A rare case of variation of both radial arteries in one female cadaver

Dong Hoon Lee,Gu Seob Roh 대한체질인류학회 2019 대한체질인류학회 학술대회 연제 초록 Vol.62 No.-

Cytoprotective Effects of Serum Hormone Deprivation against Glutamate Toxicity in HT22 Mouse Hippocampal Cells

Eunyung Son,Dong Hoon Lee,Gu Seob Roh,Hyun Joon Kim,Sang Soo Kang,Gyeong Jae Cho,Wan Sung Choi 대한해부학회 2008 Anatomy & Cell Biology Vol.41 No.3

Reactive oxygen species (ROS) are important signaling molecules or mediators in many cellular responses, including the oxidative-burst defense response. Certain hormones are neuroprotective because they are modulators of neuronal activity or ROS scavengers. We have examined the effect of a hormone-free condition on ROS levels following glutamate-induced excitotoxicity in the mouse hippocampal HT22 cell line. We show that hormone starvation slightly elevates ROS and that continuous low concentrations of ROS induce expression of antioxidant enzymes, such as heme oxygenase-1 (HO-1). In addition, N-acetyl-L-cysteine (NAC) restores the expression of ERK1/2 protein in hormone-starved HT22 cells. These findings suggest that whereas high-dose ROS are cytotoxic and lead to tissue damage in the brain low-dose ROS may act in neuroprotective signaling.

Resveratrol blocks diabetes‐induced early vascular lesions and vascular endothelial growth factor induction in mouse retinas

Kim, Young Hee,Kim, Yoon Sook,Roh, Gu Seob,Choi, Wan Sung,Cho, Gyeong Jae Blackwell Publishing Ltd 2012 Acta ophthalmologica Vol.90 No.1

<P><B>Abstract.</B></P><P><B>Purpose: </B> Vessel leakage and loss of pericytes are early signs of diabetic retinopathy (DR), which leads to vision loss. Upregulation of the vascular endothelial growth factor (VEGF) during diabetes plays a key role in mediating these vascular lesions. The aim of this study is to investigate the effects of resveratrol, a natural plant‐derived phytoalexin, on vascular damage and VEGF induction in mouse retinas of early diabetes.</P><P><B>Methods: </B> Diabetes was induced in C57BL/6 mice by five consecutive‐intraperitoneal injections of 55 mg/kg of streptozotocin (STZ). Animals injected with buffer only were used as controls. Beginning 1 month after the fifth injection of STZ or buffer, 20 mg/kg of resveratrol was administered by oral gavage daily for 4 weeks to diabetic and control mice, and all mice were killed 2 months after the injections. We assessed vessel leakage, pericyte loss and VEGF protein expression in mouse retinas of 2‐month diabetes compared with controls with or without resveratrol treatment.</P><P><B>Results: </B> Diabetes led to increase vessel leakage, pericyte loss and VEGF protein level in the mouse retinas compared with controls; however, these changes were effectively blocked by resveratrol treatment.</P><P><B>Conclusion: </B> Our data suggest that resveratrol is effective to decrease vascular lesions and VEGF induction in mouse retinas of early diabetes.</P>

Alteration of glycine receptor immunoreactivity in the auditory brainstem of mice following three months of exposure to radiofrequency radiation at SAR 4.0 W/kg

MASKEY, DHIRAJ,KIM, HYUNG GUN,SUH, MYUNG-WHAN,ROH, GU SEOB,KIM, MYEUNG JU D.A. Spandidos 2014 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.34 No.2

