• 한국육종학회지
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• 제42권5호
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• pp.565-573
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• 2010

사과의 경우 한 과총에 5개의 꽃이 피는데 그 중 한 가운데의 중심화가 먼저 개화하여 과일로 발달하고 주위의 측과 4개는 스스로 낙과되는 현상을 자가적과성이라고 한다. 적과는 인위적으로 과실의 숫자를 줄여 잎 수와 과실 수의 균형을 맞추는 작업으로 과실의 크기를 증가시키고, 수세, 수형을 유지시켜 안정적인 생산에 도움을 준다. 노동력 절감을 위해 인간에게 유용하게 사용될 수 있는 특성이 자가적과성인데, 자가적과성 품종의 사과에서 측과는 만개 후 30일 이내에 떨어지고 중심과만 남아서 성숙하게 된다. 51개의 사과 품종으로부터 비자가적과성 그룹 20종, 6월 생리적 낙과 그룹 16종, 자가적과성 그룹 15종을 분류하였다. 대표적인 자가적과성 품종인 Aori #9 로부터 중심과와 측과에서 다르게 발현이 되는 유전자들을 DD-PCR 방법으로 확인하였다. 중심과에서 30개의 clones 과 측과에서 24개의 clones을 선발하여 염기서열을 분석하였다. 주로 측과에서 발현되는 유전자들은 pathogenesis, senescence, temperature stress, protein degradation, fruit browning, sorbitol metabolism에 관여하는 유전자들과 높은 상동성을 나타내고, 중심과에서 발현되는 유전자들의 염기서열을 분석해 보면 anthocyanin의 up-regulation이나 flavonol 생합성, ethylene 생합성에 관여하는 유전자들이 분포한다. Cytochrome P450 유전자의 발현양상을 보기 위해 Real time PCR 분석을 한 결과 중심과보다 측과에서 발현량이 높게 나타났다. 중심과와 측과에서 다르게 발현되는 유전자들의 실제 발현양상을 분석하기 위해 Real time PCR을 이용해서 상대정량을 분석할 계획이며 분자수준에서의 자가적과를 조절하는 기작에 대한 앞으로의 연구는 생력 재배가 가능한 품종 육성의 육종 소재 개발에 활용될 수 있을 것이다.

• 한국가금학회지
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• 제44권1호
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• pp.1-9
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• 2017

본 연구는 한국재래계(KNC)와 백색레그혼(WLH)에서 lipopolysaccharide(LPS)감염 스트레스가 닭의 품종간 스트레스 연관 유전자들의 발현에 미치는 영향을 비교 분석하고자 실시되었다. 공시계를 대상으로 생리식염수(대조구)와 LPS(처리구)를 복강에 투여한 후, 시간(0, 48 hr) 및 처리별 각 개체로부터 간 조직을 취하고, microarray 및 quantitative RT-PCR(qRT-PCR) 분석을 하였다. 처리에 따른 유전자 발현차이를 보면, KNC(대조구)와 KNC에 LPS를 처리한 경우(KNC-LPS)를 비교한 결과, 대조구 대비 2배 이상 유전자의 발현이 증가한 유전자의 수는 1,044개, 발현이 감소한 유전자의 수는 1,000개였다. WLH(대조구)를 WLH-LPS와 비교한 경우, 유전자의 발현이 증가한 유전자의 수는 1,193개, 발현이 감소한 유전자의 수는 1,072개였다. LPS 처리에 따른 스트레스 연관 유전자들의 microarray 발현에서 스트레스연관 유전자들의 발현은 두 품종 모두에서 감소하였으며, 품종 간 차이는 없는 것으로 나타났다. Microarray의 결과를 바탕으로 HSP90, HMGCR, ATF4, SREBP1, XBP1 등의 유전자 발현을 qRT-PCR을 이용하여 검증한 결과, 대조구와 LPS 감염구 간에 유의적 차이를 나타내었다(P<0.05). 세포 수준의 스트레스(ER 스트레스)에서 ATF4, XBP1, SREBP1은 화이트레그혼에서 microarray와 qRT-PCR에서와 같이 이들 유전자들의 발현이 억제되는 것을 보여주었다. 그러나 한국 재래계에서는 ATF4를 제외한 유전자들은 LPS에 의해 영향을 받지 않거나(XBP1), 오히려 증가(SREBP)하는 양상을 보였다. ER-stress 연관 유전자들의 발현 양상으로 볼 때, KNC이 WLH에 비하여 LPS 감염에 더 민감하게 반응하는 것으로 보인다. HMGCR은 두 품종간에 LPS에 의한 상호작용이 없는 것으로 보아, HMGCR 발현에 의한 감염 차이점을 찾을 수 없었다. 한국재래계에서 HSP70은 LPS 처리 후에 대조구에 비하여 약 2.5배 이상 높은 발현을 보였으나, 백색 레그혼에서는 낮은 발현 양상을 나타내었다. 스트레스 지표 유전자들의 종류뿐만 아니라, 스트레스 종류(예: 환경스트레스, 감염스트레스)에 따라 유전자들의 발현 반응에 차이가 있음을 보여주었다. LPS 감염스트레스에 따른 스트레스연관 유전자 발현연구는 닭의 품종별 질병 저항성 및 동물복지 관련 지표의 탐색에 기여할 것으로 사료된다.

