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Cancer Selective Turn-On Fluorescence Imaging Using a Biopolymeric Nanocarrier
Jeong, Yoon,Kim, Garam,Jeong, Soohyun,Lee, Byungchul,Kim, Sangeun,Koh, Won-Gun,Lee, Kangwon American Chemical Society 2019 Biomacromolecules Vol.20 No.2
<P>Most nanoparticle-based bioresearch for clinical applications is unable to overcome the clinical barriers of efficacy (e.g., sensitivity and selectivity), safety for human use, and scalability for mass-production processes. Here, we proposed a promising concept of using a biocompatible nanocarrier that delivers natural fluorescent precursors into cancerous cells. The nanocarrier is a biopolymeric nanoparticle that can be easily loaded with fluorescent precursors to form a fluorescent moiety via a biosynthesis pathway. Once delivered into cancerous cells, the nanocarriers are selectively turned on and distinctively fluoresce upon excitation. We, therefore, demonstrated the efficacy of the selective turn-on fluorescence of the nanocarriers in in vitro coculture models and in vivo tumor-bearing models.</P> [FIG OMISSION]</BR>
Nam, Ki-Soo,Jeong, Hyun-Jeong,Kim, Hee-Kyung,Choi, Garam,Suh, Kyung-Jin,Chang, Yongmin,Kim, Tae-Jeong Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.1
The work is directed toward the synthesis of a series of DO3A conjugates of tranexamates (1c-e) and their Gd complexes (2c-e) for use as a liver-specific MRI CA. All these complexes show thermodynamic and kinetic stabilities comparable to those of structurally related clinical agents such as Dotarem$^{(R)}$. Their $R_1$ relaxivities also compare well with those of commercial agent, ranging 3.68-4.84 $mM^{-1}s^{-1}$. In vivo MR images of mice with 2a-e reveal that only 2a exhibits liver-specificity. Although 2b and 2c show strong enhancement in liver, yet no bile-excretion is observed to be termed as a liver-specific agent. The rest behaves much like ordinary ECF CAs like Dotarem$^{(R)}$. The new series possess no toxicity to be employed in vivo.
Programmed cell death 5 suppresses AKT-mediated cytoprotection of endothelium
Lee, Seung-Hyun,Seo, Jaesung,Park, Soo-Yeon,Jeong, Mi-Hyeon,Choi, Hyo-Kyoung,Lee, Chan Joo,Kim, Mi Jeong,Guk, Garam,Lee, SooYeon,Park, Hyewon,Jeong, Jae-Wook,Ha, Chang Hoon,Park, Sungha,Yoon, Ho-Geun National Academy of Sciences 2018 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.115 No.18
<P>Programmed cell death 5 (PDCD5) has been associated with human cancers as a regulator of cell death; however, the role of PDCD5 in the endothelium has not been revealed. Thus, we investigated whether PDCD5 regulates protein kinase B (PKB/AKT)-endothelial nitric oxide synthase (eNOS)-dependent signal transduction in the endothelium and affects atherosclerosis. Endothelial-specific PDCD5 knockout mice showed significantly reduced vascular remodeling compared with wild-type (WT) mice after partial carotid ligation. WT PDCD5 competitively inhibited interaction between histone deacetylase 3 (HDAC3) and AKT, but PDCD5(L6R), an HDAC3-binding-deficient mutant, did not. Knockdown of PDCD5 accelerated HDAC3-AKT interaction, AKT and eNOS phosphorylation, and nitric oxide (NO) production in human umbilical vein endothelial cells. Moreover, we found that serum PDCD5 levels reflect endothelial NO production and are correlated with diabetes mellitus, high-density lipoprotein cholesterol, and coronary calcium in human samples obtained from the cardiovascular high-risk cohort. Therefore, we conclude that PDCD5 is associated with endothelial dysfunction and may be a novel therapeutic target in atherosclerosis.</P>
Garam Jo,Hannah Oh,Gitanjali M. Singh,Dahyun Park,Min-Jeong Shin 한국영양학회 2020 Nutrition Research and Practice Vol.14 No.4