<P>The increasing use of mobile communication has triggered an interest in its possible effects on the regulation of neurotransmitter signals. Due to the close proximity of mobile phones to hearing-related brain regions during usage, its use may lead to a decrease in the ability to segregate sounds, leading to serious auditory dysfunction caused by the prolonged exposure to radiofrequency (RF) radiation. The interplay among auditory processing, excitation and inhibitory molecule interactions plays a major role in auditory function. In particular, inhibitory molecules, such a glycine, are predominantly localized in the auditory brainstem. However, the effects of exposure to RF radiation on auditory function have not been reported to date. Thus, the aim of the present study was to investigate the effects of exposure to RF radiation on glycine receptor (GlyR) immunoreactivity (IR) in the auditory brainstem region at 835 MHz with a specific absorption rate of 4.0 W/kg for three months using free-floating immunohistochemistry. Compared with the sham control (SC) group, a significant loss of staining intensity of neuropils and cells in the different subdivisions of the auditory brainstem regions was observed in the mice exposed to RF radiation (E4 group). A decrease in the number of GlyR immunoreactive cells was also noted in the cochlear nuclear complex [anteroventral cochlear nucleus (AVCN), 31.09%; dorsal cochlear nucleus (DCN), 14.08%; posteroventral cochlear nucleus (PVCN), 32.79%] and the superior olivary complex (SOC) [lateral superior olivary nucleus (LSO), 36.85%; superior paraolivary nucleus (SPN), 24.33%, medial superior olivary nucleus (MSO), 23.23%; medial nucleus of the trapezoid body (MNTB), 10.15%] of the mice in the E4 group. Auditory brainstem response (ABR) analysis also revealed a significant threshold elevation of in the exposed (E4) group, which may be associated with auditory dysfunction. The present study suggests that the auditory brainstem region is susceptible to chronic exposure to RF radiation, which may affect the function of the central auditory system.</P>

FK506 reduces calpain-regulated calcineurin activity in both the cytoplasm and the nucleus

Sun Hee Lee,Jungil Choi,Hwa jin Kim,Dong Hoon Lee,Gu Seob Roh,Hyun Joon Kim,Sang Soo Kang,Wan Sung Choi,Gyeong Jae Cho 대한해부학회 2014 Anatomy & Cell Biology Vol.47 No.2

Excessive immune responses induced by ischemia-reperfusion injury (IRI) are known to lead to necrotic and apoptotic cell death, and calcineurin plays a major role in this process. Calcineurin dephosphorylates the nuclear factor of activated T-cells (NFAT), permitting its translocation into the nucleus. As a result, calcineurin promotes the release of pro-inflammatory cytokines, such as tumor necrosis factor-α. The overproduction of pro-inflammatory cytokines causes renal cell death. Calcineurin activity is regulated by calpain, a cysteine protease present in the nucleus. Calpain-mediated proteolysis increases the phosphatase activity of calcineurin, resulting in NFAT dephosphorylation. This process has been studied in cardiomyocytes but its role in renal IRI is unknown. Thus, we examined whether calpain regulates calcineurin in renal tubule nuclei. We established an in vivo renal IRI model in mice and identified the protective role of a calcineurin inhibitor, FK506, in this process. Calcineurin is expressed in the nucleus, where it is present in its calpain-cleaved form. FK506 reduced nuclear expression of calcineurin and prevented calcineurin-mediated NFAT activation. Our study shows clearly that FK506 reduces calpain-mediated calcineurin activity. Consequently, calcineurin could not maintain NFAT activation. FK506 reduced renal cell death by suppressing the transcription of pro-inflammatory cytokine genes. This study provides evidence that FK506 protects against inflammation in a renal IRI mouse model. We also provided a mechanism of calcineurin action in the nucleus. Therefore, FK506 could improve renal function by decreasing calcineurin activity in both the cytoplasm and the nucleus of renal tubule cells.

Alpha-lipoic acid reduces retinal cell death in diabetic mice

Kim, Yoon Sook,Kim, Minjun,Choi, Mee Young,Lee, Dong Hoon,Roh, Gu Seob,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Hong, Eun-Kyung,Choi, Wan Sung Elsevier 2018 Biochemical and biophysical research communication Vol.503 No.3

