• The Korean Journal of Physiology and Pharmacology
• /
• v.8 no.4
• /
• pp.227-235
• /
• 2004

The aim of the present study was to examine the effect of leptin on CA release from the isolated perfused model of the rat adrenal gland, and to establish its mechanism of action. Leptin $(1{\sim}100\;ng/ml)$, when perfused into an adrenal vein of the rat adrenal gland for 60 min, enhanced a dose-dependently the secretory responses of CA evoked by ACh $(5.32{\times}10^{-3}\;M)$, DMPP $(10^{-4}\;M)$ and McN-A-343 $(10^{-4}\;M)$, although it alone has weak effect on CA secretion. However, it did not affect the CA secretion evoked by excess $K^+\;(5.6{\times}10^{-2}\;M)$. Leptin alone produced a weak secretory response of the CA. Moreover, leptin (10 ng/ml) in to an adrenal vein for 60 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$ ATPase. However, in the presence of U0126 $(1\;{\mu}M)$, an inhibitor of mitogen-activated protein kinase (MAPK), leptin no longer enhanced the CA secretion evoked by ACh and DMPP. Furthermore, in the presence of anti-leptin (10 ng/ml), an antagonist of Ob receptor, leptin (10 ng/ml) also no longer potentiated the CA secretory responses evoked by DMPP and Bay-K-8644. Collectively, these experimental results suggest that leptin enhances the CA secretion from the rat adrenal medulla evoked by cholinergic stimulation (both nicotininc and muscarinic receptors), but does not that by membrane depolarization. It seems that this enhanced effect of leptin may be mediated by activation of U0126-sensitive MAPK through the leptin receptors, which is probably relevant to the activation of the dihydropyridine L-type $Ca^{2+}$ channels located on the rat adrenomedullary chromaffin cells.

• KSBB Journal
• /
• v.23 no.2
• /
• pp.142-146
• /
• 2008

In order to sprout and migrate, cells must secrete proteinases which are degrading the surrounding extracellular matrix. In this study, we examined the effect of mulberry extracts and combination of mulberry extracts and VEGF on human malignant glioma U-373-MG cells. Mulberry extracts induced the secretion of matrix metalloproteinase-9 (MMP-9) and suppressed the secretion of MMP-2 and plasmin. Mulberry extracts inhibited the VEGF-induced MMP-2, MMP-9 and plasmin secretion. It is therefore, suggested that mulberry extracts can suppress the VEGF-induced tumor angiogenesis in U-373-MG cells. Also, mulberry extracts induced the secretion of MMP-9 and plasmin through PI 3'-kinase pathway in U-373-MG cells.

• Genomics & Informatics
• /
• v.5 no.2
• /
• pp.77-82
• /
• 2007

Serotonin (5-HT), the endogenous nonselective 5-HT receptor agonist, activates the inositol-1,4,5-triphosphate/calcium $(InsP3/Ca^{2+})$ signaling pathway and exerts both stimulatory and inhibitory actions on cAMP production and neuromodulin secretion in rat hypothalamic neurons. Specific mRNA transcripts for 5-HT1A, 5-HT2C and 5-HT4 were identified in rat hypothalamic neurons. These experiments were supported by combined techniques such as cAMP and a $Ca^{2+}$ assays in order to elucidate the associated receptors and signaling pathways. The cAMP production and neuromodulin release were profoundly inhibited during the activation of the Gi-coupled 5-HT1A receptor. Treatment with a selective agonist to activate the Gq-coupled 5-HT2C receptor stimulated InsP3 production and caused $Ca^{2+}$ release from the sarcoplasmic reticulum. Selective activation of the Gs-coupled 5-HT4 receptor also stimulated cAMP production, and caused an increase in neuromodulin secretion. These findings demonstrate the ability of 5-HT receptor subtypes expressed in neurons to induce neuromodulin production. This leads to the activation of single or multiple G-proteins which regulate the $InsP3/Ca^{2+}/PLC-{\gamma}$ and adenyl cyclase / cAMP signaling pathways.

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.1
• /
• pp.221-225
• /
• 2015

As metformin can inhibit endometrial carcinoma (EC) cell growth and the insulin growth factor (IGF) system is active in EC, the question of whether it can regulate endometrial carcinoma cell secretion of IGF-1 or expression of IGF-1 receptor (IGF-1R) is of interest. In this study, serum IGF-1 levels in EC patients were found to be comparable with that in the non EC patients (p>0.05). However, the IGF-1 level in the medium of cultured cells after treatment with metformin was decreased (p<0.05). IGF-1R was highly expressed in human endometrial carcinoma paraffin sections, but IGF-1R and phosphor-protein kinase B/protein kinase B (p-Akt/Akt) expression was down-regulated after metformin treatment (p<0.05). In summary, metformin can reduce the secretion of IGF-1 by Ishikawa and JEC EC cell lines and their expression of IGF-1R to deactivate downstream signaling involving the PI-3K/Akt pathway to inhibit endometrial carcinoma cell growth.

