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Lee, Jienny,Shin, Yeun-Kyung,Song, Jae-Young,Lee, Kyung-Woo Informa Healthcare 2014 International Journal of Radiation Biology Vol.90 No.1
<P><I>Purpose</I>: Ultraviolet-B (UVB) irradiation is a major inducer of DNA damage in the epidermis. Here we investigated the protective mechanism of polyphenolic phytonutrient, morin against UVB-induced DNA damage in human keratinocyte stem cells (KSC).</P><P><I>Results and conclusions</I>: After confirming the characteristics of the KSC, we examined the protective ability of morin against the cell damage of KSC under UVB irradiation condition. As a result, morin significantly inhibited the UVB-induced damage to KSC. These inhibitory effects by morin were also confirmed by the senescence-associated beta-galactosidase and alkaline comet assays. Next, we monitored the effects of morin on the UVB-induced production of inflammatory cytokines. Morin significantly decreased the production of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the UVB-irradiated KSC. Also, morin significantly inhibited the UVB-induced phosphorylation of ataxia telangiectasia mutated (ATM), serine threonine kinase checkpoint kinase 2, tumor suppressor protein 53 (p53), c-Jun N-terminal kinase/stress-activated protein kinase, p38/mitogen-activated protein kinase, S6 ribosomal protein, and histone 2A family member X in KSC. Furthermore, while UVB irradiation induced p53 reporter activation in KSC, morin significantly inhibited UVB-induced p53 reporter activation in KSC. In addition, mouse double minute 2 homolog (MDM2, p53 E3 ubiquitin protein ligase) inhibitor significantly increased the p53 reporter activation in the UVB-irradiated KSC, but morin decreased the MDM2 inhibitor-mediated increase in p53 reporter activation. On the contrary, ATM inhibitor did not affect the protective effect of morin in UVB irradiation-induced p53 reporter activation. Collectively, these findings suggest that morin could effectively enrich the p53 specific ligasing ability of MDM2 in UVB irradiation-induced p53 activation.</P>
Lee, Jienny,Byeon, Jeong Su,Lee, Keum Sil,Gu, Na-Yeon,Lee, Gyeong Been,Kim, Hee-Ryang,Cho, In-Soo,Cha, Sang-Ho Springer-Verlag 2016 Veterinary research communications Vol.40 No.1
<P>Mesenchymal stem cells (MSCs) have the ability to differentiate into multi-lineage cells, which confers great promise for use in regenerative medicine. In this study, canine adipose MSCs (cAD-MSCs) were isolated from canine adipose tissue. These cells clearly represented stemness (Oct4, Sox2, and Nanog) and differentiation potential into the mesoderm (adipocytes, chondrocytes, and osteoblasts) at early passages. The aim of this study was to evaluate the effects of hypoxia on the differentiation potential into mesoderm, and the expression of anti-apoptotic genes associated with cell survival for the optimal culturing of MSCs. We observed that the proliferation of the cAD-MSCs meaningfully increased when cultured under hypoxic condition than in normoxic condition, during 7 consecutive passages. Also, we found that hypoxia strongly expressed anti-senescence related genes such as HDAC1 (histone deacetylase 1), DNMT1 (DNA (cytosine-5)-methyltransferase 1), Bcl-2 (inhibitor of apoptosis), TERT (telomerase reverse transcriptase), LDHA (lactate dehydrogenase A), SLC2A1 (glucose transporter), and DKC1 (telomere holoenzyme complex) and differentiation potential of cAD-MSCs into chondrocytes, than seen under the normoxic culture conditions. We also examined the multipotency of hypoxic conditioned MSCs using quantitative real-time RT-PCR. We found that the expression levels of stemness genes such as Oct-4, Nanog, and Sox-2 were increased in hypoxic condition when compared to the normoxic condition. Collectively, these results suggest that hypoxic conditions have the ability to induce proliferation of MSCs and augment their chondrogenic potential. This study suggests that cell proliferation of cAD-MSC under hypoxia could be beneficial, when considering these cells for cell therapies of canine bone diseases.</P>