<P><B>Abstract</B></P> <P>Oxidative stress plays an important role in the development of diabetic retinopathy. Here, we examined whether α-lipoic acid (α-LA), a natural antioxidant, attenuated retinal injury in diabetic mice. The α-LA was orally administered to control mice or mice with streptozotocin-induced diabetes. We found that α-LA reduced oxidative stress, decreased and increased retinal 4-hydroxy-2-nonenal and glutathione peroxidase, respectively, and inhibited retinal cell death. Concomitantly, α-LA reversed the decreased activation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase, and increased the levels of peroxisome proliferator-activated receptor delta and sirtuin3 in diabetic mouse retinas, similar to results shown after metformin treatment of retinal pigment epithelial cells (RPE) exposed to high glucose. Moreover, α-LA lowered the levels of O-linked β-<I>N</I>-acetylglucosamine transferase (OGT) and thioredoxin-interacting protein (TXNIP) in diabetic retinas that were more pronounced after metformin treatment of RPE cells. Importantly, α-LA lowered interactions between AMPK and OGT as shown by co-immunoprecipitation analyses, and this was accompanied by less cell death as measured by double immunofluorescence staining by terminal deoxynucleotide transferase-mediated dUTP nick-end labelling and OGT or TXNIP in retinal ganglion cells. Consistently, α-LA lowered the levels of cleaved poly(ADP-ribose) polymerase and pro-apoptotic marker cleaved caspase-3 in diabetic retinas. Our results indicated that α-LA reduced retinal cell death partly through AMPK activation or OGT inhibition in diabetic mice.</P> <P><B>Highlights</B></P> <P> <UL> <LI> α-LA reduces oxidative stress in diabetic mouse retinas. </LI> <LI> α-LA increases p-AMPK, p-ACC, PPARδ, and SIRT3 in diabetic mouse retinas. </LI> <LI> α-LA decreases OGT, TXNIP, and cleaved-PARP and -caspase-3 in diabetic mouse retinas. </LI> <LI> α-LA decreases AMPK interaction with OGT, reducing retinal injuries in diabetic mice. </LI> </UL> </P>

Metformin protects against retinal cell death in diabetic mice

Kim, Yoon Sook,Kim, Minjun,Choi, Mee Young,Lee, Dong Hoon,Roh, Gu Seob,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Kim, Seong-Jae,Yoo, Ji-Myong,Choi, Wan Sung Elsevier 2017 Biochemical and biophysical research communication Vol.492 No.3

<P><B>Abstract</B></P> <P>Retinal degeneration is an early feature of diabetic retinopathy, the major cause of blindness in the developed world. Here we investigated how the widely used antidiabetic drug metformin reduces retinal injury in diabetic mice. Metformin was orally administered to control mice or mice with streptozotocin-induced diabetes. Western blot analysis showed that levels of O-linked β-<I>N</I>-acetylglucosamine (O-GlcNAc) transferase (OGT) and other related proteins such as carbohydrate-responsive element-binding protein (ChREBP) and thioredoxin-interacting protein (TXNIP) were significantly increased, and nuclear factor kappaB (NF-κB) and poly (ADP-ribose) polymerase (PARP) were activated in the diabetic retinas or retinal pigment epithelial (RPE) cells exposed to high glucose compared to controls. More importantly, RPE cells exposed to high glucose and treated with thiamet-G had higher levels of those proteins, demonstrating the role of elevated O-GlcNAcylation. Double immunofluorescence analysis revealed increased co-localization of terminal deoxynucleotide transferase-mediated dUTP nick-end labelling (TUNEL)-positive ganglion cells and OGT, ChREBP, TXNIP, or NF-κB in diabetic retinas compared to control retinas. Co-immunoprecipitation analysis showed that interaction between OGT and ChREBP or NF-κB was increased in diabetic retinas compared to control retinas, and this was accompanied by more cell death. Notably, metformin attenuated the increases in protein levels; reduced co-localization of TUNEL-positive ganglion cells and OGT, ChREBP, TXNIP, or NF-κB; and reduced interaction between OGT and ChREBP or NF-κB. Our results indicate that OGT inhibition might be one of the mechanisms by which metformin decreases retinal cell death.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Metformin decreases OGT, ChREBP, and TXNIP in the diabetic mouse retina. </LI> <LI> Metformin decreases NF-κB and PARP activation in diabetic mouse retinas. </LI> <LI> Metformin inhibits OGT interaction with ChREBP, decreasing retinal cell death. </LI> <LI> Metformin inhibits OGT interaction with NF-κB, decreasing retinal cell death. </LI> </UL> </P>