• 원예과학기술지
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• 제33권6호
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• pp.923-931
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• 2015

본 연구는 일시적인 고온 스트레스 처리가 복색 장미 'Pinky Girl'의 화아 착색과 안토시아닌 생합성 관련 유전자들의 발현 양상에 미치는 영향을 알아보고자 수행되었다. 꽃잎에서 cyanin의 축적은 화아의 발육단계와 연관이 있으며 화아 발육 과정에서 꽃잎이 출현하는 4단계($S_4$)에서 급격하게 일어났다. 따라서 $S_4$ 단계가 꽃잎 착색에 가장 민감한 시기로 판단된다. $S_4$ 단계에서 3일간 고온 스트레스($39/18^{\circ}C$)를 받은 고온처리구에서 개화 당시 꽃잎의 cyanin 착색이 대조구와 비교하여 45.5% 감소하였다. 한편, 안토시아닌 생합성 관련 유전자인 CHS, CHI, F3'H, DFR, ANS, 3GT, 5GT의 발현은 고온처리구에서 오히려 촉진되었다. 예외적으로 F3H의 발현은 고온처리구에서 26.7% 감소하여 'Pinky Girl'의 복색 발현에 의미 있는 유전자로 확인되었다. 하지만 대부분 안토시아닌 생합성 관련 유전자들의 발현은 꽃잎에서의 cyanin 착색 경향과 비례적이지 않았다. 따라서 장미 꽃잎의 화색소 축적은 번역 이후 효과와 조절유전자와 같은 안토시아닌 생합성과 관련된 다른 복잡한 메커니즘이 연관되어 있을 것으로 판단되었다.

• Clinical Psychopharmacology and Neuroscience
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• 제16권4호
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• pp.422-433
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• 2018

Objective: Neuropsychiatric manifestations like depression and cognitive dysfunction commonly occur in inflammatory bowel disease (IBD). In the context of the brain-gut axis model, colitis can lead to alteration of brain function in a bottom-up manner. Here, the changes in the response of the hypothalamic-pituitary-adrenal axis and inflammation-related markers in the brain in colitis were studied. Methods: Dextran sodium sulfate (DSS) was used to generate a mouse model of colitis. Mice were treated with DSS for 3 or 7 days and sacrificed. We analyzed the gene expression of brain-derived neurotrophic factor (BDNF), cyclooxygenase 2 (COX-2), and glial fibrillary acidic protein (GFAP), and the expression of GFAP, in the hippocampus, hypothalamus, and amygdala. Additionally, the levels of C-reactive protein (CRP) and serum cortisol/corticosterone were measured. Results: Alteration of inflammatory-related markers varied depending on the brain region and exposure time. In the hippocampus, COX-2 mRNA, GFAP mRNA, and GFAP expression were upregulated during exposure to DSS. However, in the hypothalamus, COX-2 mRNA was upregulated only 3 days after treatment. In the amygdala, BDNF and COX-2 mRNAs were downregulated. CRP and corticosterone expression increased with DSS treatment at day 7. Conclusion: IBD could lead to neuroinflammation in a bottom-up manner, and this effect varied according to brain region. Stress-related hormones and serum inflammatory markers, such as CRP, were upregulated from the third day of DSS treatment. Therefore, early and active intervention is required to prevent psychological and behavioral changes caused by IBD, and region-specific studies can help understand the precise mechanisms by which IBD affects the brain.

