• 한국동물학회지
• /
• 제38권4호
• /
• pp.457-464
• /
• 1995

인간의 상피세포로부터 유래된 암세포의 일종인 HeLa 세포는 거의 모든 기질분자에 부착하지만 spreading은 오직 collagen 혹은 gelatin에서만 일어난다. HeLa 세포의 spreading은 오직 collagen 결과 활성화된 phosphoipase $A_2$(PLA$_2$)에 의한 arachidonic acid(AA)의 형성으로 유도된다. PLA$_2$에 의해 분해되는 인지질을 확인하기 위해 각종 인지질의 농도변화를 spreading 과정에서 측정한 결과 단지 phosphatidylcoline 만이 감소하였으며, 또한 다양한 lysophospholipids 중 lysophosphatidylcholine 만이 spreading 과정에 생성되는 것으로 보아 phosphatidylcoline이 PLA$_2$에 의해 분해되어 AA가 형성되는 것으로 보인다. PLA$_2$의 활성화는 세포질 CA$_2$+의 농도변화 및 세포질 pH의 알칼리화에 기인하지 않으며, 또한 pertussis 혹은 cholera toxin-sensitive G protein 역시 PLA$_2$활성화와는 무관한 것으로 나타났다.

• 한국식품과학회지
• /
• 제24권2호
• /
• pp.132-136
• /
• 1992

밀가루의 지방질 조성에 대한 염소처리의 영향을 연구하기 위하여 밀가루 100파운드당 1, 2 및 4 oz의 액화염소가스를 각각 처리하여 각종 지방질 성분의 변화를 비교하였다. 염소처리에 의해 극히 적은 양이지만 유리 지방질 함량은 증가한 반면 결합지방질은 감소하였다. 중성 지방질함량은 염소처리량 증가에 따라 유리 및 결합지방질에서 모두 증가하였다. 당지방질 함량은 염소처리량 증가에 따라 유리지방질에서는 증가한 반면 결합지방질에서는 감소하는 경향이었다. Triglyceride의 함량은 염소처리량 증가에 따라 유리 및 결합지방질에서 모두 감소하였다. Digalactosyl diglyceride의 함량은 염소처리량 증가에 따라 결합지방질에서는 감소하였으며, 유리지방질에서는 4 oz 처리는 급격히 감소하였다. 유리 및 결합지방질 중 phosphatidylcholine 함량은 염소처리량 증가에 따라 감소한 반면 lysophosphatidylcholine은 증가하였다. 염소처리량 증가에 따라 유리 및 결합지방질에서 포화지방산 함량은 증가하였고 불포화지방산의 함량은 감소하는 경향이었다.

• Biomolecules & Therapeutics
• /
• 제21권6호
• /
• pp.411-422
• /
• 2013

G-protein-coupled receptors (GPCR) are the largest superfamily of receptors responsible for signaling between cells and tissues, and because they play important physiological roles in homeostasis, they are major drug targets. New technologies have been developed for the identification of new ligands, new GPCR functions, and for drug discovery purposes. In particular, intercellular lipid mediators, such as, lysophosphatidic acid and sphingosine 1-phosphate have attracted much attention for drug discovery and this has resulted in the development of fingolimod (FTY-720) and AM095. The discovery of new intercellular lipid mediators and their GPCRs are discussed from the perspective of drug development. Lipid GPCRs for lysophospholipids, including lysophosphatidylserine, lysophosphatidylinositol, lysophosphatidylcholine, free fatty acids, fatty acid derivatives, and other lipid mediators are reviewed.

• The Korean Journal of Physiology and Pharmacology
• /
• 제22권4호
• /
• pp.399-408
• /
• 2018

A lipidomic study on extensive plasma lipids in bacterial peritonitis (cecal ligation and puncture, CLP)-induced sepsis in mice was done at 24 h post-CLP. The effects of administration of lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA), compounds known to have beneficial effects in CLP, on the sepsis-induced plasma lipid changes were also examined. Among the 147 plasma lipid species from 13 lipid subgroups (fatty acid [FA], LPA, LPC, lysophosphatidylethanolamine [LPE], phosphatidic acid [PA], phosphatidylcholine [PC], phosphatidylethanolamine [PE], phosphatidylinositol [PI], monoacylglyceride [MG], diacylglyceride [DG], triacylglyceride [TG], sphingomyelin [SM], and ceramide [Cer]) analyzed in this study, 40 and 70 species were increased, and decreased, respectively, in the CLP mice. Treatments with LPC and LPA affected 14 species from 7 subgroups, and 25 species from 9 subgroups, respectively. These results could contribute to finding the much needed reliable biomarkers of sepsis.