C-jun N-terminal kinase regulates the interaction between 14-3-3 and Bad in ethanol-induced cell death

Han, Jae Yoon,Jeong, Eun Young,Kim, Yoon Sook,Roh, Gu Seob,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung Wiley Subscription Services, Inc., A Wiley Company 2008 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.86 No.14

<P>Activation of the c-jun N-terminal kinase (JNK) is known to be an important step during ethanol-induced cell death, but it has yet to be identified how JNK regulates apoptosis. Therefore, we investigated the mechanism by which JNK induces cell death following ethanol treatment. Ethanol (6 g/kg, 20% in saline) was administered subcutaneously to postnatal 7 day rat pups. Twelve hours after the first ethanol administration, rat pups were decapitated, and extracts of total protein from cerebral cortices were prepared. Ethanol exposure induced phosphorylation of JNK but did not affect the expression levels of pro- and antiapoptotic proteins. Furthermore, interactions of phospho-JNK (p-JNK) with 14-3-3 as well as with Bad were enhanced in the cerebral cortices of ethanol-treated rats. Pretreatment with JNK inhibitor (SP600125) of SH-SY5Y cells inhibited JNK phosphorylation and interaction between p-JNK and 14-3-3 resulting from ethanol. Furthermore, 14-3-3 interaction with Bad was diminished in the cerebral cortices of ethanol-treated rats. These findings suggest that JNK induces Bad release from 14-3-3 by inhibiting their interaction. After this event, Bad binds to Bcl-xL, releasing Bax from Bcl-xL and leading to cell death. We hypothesize that JNK may play an important role during ethanol-induced cell death via the inhibition of antiapoptotic function of 14-3-3 as well as activation of proapoptotic function of Bad. © 2008 Wiley-Liss, Inc.</P>

Anti-obesity Activity of Ethanol Extract from Bitter Melon in Mice Fed High-Fat Diet

Yoon, Nal Ae,Park, Juyeong,Jeong, Joo Yeon,Rashidova, Nilufar,Ryu, Jinhyun,Roh, Gu Seob,Kim, Hyun Joon,Cho, Gyeong Jae,Choi, Wan Sung,Lee, Dong Hoon,Kang, Sang Soo The Korean Society of Developmental Biology 2019 발생과 생식 Vol.23 No.2

In many cases, obesity is associated with metabolic disorders. Recently, natural compounds that may be beneficial for improving obesity have received increasing attention. Bitter melon has received attention as a diabetes treatment. $NAD^+$-dependent deacetylase (Sirtuin 1, SIRT1) has emerged as a novel therapeutic target for metabolic diseases. In this study, ethanol extract of bitter melon (BME) suppressed adipocyte differentiation and significantly increased the expression of SIRT1 in fully differentiated 3T3-L1 cells. Moreover, it enhanced the activation of AMP-activated protein kinase (AMPK). In high-fat diet (HFD)-fed induced-obesity mice, BME suppressed HFD-induced increases in body weight and white adipose tissue (WAT) weight. BME also increased the expression of SIRT1 and suppressed peroxisome proliferator-activated receptor and sterol regulatory element binding protein 1 expressions of WAT from HFD-fed mice. These findings suggest that BME prevents obesity by activating the SIRT1 and AMPK pathway and that it may be a useful dietary supplement for preventing obesity.

Altered gene expression of caspase-10, death receptor-3 and IGFBP-3 in preeclamptic placentas /

Han, Jae Yoon,Kim, Yoon Sook,Cho, Gyeong Jae,Roh, Gu Seob,Kim, Hyun Joon,Choi, Won Jun,Paik, Won Young,Rho, Gyu Jin,Kang, Sang Soo,Choi, Wan Sung Korean Society for Molecular and Cellular Biology 2006 Molecules and cells Vol.22 No.2