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Lee, Youngjeon,Lee, Seunghoon,Lee, Sang-Rae,Park, Kanghui,Hong, Yunkyung,Lee, Minkyung,Park, Sookyoung,Jin, Yunho,Chang, Kyu-Tae,Hong, Yonggeun Molecular Diversity Preservation International (MD 2014 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.15 No.2
<P>Endogenous neural stem/progenitor cells (eNSPCs) proliferate and differentiate into neurons and glial cells after spinal cord injury (SCI). We have previously shown that melatonin (MT) plus exercise (Ex) had a synergistic effect on functional recovery after SCI. Thus, we hypothesized that combined therapy including melatonin and exercise might exert a beneficial effect on eNSPCs after SCI. Melatonin was administered twice a day and exercise was performed on a treadmill for 15 min, six days per week for 3 weeks after SCI. Immunohistochemistry and RT-PCR analysis were used to determine cell population for late response, in conjunction with histological examination and motor function test. There was marked improvement in hindlimb function in SCI+MT+Ex group at day 14 and 21 after injury, as documented by the reduced size of the spinal lesion and a higher density of dendritic spines and axons; such functional improvements were associated with increased numbers of BrdU-positive cells. Furthermore, MAP2 was increased in the injured thoracic segment, while GFAP was increased in the cervical segment, along with elevated numbers of BrdU-positive nestin-expressing eNSPCs in the SCI+MT+Ex group. The dendritic spine density was augmented markedly in SCI+MT and SCI+MT+Ex groups. These results suggest a synergistic effect of SCI+MT+Ex might create a microenvironment to facilitate proliferation of eNSPCs to effectively replace injured cells and to improve regeneration in SCI.</P>
Therapeutically Targeting Neuroinflammation and Microglia after Acute Ischemic Stroke
Lee, Youngjeon,Lee, Sang-Rae,Choi, Sung S.,Yeo, Hyeon-Gu,Chang, Kyu-Tae,Lee, Hong J. Hindawi Publishing Corporation 2014 BioMed research international Vol.2014 No.-
<P>Inflammation has a pivotal role in the pathogenesis of ischemic stroke, and recent studies posit that inflammation acts as a double-edged sword, not only detrimentally augmenting secondary injury, but also potentially promoting recovery. An initial event of inflammation in ischemic stroke is the activation of microglia, leading to production of both pro- and anti-inflammatory mediators acting through multiple receptor signaling pathways. In this review, we discuss the role of microglial mediators in acute ischemic stroke and elaborate on preclinical and clinical studies focused on microglia in stroke models. Understanding how microglia can lead to both pro- and anti-inflammatory responses may be essential to implement therapeutic strategies using immunomodulatory interventions in ischemic stroke.</P>
Identification of hyperacute ischemic stroke with a more homogenous nature
Yi, Kyung,Lee, Hong,Lee, Sang-Rae,Lee, Youngjeon,Lee, Seung,Lee, Chulhyun,Cha, Sang-Hoon De Gruyter Open Sp. z o.o. 2014 Translational neuroscience Vol.5 No.2
<B>Abstract</B><P>Previous reports revealed that middle cerebral artery occlusion (MCAO) models in rats were very diverse in nature, and experimental stroke of a more homogenous nature had not been previously documented. This paper aims to present our novel observations of experimental stroke in rats with similar MRI characteristics after MCAO. Immediately after MCAO, 19 rats were placed into a 4.7 T MRI scanner, and diffusion weighted imaging (DWI) of axial and coronal planes was repeated every 10 minutes up to post-occlusion 115 minutes. Apparent diffusion coefficient (ADC) values of the ischemic lesions were calculated and compared to those of the unaffected contra-lateral hemispheres. Successful MCAO was defined when the whole left MCA territory showed ADC abnormality on DWI. Percentage of hemispheric lesion volume (% HLV), relative ADC value (rADC), and relative DWI signal intensity (rDWI) were serially evaluated for quantitative analysis of ADC-derived lesion characteristics. Successful MCA territorial infarction was induced in nine rats (9/19, 47.4%). In quantitative analysis of ADC-derived lesion characteristics, lesion volumes of seven rats (group 1) were very similar, but larger than those of the other two rats (group 2): % HLV of initial MRI = 45.4 ± 2.5 / 19.1 ± 6.6. rADCs and rDWIs of group 1 showed similar patterns of temporal change, which was different from those of group 2. Using prospective diffusion MRI after MCAO in rats, we identified territorial hyperacute ischemic lesions with similar MRI characteristics. This observation would contribute to the establishment of more homogenous rodent models for ischemic stroke translational research.</P>
Alu-Derived Alternative Splicing Events Specific to Macaca Lineages in CTSF Gene
Lee, Ja-Rang,Park, Sang-Je,Kim, Young-Hyun,Choe, Se-Hee,Cho, Hyeon-Mu,Lee, Sang-Rae,Kim, Sun-Uk,Kim, Ji-Su,Sim, Bo-Woong,Song, Bong-Seok,Jeong, Kang-Jin,Lee, Youngjeon,Jin, Yeung Bae,Kang, Philyong,Hu Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.2
Cathepsin F, which is encoded by CTSF, is a cysteine proteinase ubiquitously expressed in several tissues. In a previous study, novel transcripts of the CTSF gene were identified in the crab-eating monkey deriving from the integration of an Alu element-AluYRa1. The occurrence of AluYRa1-derived alternative transcripts and the mechanism of exonization events in the CTSF gene of human, rhesus monkey, and crabeating monkey were investigated using PCR and reverse transcription PCR on the genomic DNA and cDNA isolated from several tissues. Results demonstrated that AluYRa1 was only integrated into the genome of Macaca species and this lineage-specific integration led to exonization events by producing a conserved 3' splice site. Six transcript variants (V1-V6) were generated by alternative splicing (AS) events, including intron retention and alternative 5' splice sites in the 5' and 3' flanking regions of CTSF_AluYRa1. Among them, V3-V5 transcripts were ubiquitously expressed in all tissues of rhesus monkey and crab-eating monkey, whereas AluYRa1-exonized V1 was dominantly expressed in the testis of the crab-eating monkey, and V2 was only expressed in the testis of the two monkeys. These five transcript variants also had different amino acid sequences in the C-terminal region of CTSF, as compared to reference sequences. Thus, species-specific Alu-derived exonization by lineage-specific integration of Alu elements and AS events seems to have played an important role during primate evolution by producing transcript variants and gene diversification.
