• BMB Reports
• /
• v.44 no.7
• /
• pp.478-483
• /
• 2011

Hairless (HR), a transcriptional cofactor, is highly expressed in the skin and brain. To characterize the effects of HR expression in the skin, we examined its capacity for transcriptional regulation of its target genes in mouse skin and keratinocytes. We found that Foxe1 mRNA expression was suppressed in HR-overexpressing skin, as well as in HR-expressing keratinocytes. In turn, Msx1 expression was downregulated contingent on Foxe1 downregulation in skin and keratinocytes. We also found that expression of Sfrp1 was also correlated with that of Foxe1. Further investigation of the mechanisms involved in the transcriptional regulation of these genes will facilitate our understanding of the relationship among genes involved in hair follicle morphogenesis and cycling.

• BMB Reports
• /
• v.49 no.8
• /
• pp.405-413
• /
• 2016

Tau proteins, which stabilize the structure and regulate the dynamics of microtubules, also play important roles in axonal transport and signal transduction. Tau proteins are missorted, aggregated, and found as tau inclusions under many pathological conditions associated with neurodegenerative disorders, which are collectively known as tauopathies. In the adult human brain, tau protein can be expressed in six isoforms due to alternative splicing. The aberrant splicing of tau pre-mRNA has been consistently identified in a variety of tauopathies but is not restricted to these types of disorders as it is also present in patients with non-tau proteinopathies and RNAopathies. Tau mis-splicing results in isoform-specific impairments in normal physiological function and enhanced recruitment of excessive tau isoforms into the pathological process. A variety of factors are involved in the complex set of mechanisms underlying tau mis-splicing, but variation in the cis-element, methylation of the MAPT gene, genetic polymorphisms, the quantity and activity of spliceosomal proteins, and the patency of other RNA-binding proteins, are related to aberrant splicing. Currently, there is a lack of appropriate therapeutic strategies aimed at correcting the tau mis-splicing process in patients with neurodegenerative disorders. Thus, a more comprehensive understanding of the relationship between tau mis-splicing and neurodegenerative disorders will aid in the development of efficient therapeutic strategies for patients with a tauopathy or other, related neurodegenerative disorders.

• Molecular & Cellular Toxicology
• /
• v.5 no.1
• /
• pp.1-6
• /
• 2009

Microglial cells constitute the first line of defense against infection and injury in the brain. This study was conducted to evaluate the protective mechanisms of Agrimonia pilosa (AP) on LPS-induced activation of BV-2 microglial cells. The effects of AP on gene expression profiles in activated BV-2 microglial cells were evaluated using microarray analysis. BV-2 microglial cells were cultured in a 100 mm dish ($1{\times}10^7/mL$) for 24 hr and then pretreated with 1 g/mL AP or left untreated for 30 min. Next, 1 g/mL LPS was added to the samples and the cells were reincubated at $37^{\circ}C$ for 30 min, 3 hr and 6 hr. The gene expression profiles of the BV-2 microglial cells varied depending on the AP. The microarray analysis revealed that MAPK signaling pathway-related genes were down-regulated and IL10 gene was up-regulated in AP-treated BV-2 microglial cells. AP can affect the inflammatory response and MAPK pathway in BV-2 microglial cells.

• The Journal of Korean Physical Therapy
• /
• v.22 no.3
• /
• pp.31-35
• /
• 2010

Purpose: The aim of this study was to use fMRI and clinical prognosis criteria to evaluate therapeutic interventions in stroke patients with corona radiata infarct and acquire fundamental information about recovery mechanisms. Methods: Four subjects (2 men, 2 women) who had strokes with corona radiata infarct were recruited. For all subjects, motor functions such as motricity index (MI), modified brunnstrom classification (MBC), functional ambulatory category (FAC), and bathel index (BI) were evaluated. Evaluations were done at least 4 times over a period of approximately 6~7 months from stroke onset. We compared the final evaluation with the first. Results: All patients with corona radiata infarct showed improvement in motor outcomes with the passing of time. The strength of all patients improved from zero or trace levels to normal or good levels in the MI (Motricity Index) test. Other motor outcomes including the modified brunnstrom classification (MBC), the functional ambulatory category (FAC), and the bathel index (BI) also improved with the passing of time. Conclusion: Stroke patients with corona radiata infarcts change for the better over time. Therefore, one can introduce clinical interventions by the aspect of progress in functional motor recovery.

• Toxicological Research
• /
• v.24 no.3
• /
• pp.169-174
• /
• 2008

This study examined the mechanisms underlying the effects of the vasorelaxation active substance(VAS), dimethyladenosine-5'-L-arabinose, and its partial purification fraction on nitric oxide synthase in improving erectile dysfunction with particular focus on the nitric oxide (NO)-cGMP pathways. Two rat models, 9-month-old SD rats and 11-month-old SD rats, were given VAS(40 mg/kg per day) for 4 days, The aqueous fraction of silworm male pupae extract; semi-purified VAS(100 mg/kg per day) for 10 days, respectively. The NOS activities of the following three enzymes were examined: neuronal NO synthase(nNOS), inducible NOS(iNOS), endothelial NOS(eNOS), vascular endothelial growth factor on endothelial cells(VEGF) and anti-inflammation effect of Tumor necrosis factor-$\alpha$. The results showed increases in the nitric oxide synthase activities. Western blotting of the tissue homogenate showed an increase in the nNOS level in the brain and tongue, and an increase in the endothelial NO synthase(eNOS) level in penis. However, there was little association with VEGF production in HUVEC endothelial cells and no relationship with TNF-$\alpha$ which showed low levels.

