additional, Park, Sang Ki, additional, Yoo, Joo‐Yeon, additional, Kim, Sanguk, additional, and Lee, Seung‐Jae V., additional

Published
2019
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15. Prefoldin 6 mediates longevity response from heat shock factor 1 to FOXO in C. elegans

Author

Son, Heehwa G., primary, Seo, Keunhee, additional, Seo, Mihwa, additional, Park, Sangsoon, additional, Ham, Seokjin, additional, An, Seon Woo A., additional, Choi, Eun-Seok, additional, Lee, Yujin, additional, Baek, Haeshim, additional, Kim, Eunju, additional, Ryu, Youngjae, additional, Ha, Chang Man, additional, Hsu, Ao-Lin, additional, Roh, Tae-Young, additional, Jang, Sung Key, additional, and Lee, Seung-Jae V., additional

Published
2018
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16. Diacetyl odor shortens longevity conferred by food deprivation in C. elegans via downregulation of DAF‐16/FOXO.

Author

Park, Sangsoon, Artan, Murat, Jeong, Dae‐Eun, Park, Hae‐Eun H., Son, Heehwa G., Kim, Sieun S., Jung, Yoonji, Choi, Yunji, Lee, Jin I., Kim, Kyuhyung, and Lee, Seung‐Jae V.

Subjects
CAENORHABDITIS elegans, LONGEVITY, DIACETYL, ODORS, LACTIC acid bacteria, SENSORY neurons, LACTIC acid
Abstract

Dietary restriction extends lifespan in various organisms by reducing the levels of both nutrients and non‐nutritional food‐derived cues. However, the identity of specific food‐derived chemical cues that alter lifespan remains unclear. Here, we identified several volatile attractants that decreased the longevity on food deprivation, a dietary restriction regimen in Caenorhabditis elegans. In particular, we found that the odor of diacetyl decreased the activity of DAF‐16/FOXO, a life‐extending transcription factor acting downstream of insulin/IGF‐1 signaling. We then demonstrated that the odor of lactic acid bacteria, which produce diacetyl, reduced the nuclear accumulation of DAF‐16/FOXO. Unexpectedly, we showed that the odor of diacetyl decreased longevity independently of two established diacetyl receptors, ODR‐10 and SRI‐14, in sensory neurons. Thus, diacetyl, a food‐derived odorant, may shorten food deprivation‐induced longevity via decreasing the activity of DAF‐16/FOXO through binding to unidentified receptors. [ABSTRACT FROM AUTHOR]

Published
2021
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21. Myricetin improves endurance capacity and mitochondrial density by activating SIRT1 and PGC-1α

Author

Jung, Hoe-Yune, primary, Lee, Dongyeop, additional, Ryu, Hye Guk, additional, Choi, Bo-Hwa, additional, Go, Younghoon, additional, Lee, Namgyu, additional, Lee, Dohyun, additional, Son, Heehwa G., additional, Jeon, Jongsu, additional, Kim, Seong-Hoon, additional, Yoon, Jong Hyuk, additional, Park, Seon-Min, additional, Lee, Seung-Jae V., additional, Lee, In-Kyu, additional, Choi, Kwan Yong, additional, Ryu, Sung Ho, additional, Nohara, Kazunari, additional, Yoo, Seung-Hee, additional, Chen, Zheng, additional, and Kim, Kyong-Tai, additional

Published
2017
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23. Mitochondrial chaperoneHSP‐60 regulates anti‐bacterial immunity via p38MAPkinase signaling

Author

Jeong, Dae‐Eun, primary, Lee, Dongyeop, additional, Hwang, Sun‐Young, additional, Lee, Yujin, additional, Lee, Jee‐Eun, additional, Seo, Mihwa, additional, Hwang, Wooseon, additional, Seo, Keunhee, additional, Hwang, Ara B, additional, Artan, Murat, additional, Son, Heehwa G, additional, Jo, Jay‐Hyun, additional, Baek, Haeshim, additional, Oh, Young Min, additional, Ryu, Youngjae, additional, Kim, Hyung‐Jun, additional, Ha, Chang Man, additional, Yoo, Joo‐Yeon, additional, and Lee, Seung‐Jae V, additional