Autophagy contributes to retardation of cardiac growth in diabetic rats
Youngjeon Lee,Yunkyung Hong,Sang-Rae Lee,Kyu-Tae Chang,Yonggeun Hong 한국실험동물학회 2012 Laboratory Animal Research Vol.28 No.2
Diabetes mellitus is a major predictor of heart failure, although the mechanisms by which the disease causes cardiomyopathy are not well understood. The purpose of this study was to determine whether prolonged exposure of cardiomyocytes to high glucose concentrations induces autophagy and contributes to cardiomyopathy. Interestingly, there were no differences in the autophagic activation produced by different glucose concentrations. However, cell viability was decreased by high glucose. In the diabetic rats, we found a higher level of microtubule-associated protein light chain 3 (LC3) expression and a reduction in the size of the left ventricle (LV) (P<0.05) caused by growth retardation, suggesting activated autophagy. Our in vitro findings indicate that hyperglycemic oxidative stress induces autophagy, and our in vivo studies reveal that autophagy is involved in the progression of pathophysiological remodeling of the heart. Taken together, the studies suggest that autophagy may play a role in the pathogenesis of juvenile diabetic cardiomyopathy.
Prophylactic effects of swimming exercise on autophagy-induced muscle atrophy in diabetic rats
Youngjeon Lee,Joo-Heon Kim,Yunkyung Hong,Sang-Rae Lee,Kyu-Tae Chang,Yonggeun Hong 한국실험동물학회 2012 Laboratory Animal Research Vol.28 No.3
Diabetes decreases skeletal muscle mass and induces atrophy. However, the mechanisms by which hyperglycemia and insulin deficiency modify muscle mass are not well defined. In this study, we evaluated the effects of swimming exercise on muscle mass and intracellular protein degradation in diabetic rats, and proposed that autophagy inhibition induced by swimming exercise serves as a hypercatabolic mechanism in the skeletal muscles of diabetic rats, supporting a notion that swimming exercise could efficiently reverse the reduced skeletal muscle mass caused by diabetes. Adult male Sprague-Dawley rats were injected intraperitoneally with streptozotocin (60 mg/kg body weight) to induce diabetes and then submitted to 1 hr per day of forced swimming exercise, 5 days per week for 4 weeks. We conducted an intraperitoneal glucose tolerance test on the animals and measured body weight, skeletal muscle mass, and protein degradation and examined the level of autophagy in the isolated extensor digitorum longus, plantaris, and soleus muscles. Body weight and muscle tissue mass were higher in the exercising diabetic rats than in control diabetic rats that remained sedentary. Compared to control rats, exercising diabetic rats had lower blood glucose levels, increased intracellular contractile protein expression, and decreased autophagic protein expression. We conclude that swimming exercise improves muscle mass in diabetes-induced skeletal muscle atrophy, suggesting the activation of autophagy in diabetes contributes to muscle atrophy through hypercatabolic metabolism and that aerobic exercise, by suppressing autophagy, may modify or reverse skeletal muscle wasting in diabetic patients.
Lee, Ja-Rang,Kim, Young-Hyun,Park, Sang-Je,Choe, Se-Hee,Cho, Hyeon-Mu,Lee, Sang-Rae,Kim, Sun-Uk,Kim, Ji-Su,Sim, Bo-Woong,Song, Bong-Seok,Jeong, Kang-Jin,Lee, Youngjeon,Jin, Yeung Bae,Kang, Philyong,Hu Hindawi Publishing Corporation 2016 International journal of genomics Vol.2016 No.-
<P><I>TSEN54</I> encodes a subunit of the tRNA-splicing endonuclease complex, which catalyzes the identification and cleavage of introns from precursor tRNAs. Previously, we identified an<I> AluSx</I>-derived alternative transcript in<I> TSEN54</I> of cynomolgus monkey. Reverse transcription-polymerase chain reaction (RT-PCR) amplification and<I> TSEN54</I> sequence analysis of primate and human samples identified five novel alternative transcripts, including the<I> AluSx</I> exonized transcript. Additionally, we performed comparative expression analysis via RT-qPCR in various cynomolgus, rhesus monkey, and human tissues. RT-qPCR amplification revealed differential expression patterns. Furthermore, genomic PCR amplification and sequencing of primate and human DNA samples revealed that<I> AluSx</I> elements were integrated in human and all of the primate samples tested. Intriguingly, in langur genomic DNA, an additional<I> AluY</I> element was inserted into<I> AluSx</I> of intron eight of<I> TSEN54</I>. The new<I> AluY</I> element showed polymorphic insertion. Using standardized nomenclature for<I> Alu</I> repeats, the polymorphic<I> AluY</I> of the langur<I> TSEN54</I> was designated as being of the<I> AluYl17</I> subfamily. Our results suggest that integration of the<I> AluSx</I> element in<I> TSEN54</I> contributed to diversity in transcripts and induced lineage- or species-specific evolutionary events such as alternative splicing and polymorphic insertion during primate evolution.</P>