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Biomedical subjects

Y J Jeon

Publications and source records attributed to Y J Jeon.

45 records · Page 3Linked to original sources
PubMed1995

Suppression of cytochrome P450 (Cyp1a-1) induction in mouse hepatoma Hepa-1C1C7 cells by methoxsalen.

Cultured mouse hepatoma cell line Hepa-1c1c7 cells were treated with methoxsalen to assess the role of methoxsalen in the process of Cyp1a-1 induction. Treatment of Hepa-1c1c7 cultures with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced Cyp1a-1, as indicated by analysis of 7-ethoxyresorufin O-deethylation (EROD) activity and P4501A1 protein. When methoxsalen and TCDD were both added to cultures, TCDD-inducible EROD activity was greatly suppressed by methoxsalen in a dose-dependent manner. We find that treatment of Hepa-1c1c7 cells with methoxsalen inhibited CYP1A1 mRNA induction by TCDD as well as the concomitant increase P4501A1 protein. Formation of DNA-protein complexes between the dioxin receptor and its DRE target was inhibited by methoxsalen, as determined by gel mobility shift assays using oligonucleotides corresponding to DRE 3 of the Cyp1a-1 gene. These results suggest that the inhibitory action of methoxsalen on TCDD induction of the Cyp1a-1 gene expression in Hepa-1c1c7 cells might be antagonism of the DNA binding potential of nuclear dioxin receptor.

Animals↗
PubMed1995

Distribution of extracellular matrices, matrix receptors, and transforming growth factor-beta 1 in human and experimental lung granulomatous inflammation.

Aberrant deposition of extracellular matrices (ECMs) may affect lung inflammation by influencing cell adhesion, migration, and activation. Little is known about the expression of ECMs in lungs with granulomatous inflammation. Therefore the authors investigated the distribution of ECMs, matrix receptors of the integrin family, and transforming growth factor-beta 1 (TGF-beta 1) in lungs from patients with pulmonary sarcoidosis and animals with experimental granulomatosis. Immunohistochemistry revealed increased deposition of type I collagen and fibronectin in human lung granulomas when compared with healthy human lungs. Procollagen type I and cellular fibronectin also were increased, suggesting local synthesis of ECM in sarcoid granulomas. These findings were accompanied by increased staining for fibronectin (alpha 5 beta 1) and collagen (alpha 2 beta 1) integrin receptors. The matrix-inducing cytokine TGF-beta 1 was co-distributed with the aforementioned molecules in the granulomas, whereas no significant staining for TGF-beta 1 was found in healthy lungs. Similar to sarcoid lungs, analysis of lung sections obtained from a murine model of granuloma formation revealed increased expression of fibronectin, collagen, integrin receptors, and TGF-beta 1 within granulomas. Based on these observations, there is increased expression of ECM and matrix receptors in both human and experimental lung granulomas. Such alterations may influence the recruitment and activation of inflammatory cells and fibroblasts, promoting granuloma formation and remodeling of tissue by fibrosis. Activation of mononuclear cells resulting in production of TGF-beta 1 is likely to contribute to the changes described.

Animals↗
PubMed1995

Expression of transglutaminase C during the prenatal development of human submandibular glands.

The involvement of transglutaminase C (TGase C) in morphogenesis and cytodifferentiation during glandular tubule formation was addressed by immunolocalization of the protein at different stages of prenatal human submandibular gland development in 100 fetuses and 20 adult salivary glands. Immunocytochemical detection was carried out using a monospecific antibody to TGase C. The results showed TGase C reactivity in both acini and ducts early in development (from 10 to 14 weeks), followed by a marked increase in ductal activity and a decline in acinar activity up to 32 weeks. During the peak of reactivity at 25 to 32 weeks, staining was concentrated in the apical ends of the columnar cells. In the adult, staining was weakly and diffusely distributed in the striated and excretory ducts. Western blot analysis of the cellular extracts of pooled samples from various stages of salivary gland development showed a single strong band at 76 kDa early in development. This band became weaker after 32 weeks of prenatal development and in the adult. These findings of transient high expression of TGase C, which coincide with the development of tubulo-alveolar structure, suggest that TGase C may play a role in morphogenesis in human salivary gland development.

Adult↗
PubMed1994

The 100-kDa protein, whose phosphorylation precedes the fusion of chick embryonic myoblasts, is the eukaryotic elongation factor-2.