Published
2017
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24. RNA surveillance via nonsense-mediated mRNA decay is crucial for longevity in daf-2/insulin/IGF-1 mutant C. elegans

Author

Son, Heehwa G., primary, Seo, Mihwa, additional, Ham, Seokjin, additional, Hwang, Wooseon, additional, Lee, Dongyeop, additional, An, Seon Woo A., additional, Artan, Murat, additional, Seo, Keunhee, additional, Kaletsky, Rachel, additional, Arey, Rachel N., additional, Ryu, Youngjae, additional, Ha, Chang Man, additional, Kim, Yoon Ki, additional, Murphy, Coleen T., additional, Roh, Tae-Young, additional, Nam, Hong Gil, additional, and Lee, Seung-Jae V., additional

Published
2017
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29. Mitochondrial chaperone HSP-60 regulates anti-bacterial immunity via p38 MAP kinase signaling.

Author

Jeong, Dae‐Eun, Lee, Dongyeop, Hwang, Sun‐Young, Lee, Yujin, Lee, Jee‐Eun, Seo, Mihwa, Hwang, Wooseon, Seo, Keunhee, Hwang, Ara B, Artan, Murat, Son, Heehwa G, Jo, Jay‐Hyun, Baek, Haeshim, Oh, Young Min, Ryu, Youngjae, Kim, Hyung‐Jun, Ha, Chang Man, Yoo, Joo‐Yeon, and Lee, Seung‐Jae V

Subjects
MITOGEN-activated protein kinases, IMMUNOLOGY, EXTRACHROMOSOMAL DNA, CAENORHABDITIS elegans, PSEUDOMONAS aeruginosa
Abstract

Mitochondria play key roles in cellular immunity. How mitochondria contribute to organismal immunity remains poorly understood. Here, we show that HSP-60/ HSPD1, a major mitochondrial chaperone, boosts anti-bacterial immunity through the up-regulation of p38 MAP kinase signaling. We first identify 16 evolutionarily conserved mitochondrial components that affect the immunity of Caenorhabditis elegans against pathogenic Pseudomonas aeruginosa ( PA14). Among them, the mitochondrial chaperone HSP-60 is necessary and sufficient to increase resistance to PA14. We show that HSP-60 in the intestine and neurons is crucial for the resistance to PA14. We then find that p38 MAP kinase signaling, an evolutionarily conserved anti-bacterial immune pathway, is down-regulated by genetic inhibition of hsp-60, and up-regulated by increased expression of hsp-60. Overexpression of HSPD1, the mammalian ortholog of hsp-60, increases p38 MAP kinase activity in human cells, suggesting an evolutionarily conserved mechanism. Further, cytosol-localized HSP-60 physically binds and stabilizes SEK-1/ MAP kinase kinase 3, which in turn up-regulates p38 MAP kinase and increases immunity. Our study suggests that mitochondrial chaperones protect host eukaryotes from pathogenic bacteria by up-regulating cytosolic p38 MAPK signaling. [ABSTRACT FROM AUTHOR]

Published
2017
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30. Age‐dependent changes and biomarkers of aging in Caenorhabditis elegans.

Author

Son, Heehwa G., Altintas, Ozlem, Kim, Eun Ji E., Kwon, Sujeong, and Lee, Seung‐Jae V.

Subjects
*CAENORHABDITIS elegans, *CAENORHABDITIS, *BIOMARKERS
Abstract

Caenorhabditis elegans is an exceptionally valuable model for aging research because of many advantages, including its genetic tractability, short lifespan, and clear age‐dependent physiological changes. Aged C. elegans display a decline in their anatomical and functional features, including tissue integrity, motility, learning and memory, and immunity. Caenorhabditis elegans also exhibit many age‐associated changes in the expression of microRNAs and stress‐responsive genes and in RNA and protein quality control systems. Many of these age‐associated changes provide information on the health of the animals and serve as valuable biomarkers for aging research. Here, we review the age‐dependent changes in C. elegans and their utility as aging biomarkers indicative of the physiological status of aging. [ABSTRACT FROM AUTHOR]

Published
2019
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31. Cytotoxic CD4+ T cells eliminate senescent cells by targeting cytomegalovirus antigen.