Zingerone protects keratinocyte stem cells from UVB-induced damage
Lee, Jienny,Oh, Sae Woong,Shin, Seoung Woo,Lee, Kyung-Woo,Cho, Jae-Youl,Lee, Jongsung Elsevier 2018 Chemico-biological interactions Vol.279 No.-
<P><B>Abstract</B></P> <P>The epidermis, the outermost layer of the skin, is a stratified epithelium that protects the body from the external environment. Keratinocyte stem cells (KSCs) are involved in epidermis homeostasis by maintaining epidermal integrity through a process of constant regeneration. Ultraviolet B (UVB) radiation is a major inducer of cellular damage in the epidermis. In this study, we investigated the effects of zingerone (a phenolic compound derived from spices) on UVB-induced cellular damage in KSCs. We found that zingerone significantly inhibited cellular senescence of KSCs in response to UVB irradiation. These effects were confirmed by the senescence-associated β-galactosidase and comet assays. Zingerone decreased the production of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in UVB-irradiated KSCs. Moreover, UVB-induced expression of p21, a cell cycle arrest-related gene, was reduced by zingerone treatment, whereas zingerone upregulated the expression of proliferation-related genes such as proliferating cell nuclear antigen (PCNA) and vascular endothelial growth factor (VEGF), in addition to anti-senescence-related genes including telomerase reverse transcriptase (TERT), histone deacetylase 1 (HDAC1), and DNA (cytosine-5)-methyltransferase 1 (DNMT1). The UVB-protective effects of zingerone were mediated by inhibition of p42/44 MAPK and p38 MAPK. Therefore, zingerone could potentially be used to protect the epidermis from UVB-induced damage.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Zingerone inhibited the UVB-induced cellular senescence in KSCs. </LI> <LI> Zingerone reduced the UVB-induced production of proinflammatory cytokines. </LI> <LI> Zingerone reduced the UVB-induced expression of p21 gene. </LI> <LI> Zingerone increased expression of genes such as PCNA, VEGF, TERT, HDAC1, and DNMT1. </LI> <LI> Zingerone inhibited UVB-induced activation of p42/44 MAPK and p38 MAPK. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Development and characterization of mouse small intestinal enteroids
Siu Lee,Na-Yeon Gu,Se-A Lee,Jienny Lee,Yoon-Hee Lee,Bang-Hun Hyun 한국예방수의학회 2020 예방수의학회지 Vol.44 No.2
The culture of the intestinal epithelium into three dimensional (3D) structures typically termed organoid culture. Organoid culture is based on the ability of intestinal stem cells (ISCs), at the base of the crypt, perpetually to divide and produce a fully differentiated, polarized epithelium. Leucine-rich-repeat-containing G-protein-coupled receptor 5 (Lgr5) positive ISCs isolated from the intestine can form organoids in long-term culture. Thus, when cultured under the appropriate 3D conditions, single Lgr5⁺ ISCs undergo cycles of self-renewal, differentiation and morphogenesis, and self-organize into crypt-villus domains that house cycling ISCs and differentiated intestinal epithelial cells (IECs). In this study, we performed isolation, characterization and consecutive subculture of small intestinal crypts from BALB/c-nude mouse. Briefly, isolated mouse crypts were embedded in matrigel, cast into 40 μL droplets at the bottom of well in a 48-well plate. Following polymerization, the gels were overlaid with ISCs expansion medium containing B27, N2, N-acetylcysteine, epidermal growth factor, noggin, and R-spondin 1. As a result, mouse crypt-derived ISCs had enteroids and spheroid morphologies. We also confirmed by quantitative real-time RT-PCR that expression of ISCs-related specific genes (Lgr5, sox9) and IECs-related specific genes (chromogranin A, defensin-5, mucin-1, mucin-2, and villin) was maintained at eight passages or more. Thus, we observed that expression of specific markers and consecutive self-renewing in the mouse small intestinal crypt-derived organoids.