• The Korean Journal of Physiology and Pharmacology
• /
• 제13권1호
• /
• pp.27-32
• /
• 2009

The effects of oxidized low-density lipoprotein(OxLDL) and its major lipid constituent lysophosphatidylcholine(LPC) on $Ca^{2+}$ entry were investigated in cultured human umbilical endothelial cells(HUVECs) using fura-2 fluorescence and patch-clamp methods. OxLDL or LPC increased intracellular $Ca^{2+}$ concentration($[Ca^{2+}]_i$), and the increase of $[Ca^{2+}]_i$ by OxLDL or by LPC was inhibited by $La^{3+}$ or heparin. LPC failed to increase $[Ca^{2+}]_i$ in the presence of an antioxidant tempol. In addition, store-operated $Ca^{2+}$ entry(SOC), which was evoked by intracellular $Ca^{2+}$ store depletion in $Ca^{2+}$-free solution using the sarcoplasmic reticulum $Ca^{2+}$ pump blocker, 2, 5-di-t-butyl-l,4-benzohydroquinone(BHQ), was further enhanced by OxLDL or by LPC. Increased SOC by OxLDL or by LPC was inhibited by U73122. In voltage-clamped cells, OxLDL or LPC increased $[Ca^{2+}]_i$ and simultaneously activated non-selective cation(NSC) currents. LPC-induced NSC currents were inhibited by 2-APB, $La^{3+}$ or U73122, and NSC currents were not activated by LPC in the presence of tempol. Furthermore, in voltage-clamped HUVECs, OxLDL enhanced SOC and evoked outward currents simultaneously. Clamping intracellular $Ca^{2+}$ to 1 ${\mu}M$ activated large-conductance $Ca^{2+}$-activated $K^+(BK_{ca})$ current spontaneously, and this activated $BK_{ca}$ current was further enhanced by OxLDL or by LPC. From these results, we concluded that OxLDL or its main component LPC activates $Ca^{2+}$-permeable $Ca^{2+}$-activated NSC current and $BK_{ca}$ current simultaneously, thereby increasing SOC.

• Applied Biological Chemistry
• /
• 제39권3호
• /
• pp.206-211
• /
• 1996

Orotic acid의 과잉 섭취는 지질대사의 이상으로 인한 간 장해를 야기시키는 것이 알려져있다. 특히 지방간 생성에 대하여 관심을 가지게 되어서 본 연구는 orotic acid에 의한 혈청, 신장(腎臟) 및 간장(肝臟)의 지질 농도에 미치는 영향에 대하여 검토하였다. 시판 분말 chow 식이에 orotic acid 1% 첨가, 무첨가한 식이를 21일간 90g 전후의 성장기 Sprague-Dawley 계(系) 웅성 쥐에 급여하였다. 그 결과 orotic acid 1% 첨가 식이에서 혈청cholesterol, triglyceride 및 phospholipid 농도는 각각 5% 수준에서 유의하게 저하 하였다. 간장(肝臟)의 triglyceride 농도는 5% 수준에서 유의하게 저하 하였다. Orotic acid 첨가 식이에서 간장(肝臟)중량은 증가한 반면 신장(腎臟)중량은 저하하였다. Orotic acid 1% 첨가한 군에서 간장(肝臟) 및 신장(腎臟)의 phospholipid조성에의 영향은 인정되지 않았으나, 신장(腎臟)의 lysophosphatidylcholine은 높은 증가율을 보였다. 간장(肝臟) phospholipid와 비교하여 신장(腎臟)에서는 sphingomyeline phosphatidylethanolamine은 유의하게 높은 분포를 나타냈다. 신장(腎臟) phospholipid의 지방산 조성중에서 linoleic acid(18:2)가 상승하고 arachidonic acid(20:4)가 감소하였다.

• BMB Reports
• /
• 제31권4호
• /
• pp.350-354
• /
• 1998

To understand the role of protein kinase C (PKC) in the regulation of chondrogenesis, we examined proteins which are phosphorylated by PKC. Stage 23/24 chick embryo wing mesenchymes were micromass-cultured to induce chondrogenesis and cell extracts were phosphorylated in a condition that activates PKC. Several proteins including 63 and 66 kDa proteins were phosphorylated. The 66 kDa protein was phosphorylated only in the presence of phorbol 12-myristate 13-acetate (PMA) and phosphatidylserine CPS), and the phosphorylation was almost completely diminished by bisindolylmaleimide, a PKC inhibitor. In addition, partially purified PKC increased the phosphorylation of the 66 kDa protein. Treatment of cultures with lysophosphatidylcholine (LPC) promoted chondrogenesis and phosphorylation of 66 kDa protein, while PMA and thymeleatoxin inhibited both of the two events. Our results suggest that the 66 kDa protein is a putative substrate of PKC, and phosphorylation of the 66 kDa protein, probably by $PKC\alpha$ is required for chondrogenesis.