• BMB Reports
• /
• v.49 no.10
• /
• pp.529-535
• /
• 2016

The NLRP3 inflammasome is activated by a variety of external or host-derived stimuli and its activation initiates an inflammatory response through caspase-1 activation, resulting in inflammatory cytokine IL-1β maturation and secretion. The NLRP3 inflammasome activation is a kind of innate immune response, most likely mediated by myeloid cells acting as a host defense mechanism. However, if this activation is not properly regulated, excessive inflammation induced by overactivated NLRP3 inflammasome can be detrimental to the host, causing tissue damage and organ dysfunction, eventually causing several diseases. Previous studies have suggested that mitochondrial damage may be a cause of NLRP3 inflammasome activation and autophagy, which is a conserved self-degradation process that negatively regulates NLRP3 inflammasome activation. Recently, mitochondria-selective autophagy, termed mitophagy, has emerged as a central player for maintaining mitochondrial homeostasis through the elimination of damaged mitochondria, leading to the prevention of hyperinflammation triggered by NLRP3 inflammasome activation. In this review, we will first focus on the molecular mechanisms of NLRP3 inflammasome activation and NLRP3 inflammasome-related diseases. We will then discuss autophagy, especially mitophagy, as a negative regulator of NLPP3 inflammasome activation by examining recent advances in research.

• Journal of Korean Neurosurgical Society
• /
• v.30 no.10
• /
• pp.1220-1223
• /
• 2001

Authors experienced a unique case of craniopharyngioma which had evolved rapidly after 4 years of total resection for supratentorial meningioma. A 58-year-old woman presented with headache and visual deterioration. Previously, she had undertaken surgical removal of frontal convexity meningioma 4 years ago and had been well without any postoperative sequelae thereafter. Brain magnetic resonance imaging demonstrated a newly developed suprasellar mass. Pertinent operative procedure was performed and histological verification was made as an adamantinomatous craniopharyngioma. She has been showing unremarkable clinical course up to date. Possible pathogenic mechanisms of de novo development of craniopharyngioma are disscussed with review of case.

• Korean Journal of Biological Psychiatry
• /
• v.5 no.2
• /
• pp.197-209
• /
• 1998

In mordern society, nutritional and appetite disorders occur in epidemic proportions and are serious health harzards. Obesity and diabetes affect over 30% of American population, while eating disorders, such as anorexia nervosa and bulimia nervosa occur in a growing number of adolescences and young adults. The changes in various sociocultural aspects with the introduction of Westernized culture have had the effect of increasing the risk of same problems in Korea. Disorderd eating patterns are a primary symptom of numerous psychiatric disorders and loss of appetite and cachexia, during illness or in the elderly, preclude proper medical treatment for restoring good health or preserving life. Increased understanding of the systems of the body and brain, related to energy and nutrient balance, may help us to treatment and ultimately prevent these commom disorders. In this review, the author highlights the psychobiological mechanisms or factors which are associated with eating behavior, especially in the view of intake psychobiology. This review would be concentrated on 1) the theoretical concepts and theories of eating behavior ; 2) the psychobiological determinants of food intake ; and 3) the psychobiological control of eating behavior.

• BMB Reports
• /
• v.46 no.12
• /
• pp.567-574
• /
• 2013

Liver plays a major role in maintaining glucose homeostasis in mammals. Under fasting conditions, hepatic glucose production is critical as a source of fuel to maintain the basic functions in other tissues, including skeletal muscle, red blood cells, and the brain. Fasting hormones glucagon and cortisol play major roles during the process, in part by activating the transcription of key enzyme genes in the gluconeogenesis such as phosphoenol pyruvate carboxykinase (PEPCK) and glucose 6 phosphatase catalytic subunit (G6Pase). Conversely, gluconeogenic transcription is repressed by pancreatic insulin under feeding conditions, which effectively inhibits transcriptional activator complexes by either promoting post-translational modifications or activating transcriptional inhibitors in the liver, resulting in the reduction of hepatic glucose output. The transcriptional regulatory machineries have been highlighted as targets for type 2 diabetes drugs to control glycemia, so understanding of the complex regulatory mechanisms for transcription circuits for hepatic gluconeogenesis is critical in the potential development of therapeutic tools for the treatment of this disease. In this review, the current understanding regarding the roles of two key transcriptional activators, CREB and FoxO1, in the regulation of hepatic gluconeogenic program is discussed.

• The Korean Journal of Physiology and Pharmacology
• /
• v.24 no.4
• /
• pp.349-362
• /
• 2020

Temperature affects the firing pattern and electrical activity of neurons in animals, eliciting diverse responses depending on neuronal cell type. However, the mechanisms underlying such diverse responses are not well understood. In the present study, we performed in vitro recording of abdominal ganglia cells of Aplysia juliana, and analyzed their burst firing patterns. We identified atypical bursting patterns dependent on temperature that were totally different from classical bursting patterns observed in R15 neurons of A. juliana. We classified these abnormal bursting patterns into type 1 and type 2; type 1 abnormal single bursts are composed of two kinds of spikes with a long interspike interval (ISI) followed by short ISI regular firing, while type 2 abnormal single bursts are composed of complex multiplets. To investigate the mechanism underlying the temperature dependence of abnormal bursting, we employed simulations using a modified Plant model and determined that the temperature dependence of type 2 abnormal bursting is related to temperature-dependent scaling factors and activation or inactivation of potassium or sodium channels.