BACKGROUND/OBJECTIVES: Dietary factors are important contributors to cardiometabolic and cancer mortality. We examined the secular trends of nine dietary factors (fruits, vegetables, whole grains, nuts and seeds, milk, red meat, processed meat, sugar-sweetened beverages, and calcium) and the associated burdens of cardiometabolic and cancer mortality in Korea using representative cross-sectional survey data from 1998 to 2016. SUBJECTS/METHODS: Using dietary data from Korean adults aged ≥ 25 years in the Korea National Health and Nutrition Examination Survey (KNHANES), we characterized secular trends in intake levels. We performed comparative risk assessment to estimate the population attributable fraction and the number of cardiometabolic and cancer deaths attributable to each dietary factor. RESULTS: A total of 231,148 cardiometabolic and cancer deaths were attributable to nine dietary risk factors in Korea from 1998 to 2016. Suboptimal intakes of fruits and whole grains were the leading contributors. Although the intakes of fruits, vegetables, and whole grains moderately improved over time, the intake levels in 2016 (192.1 g/d, 225.6 g/d, and 10.9 g/d, respectively) remained far below the optimal levels. Deaths attributable to the low intakes of nuts and seeds (4.5 g/d), calcium (440.5 mg/d), and milk (37.1 g/d) and the high intakes of red meat (54.7 g/d), processed meat (4.7 g/d), and sugar-sweetened beverages (33.0 g/d) increased since 1998. Compared with older age groups (≥ 45 years), more unfavorable changes in dietary patterns were observed in the younger population aged 25–44 years, including more sharply increased intakes of processed meat. CONCLUSIONS: We observed improvement in the intakes of fruits, vegetables, and whole grains and unfavorable changes in the intakes of processed meat and sugar-sweetened beverages over the past few decades. Our data suggest that to reduce the chronic disease burden in Korea, more effective nutritional policies and interventions are needed to target these dietary risk factors.
Kim, Garam,Khanal, Prem,Lim, Sung-Chul,Yun, Hyo Jeong,Ahn, Sang-Gun,Ki, Sung Hwan,Choi, Hong Seok IRL Press] ; Oxford University Press 2013 Carcinogenesis Vol.34 No.2
<P>Inflammatory conditions elicited by extrinsic environmental factors promote malignant transformation, tumor growth and metastasis. Although the role of T cells in cancer promotion has been examined, little is known about the underlying molecular mechanisms of interleukin-17 A (IL-17A), a proinflammatory cytokine produced by activated CD4(+) memory T cells, in carcinogenesis. Here, we report that IL-17A induces neoplastic transformation of JB6 Cl41 cells through activation of tumor progression locus 2 (TPL2). IL-17A dose- and time-dependently increases TPL2 phosphorylation in JB6 Cl41 cells through IL-17A receptor. IL-17A activates mitogen-activated protein kinase/extracellular signal-regulated kinase kinases, c-jun N-terminal kinases and STAT3 signaling pathways, which are inhibited by a TPL2 kinase inhibitor (TKI). Furthermore, IL-17A activates c-fos and c-jun promoter activity, resulting in increased activator protein-1 (AP-1) activity. When small interfering RNA of IL-17A receptor (IL-17R), IL-17A and TPL2 were introduced into JB6 Cl41 cells, respectively, IL-17A-induced AP-1 activity was significantly decreased compared with control cells. Similarly, TPL2 inhibition suppressed AP-1 activity induced by IL-17A. The knockdown of IL-17R and TKI treatment in JB6 Cl41 cells resulted in decreased IL-17A-induced cell transformation. The in vivo chorioallantoic membrane assay also showed that IL-17A increased tumor formation of JB6 Cl41 cells, whereas TKI inhibited the tumorigenesis promoted by IL-17A. Consistent with these observations, knockdown of IL-17A and/or inhibition of TPL2 attenuated tumorigenicity of human breast cancer MCF7 cells. Together, our findings point to a critical role for the IL-17A-induced TPL2 signaling pathway in supporting cancer-associated inflammation in the tumor microenvironment. Therapeutic approaches that target this pathway may, therefore, effectively inhibit carcinogenesis.</P>