• Toxicological Research
• /
• v.30 no.2
• /
• pp.77-81
• /
• 2014

In contrast to animals, plants do not have a circulatory system as well as mobile immune cells that allow them to protect themselves against pathogens. Instead, plants exclusively depend on the innate immune system to defend against pathogens. As typically observed in the animal innate immunity, plant immune responses are composed of pathogen detection, defense signaling which includes transcriptional reprogramming, and secretion of antimicrobial compounds. Although knowledge on recognition and subsequent signaling of pathogen-derived molecules called elicitors is now expanding, the mechanisms of how these immune molecules are excreted are yet poorly understood. Therefore, current understandings of how plants secrete defense products especially via exocytosis will be discussed in this review.

• Biomedical Science Letters
• /
• v.28 no.2
• /
• pp.59-66
• /
• 2022

The Cyr61/CTGF/NOV (CCN) family is dynamically expressed in various tissues, including the nervous system, from the prenatal period to adulthood. However, major studies have been conducted only in limited fields, such as the cardiovascular and muscular systems, skeletal development, and cancer. In addition, although the CCN family is a secretory protein, very few studies have described its mechanism of secretion. Recently, it has been suggested that overexpression of CCN3 or intracellular accumulation due to problems in the secretory pathway can inhibit neuronal axonal growth. In this review, we have briefly summarized the structure and characteristics of the CCN family and its related diseases, with particular emphasis on the secretory mechanism and modifiers of the CCN family, newly identified in the nervous system.

• Genomics & Informatics
• /
• v.12 no.4
• /
• pp.195-202
• /
• 2014

Metabolic syndrome (MetS) is a complex disorder related to insulin resistance, obesity, and inflammation. Genetic and environmental factors also contribute to the development of MetS, and through genome-wide association studies (GWASs), important susceptibility loci have been identified. However, GWASs focus more on individual single-nucleotide polymorphisms (SNPs), explaining only a small portion of genetic heritability. To overcome this limitation, pathway analyses are being applied to GWAS datasets. The aim of this study is to elucidate the biological pathways involved in the pathogenesis of MetS through pathway analysis. Cohort data from the Korea Associated Resource (KARE) was used for analysis, which include 8,842 individuals (age, $52.2{\pm}8.9years$ ; body mass index, $24.6{\pm}3.2kg/m^2$). A total of 312,121 autosomal SNPs were obtained after quality control. Pathway analysis was conducted using Meta-analysis Gene-Set Enrichment of Variant Associations (MAGENTA) to discover the biological pathways associated with MetS. In the discovery phase, SNPs from chromosome 12, including rs11066280, rs2074356, and rs12229654, were associated with MetS (p < $5{\times}10^{-6}$), and rs11066280 satisfied the Bonferroni-corrected cutoff (unadjusted p < $1.38{\times}10^{-7}$, Bonferroni-adjusted p < 0.05). Through pathway analysis, biological pathways, including electron carrier activity, signaling by platelet-derived growth factor (PDGF), the mitogen-activated protein kinase kinase kinase cascade, PDGF binding, peroxisome proliferator-activated receptor (PPAR) signaling, and DNA repair, were associated with MetS. Through pathway analysis of MetS, pathways related with PDGF, mitogen-activated protein kinase, and PPAR signaling, as well as nucleic acid binding, protein secretion, and DNA repair, were identified. Further studies will be needed to clarify the genetic pathogenesis leading to MetS.

• The Journal of the Korean Society for Microbiology
• /
• v.35 no.5_6
• /
• pp.350-350
• /
• 2000

• Proceedings of the PSK Conference
• /
• 2002.10a
• /
• pp.268.2-269
• /
• 2002

The recombinant histamine-releasing factor (rHRF) has been reported to induce a secretion of histamine and cytokines from inflammation-related cell types such as basophils and eosinophils. and to function as a growth factor in immune B cells. Recently. decreased expression level of HRF protein was observed in brain of patients with Alzheimer disease and Downs syndrome. suggesting a possible significant role in neurological systems. (omitted)

• Proceedings of the Zoological Society Korea Conference
• /
• 2001.10a
• /
• pp.205.1-205
• /
• 2001

No Abstract, See Full Text