• Biomolecules & Therapeutics
• /
• 제7권3호
• /
• pp.263-270
• /
• 1999

The in vitro permeation of thyrotropin-releasing hormone (TRH) through rabbit nasal, rectal and duodenal mucosae was studied in the absence and presence of an enzyme inhibitor and permeation enhancer. TRH in the donor and receptor solutions was assayed by HPLC. When thimerosal (TM, 0.5 mM) was added to the donor cell as an inhibitor, the permeation rate of TRH (200 $\mu\textrm{g}$/ml) increased linearly as a function of time. Fluxes of TRH through the nasal, rectal and duodenal mucosae were found to be 33.3$\pm$5.9, 11.8$\pm$1.9 and 9.6$\pm$0.7 $\mu\textrm{g}$/$\textrm{Cm}^2$/hr, respectively. The addition of sodium glycocholate, glycyrrhizic acid ammonium salt, sodium taurodihydrofusidate or L-$\alpha$-lysophosphatidylcholine to the donor solution containing TM did not result in the significant increase of permeation flux except for the duodenal mucosa, comparing with that in the presence of TM alone. Consequently, it was suggested that the nasal route was advantageous for systemic delivery of TRH, and the addition of TM and/or an enhancer was necessary to maximize the transmucosal permeation of TRH.

• Animal cells and systems
• /
• 제4권4호
• /
• pp.361-366
• /
• 2000

In order to investigate the role of protein kinase C (PKC) in chondrogenic differentiation, we examined the localization of PKC isoforms in a limb bud micromass culture system. PKC$\alpha$ is specifically localized in the regions which would become cartilage nodules, while PKC$\lambda/l$ and $\zeta$ display widespread distribution in the whole culture. Distribution of PKC$\alpha$ change along with promotion or inhibition of chondrogenesis by lysophosphatidylcholine or phorbol 12-myristate 13-acetate. On the other hand, localization of PKC$\lambda/l$ or $\zeta$ a was not changed by the modulation of chondrogenesis. Peanut agglutinin binding protein which is associated with cell aggregation during chondrogenesis was present in the cell condensation regions and its expression in those regions was influenced by PKC activity. Expression of fibronectin and N-cadherin in the cell condensing area were also affected by modulation of PKC activity. These results suggest involvement of PKC$\alpha$ in the cell condensation, possibly through regulating expression of fibronectin and N-cadherin.

• The Korean Journal of Physiology and Pharmacology
• /
• 제26권4호
• /
• pp.229-238
• /
• 2022

Severe bacterial infections are frequently accompanied by depressed neutrophil functions. Thus, agents that increase the microbicidal activity of neutrophils could add to a direct antimicrobial therapy. Lysophosphatidylcholine augments neutrophil bactericidal activity via the glycine (Gly)/glycine receptor (GlyR) α2/TRPM2/p38 mitogen-activated protein kinase (MAPK) pathway. However, the direct effect of glycine on neutrophil bactericidal activity was not reported. In this study, the effect of glycine on neutrophil bactericidal activity was examined. Glycine augmented bactericidal activity of human neutrophils (EC₅₀ = 238 μM) in a strychnine (a GlyR antagonist)-sensitive manner. Glycine augmented bacterial clearance in mice, which was also blocked by strychnine (0.4 mg/kg, s.c.). Glycine enhanced NADPH oxidase-mediated reactive oxygen species (ROS) production and TRPM2-mediated [Ca²⁺]_i increase in neutrophils that had taken up E. coli. Glycine augmented Lucifer yellow uptake (fluid-phase pinocytosis) and azurophil granule-phagosome fusion in neutrophils that had taken up E. coli in an SB203580 (a p38 MAPK inhibitor)-sensitive manner. These findings indicate that glycine augments neutrophil microbicidal activity by enhancing azurophil granule-phagosome fusion via the GlyRα2/ROS/calcium/p38 MAPK pathway. We suggest that glycine could be a useful agent for increasing neutrophil bacterial clearance.