• Asian Pacific Journal of Cancer Prevention
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• 제17권4호
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• pp.1967-1971
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• 2016

Background: In tumor cells, aberrant differentiation programs have been described. Several neuronal proteins have been found associated with morphological neuronal-glial changes in breast cancer (BCa). These neuronal proteins have been related to mechanisms that are involved in carcinogenesis; however, this regulation is not well understood. Microtubule-associated protein-tau (MAP-Tau) has been describing in BCa but not its variants. This finding could partly explain the neuronal-glial morphology of BCa cells. Our aim was to determine mRNA expression of MAP-tau variants 2, 4 and 6 in breast cancer cell lines. Materials and Methods: Cultured cell lines MCF-10A, MDA-MB-231, SKBR3 and T47D were observed under phase-contrast microscopy for neural morphology and analyzed for gene expression of MAP-Tau transcript variants 2, 4 and 6 by real-time PCR. Results: Regarding morphology like neural/glial cells, T47D line shown more cells with these features than MDA-MB-231 and SKBR. In another hand, we found much greater mRNA expression of MAP-Tau transcript variants 2, and to a lesser extent 4 and 6, in T47D cells than the other lines. In conclusion, regulation of MAP-Tau could bring about changes in cytoskeleton, cell morphology and motility; these findings cast further light on neuronal transdifferentiation in BCa.

• IMMUNE NETWORK
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• 제11권6호
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• pp.376-382
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• 2011

Background: Carbon monoxide (CO) is a cytoprotective and homeostatic molecule with important signaling capabilities in physiological and pathophysiological situations. CO protects cells/tissues from damage by free radicals or oxidative stress. NAD(P)H:quinone oxidoreductase (NQO1) is a highly inducible enzyme that is regulated by the Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway, which is central to efficient detoxification of reactive metabolites and reactive oxygen species (ROS). Methods: We generated NQO1 promoter construct. HepG2 cells were treated with CO Releasing Molecules-2 (CORM-2) or CO gas and the gene expressions were measured by RT-PCR, immunoblot, and luciferase assays. Results: CO induced expression of NQO1 in human hepatocarcinoma cell lines by activation of Nrf2. Exposure of HepG2 cells to CO resulted in significant induction of NQO1 in dose- and time-dependent manners. Analysis of the NQO1 promoter indicated that an antioxidant responsible element (ARE)-containing region was critical for the CO-induced Nrf2-dependent increase of NQO1 gene expression in HepG2 cells. Conclusion: Our results suggest that CO-induced Nrf2 increases the expression of NQO1 which is well known to detoxify reactive metabolites and ROS.

• IMMUNE NETWORK
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• 제6권1호
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• pp.6-12
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• 2006

Background: The Hypothalamo-Pituitary-Adrenal (HPA) axis is an important regulator for the body's stress response. As a primary stress responsive system, HPA-axis secretes various neurotransmitters, hormones, and cytokines, which regulates the immune system. Natural killer (NK) cell which is plays an important role in the innate immune response, is specially decreased their numbers and loose cytolytic activity in response to stress. However, the effect of HPA-axis secreted proteins on NK cell activity has not been defined. Herein, we studied the effect of adrenal secreted adiponectin on NK cell cytotoxicity. Adiponectin which is well-known metabolic control protein, plays important roles in various diseases, including hypertension, cardiovascular diseases, inflammatory disorders, and cancer. Methods: Signal sequence trap was used to find stress novel secretory protein from HP A-axis. Selected adiponectin was treated mouse mature primary NK cells and then examined the effect of adiponectin to NK cell cytotoxicity and cytokine expression level. Results: We found that adiponectin which is secreted from adrenal gland, suppress IL-2 induced NK cell cytotoxicity. And also investigated cytolytic cytokines are suppressed by adiponectin. Conclusion: These data suggest that adiponectin inhibites NK cell cytotoxicity via suppression of cytotoxicity related target gene.