We have previously shown that Ca2+/calmodulin-dependent phosphorylation of the 100-kDa protein dramatically increases during the early period of myoblast fusion and inhibition of the protein phosphorylation prevents the fusion. Here, we show that the protein phosphorylation occurs exclusively at Thr residue(s) and the purified 100-kDa protein can be ADP-ribosylated upon treatment with diphtheria toxin. Furthermore, the 13 N-terminal amino acid sequence of the 100-kDa protein, N-Val-Asn-Phe-Val-Asp-Gln-Ile-Arg-Ala-Ile-Met-Asp-Lys, exactly matches with that of elongation factor-2 from rat and hamster. These results indicate that the 100-kDa protein in chick embryonic myoblasts is identical to the eukaryotic elongation factor-2.

Adenosine Diphosphate Ribose↗
PubMed1994

Cyclic AMP negatively modulates both Ca2+/calmodulin-dependent phosphorylation of the 100-kDa protein and membrane fusion of chick embryonic myoblasts.

We have previously shown that Ca2+/calmodulin-dependent phosphorylation of the 100-kDa protein dramatically increases during the early period of myoblast fusion and treatment of calmodulin antagonists, such as trifluoperazine, blocks the fusion. Here, we show that cAMP treatment of primary cultures of chick embryonic myoblasts blocks 100-kDa protein phosphorylation. This effect is dose-dependent and can be reversed upon removal of the nucleotide from the culture media. However, cAMP shows little or no effect on accumulation of the 100-kDa protein. Furthermore, phosphorylation of the 100-kDa protein by the partially purified Ca2+/calmodulin-dependent protein kinase (CaM kinase III) from cAMP-treated cells occurs to a much lower extent than that from untreated cells. Nevertheless, cAMP-sensitive protein kinase does not seem to be directly involved in phosphorylation and inactivation of CaM kinase III, because preincubation of cAMP with the myoblast extracts lacking the endogenous 100-kDa protein does not show any effect on activity of CaM kinase III. Similar to its effect on 100-kDa protein phosphorylation, cAMP reversibly inhibits the fusion of cultured myoblasts. Moreover, treatment with forskolin or theophylline, which is known to elevate the intracellular cAMP level, also reversibly blocks both protein phosphorylation and myoblast fusion. On the other hand, cAMP shows little or no effect on accumulation of muscle-specific proteins, such as creatine kinase and tropomyosin. These results suggest that cAMP is involved in down-regulation of both 100-kDa protein phosphorylation and membrane fusion of cultured myoblasts. These results also suggest that the cAMP-mediated inhibition of 100-kDa protein phosphorylation may be associated with its inhibitory effect on myoblast fusion.

Animals↗
PubMed1993

Sphingosine blocks both membrane fusion and calmodulin-dependent phosphorylation of the 100-kDa protein of chick embryonic myoblasts.

Sphingosine, a potent inhibitor of protein kinase C, was found to block membrane fusion of chick embryonic myoblasts in culture. This effect was dose-dependent and could be reversed upon removal of the drug. Treatment with 12-O-tetradecanoylphorbol 13-acetate, which is a powerful activator of protein kinase C and capable of preventing myoblast fusion, further potentiated the inhibitory effect of sphingosine. Thus, the sphingosine-mediated inhibition of myoblast fusion appears to be independent of protein kinase C. Sphingosine also decreased the phosphorylation state of the 100-kDa protein when given to the cell extracts, and this inhibition was competitive with calmodulin. Thus, sphingosine seems to act as a calmodulin antagonist. These results suggest that the sphingosine-mediated inhibition of myoblast fusion may be associated with the inhibitory effect of the drug against the calmodulin-dependent phosphorylation of the 100-kDa protein.

Animals↗
PubMedDate not supplied

Protective effects of (-)-epigallocatechin-3-gallate on UVA- and UVB-induced skin damage.

It has been known that green tea and its components possess significant chemopreventive effects against chemical carcinogens and photo-caused skin tumor formation. In this study, the protective effects of (-)-epigallocatechin-3-gallate (EGCG), a major green tea catechin, on the ultraviolet (UV)-induced skin damage (photoaging) were studied in guinea pigs, hairless mice and human dermal fibroblast cultures. The lipid peroxidation was significantly reduced in the EGCG-treated group. The amount of lipid peroxides produced in the control and EGCG treated group were 838 +/- 144 and 286 +/- 57 nmol/mg at 18 h after UV irradiation, respectively. UVB-induced erythema was also significantly reduced in the EGCG treated group. The erythema relative index of the control and the EGCG treated group were 311 +/- 45 and 191 +/- 49 at 16 h after UV irradiation, respectively. EGCG treatment reduced UVA-induced skin damage (roughness and sagginess) and protected from the decrease of dermal collagen in hairless mouse skin. EGCG treatment blocked the UV-induced increase of collagen secretion and collagenase mRNA level in fibroblast culture. The nuclear transcription factors NF-kappaB and AP-1 binding activities were also inhibited by EGCG treatment.

Animals↗