Author

Hasegawa, Tatsuya, Oka, Tomonori, Son, Heehwa G., Oliver-García, Valeria S., Azin, Marjan, Eisenhaure, Thomas M., Lieb, David J., Hacohen, Nir, and Demehri, Shadmehr

Subjects
*IMMUNOSENESCENCE, *CYTOTOXIC T cells, *T cells, *HLA histocompatibility antigens, *ORGANS (Anatomy), *CELLULAR aging, *ANTIGENS, *CYTOMEGALOVIRUSES
Abstract

Senescent cell accumulation has been implicated in the pathogenesis of aging-associated diseases, including cancer. The mechanism that prevents the accumulation of senescent cells in aging human organs is unclear. Here, we demonstrate that a virus-immune axis controls the senescent fibroblast accumulation in the human skin. Senescent fibroblasts increased in old skin compared with young skin. However, they did not increase with advancing age in the elderly. Increased CXCL9 and cytotoxic CD4+ T cells (CD4 CTLs) recruitment were significantly associated with reduced senescent fibroblasts in the old skin. Senescent fibroblasts expressed human leukocyte antigen class II (HLA-II) and human cytomegalovirus glycoprotein B (HCMV-gB), becoming direct CD4 CTL targets. Skin-resident CD4 CTLs eliminated HCMV-gB+ senescent fibroblasts in an HLA-II-dependent manner, and HCMV-gB activated CD4 CTLs from the human skin. Collectively, our findings demonstrate HCMV reactivation in senescent cells, which CD4 CTLs can directly eliminate through the recognition of the HCMV-gB antigen. [Display omitted] • Senescent fibroblasts do not increase with advancing age in the skin of the elderly • CD4 CTLs negatively correlate with senescent fibroblast accumulation in the old skin • Senescent fibroblasts highly express HLA-II, NKG2D ligands, and HCMV-glycoprotein B • CD4 CTLs eliminate HCMV-gB+ senescent fibroblasts in an HLA-II-dependent manner In humans, senescent fibroblasts do not seem to increase with advancing age in the elderly because their populations are controlled by cytotoxic CD4+ T cells. The expression of T cell-activating ligands and the human cytomegalovirus glycoprotein B marks the senescent fibroblasts for elimination. [ABSTRACT FROM AUTHOR]

Published
2023
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32. Rejection of benign melanocytic nevi by nevus-resident CD4+ T cells.

Author

Schiferle, Erik B., Se Yun Cheon, Seokjin Ham, Son, Heehwa G., Messerschmidt, Jonathan L., Lawrence, Donald P., Cohen, Justine V., Flaherty, Keith T., Moon, James J., Lian, Christine G., Sullivan, Ryan J., and Demehri, Shadmehr

Subjects
*NEVUS, *T cells, *BASILIXIMAB, *CYTOTOXIC T cells, *REGULATORY T cells, *T helper cells, *TOLUIDINE blue, *DYSPLASTIC nevus syndrome
Published
2021
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33. Compromised T Cell Immunity Links Increased Cutaneous Papillomavirus Activity to Squamous Cell Carcinoma Risk.

Author

Johnson LH, Son HG, Ha DT, Strickley JD, Joh J, and Demehri S

Abstract

Cutaneous squamous cell carcinoma (cSCC) is the second most common cancer, with increased incidence in immunosuppressed patients. β-Human papillomavirus has been proposed as a contributor to cSCC risk partly on the basis of increased β-human papillomavirus viral load and seropositivity observed among patients with cSCC. Experimental data in mice colonized with mouse papillomavirus type 1 suggest that T cell immunity against β-human papillomavirus suppresses skin cancer in immunocompetent hosts, and the loss of this immunity leads to the increased risk of cSCC. In this study, we show that CD8 + T cell depletion in mouse papillomavirus type 1‒colonized mice that underwent skin carcinogenesis protocol led to increased viral load in the skin and seropositivity for anti‒mouse papillomavirus type 1 antibodies. These findings provide evidence that compromised T cell immunity can be the link that connects increased β-human papillomavirus detection to cSCC risk., (© 2022 The Authors.)

Published
2022
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