• Genomics & Informatics
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• 제7권2호
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• pp.97-106
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• 2009

Epigallocatechin gallate (EGCG), a well-known antioxidant molecule, has been reported to cause hepatotoxicity when used in excess. However, the mechanism underlying EGCG-induced hepatotoxicity is still unclear. To better understand the mode of action of EGCG-induced hepatotoxicity, we examined the effect of EGCG on human hepatic gene expression in HepG2 cells using microarrays. Analyses of microarray data revealed more than 1300 differentially expressed genes with a variety of biological processes. Upregulated genes showed a primary involvement with protein-related biological processes, such as protein synthesis, protein modification, and protein trafficking, while downregulated genes demonstrated a strong association with lipid transport. Genes involved in cellular stress responses were highly upregulated by EGCG treatment, in particular genes involved in endoplasmic reticulum (ER) stress, such as GADD153, GADD34, and ATF3. In addition, changes in genes responsible for cholesterol synthesis and lipid transport were also observed, which explains the high accumulation of EGCG-induced lipids. We also identified other regulatory genes that might aid in clarifying the molecular mechanism underlying EGCG-induced hepatotoxicity.

• 한국식품저장유통학회지
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• 제24권4호
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• pp.536-541
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• 2017

Hyperglycemia found in diabetes mellitus causes several physiological abnormalities including the formation of advanced glycation end products (AGEs) and oxidative stress. Accumulation of AGEs and elevation of oxidative stress plays major roles in the development of diabetic complications. Adiponectin secreted from adipocytes is known to improve insulin sensitivity and blood glucose level. Curcumin (CCM), a bioactive component of turmeric, has been reported as a potent antioxidant. Present work aimed to elucidate the roles of CCM in high glucose-induced protein glycation and intracellular events in mature adipocytes. The results demonstrated that CCM inhibited the formation of fluorescent AGEs by approximated 52% at 3 weeks of bovine serum albumin (BSA) glycation with glucose. Correspondingly, CCM decreased the levels of fructosamine and ${\alpha}-dicarbonyl$ compounds during BSA glycation with glucose. These data suggested that CCM might be a new promising anti-glycation agent. Also, CCM reduced high glucose-induced oxidative stress in a dose dependent manner, whereas CCM treatment time-dependently elevated the expression of adiponectin gene in 3T3-L1 adipocytes. The findings from this study suggested the possibility of therapeutic use of CCM for the prevention of diabetic complications and obesity-related diseases.

• 생물정신의학
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• 제8권1호
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• pp.3-19
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• 2001

Recent basic and clinical studies demonstrate a major role for neural plasticity in the etiology and treatment of depression and stress-related illness. The neural plasticity is reflected both in the birth of new cell in the adult brain(neurogenesis) and the death of genetically healthy cells(apoptosis) in the response to the individual's interaction with the environment. The neural plasticity includes adaptations of intracellular signal transduction pathway and gene expression, as well as alterations in neuronal morphology and cell survival. At the cellular level, repeated stress causes shortening and debranching of dendrite in the CA3 region of hippocampus and suppress neurogenesis of dentate gyrus granule neurons. At the molecular level, both form of structural remodeling appear to be mediated by glucocorticoid hormone working in concert with glutamate and N-methyl-D-aspartate(NMDA) receptor, along with transmitters such as serotonin and GABA-benzodiazepine system. In addition, the decreased expression and reduced level of brain-derived neurotrophic factor(BDNF) could contribute the atrophy and decreased function of stress-vulnerable hippocampal neurons. It is also suggested that atrophy and death of neurons in the hippocampus, as well as prefrontal cortex and possibly other regions, could contribute to the pathophysiology of depression. Antidepressant treatment could oppose these adverse cellular effects, which may be regarded as a loss of neural plasticity, by blocking or reversing the atrophy of hippocampal neurons and by increasing cell survival and function via up-regulation of cyclic adenosine monophosphate response element-binding proteins(CREB) and BDNF. In this article, the molecular and cellular mechanisms that underlie stress, depression, and action of antidepressant are precisely discussed.