Apoptosis in Cultured Human Fetal Membrane Cells Infected with Influenza Virus.

Uchide, Noboru; Ohyama, Kunio; Bessho, Toshio; Yuan, Bo; Yamakawa, Toshio

doi:10.1248/bpb.25.109

Cited by 28 publications

(79 citation statements)

References 26 publications

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“…Interestingly, we have reported that influenza virus infection induced apoptosis and the gene expression of interleukin (IL)-6, tumor necrosis factor (TNF)-α and interferon (IFN)-β in cultured human fetal membrane chorion trophoblast cells. [12][13][14] However, even though the virus proliferated in cultured amnion epithelial cells, it should be noted that we did not observe the above phenomena in these cells. [12][13][14] Overall, these findings suggest that the induction of apoptosis and gene expression of pro-inflammatory cytokines in chorion trophoblast cells may have a possible role in the etiology of adverse pregnancy outcomes that are associated with an intrauterine infection caused by an influenza virus.…”

contrasting

confidence: 69%

Regulation of Matrix Metalloproteinases-2 and -9 Gene Expression in Cultured Human Fetal Membrane Cells by Influenza Virus Infection

Uchide

Obatake

Yamada

et al. 2016

Biological & Pharmaceutical Bulletin

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confidence: 69%

Regulation of Matrix Metalloproteinases-2 and -9 Gene Expression in Cultured Human Fetal Membrane Cells by Influenza Virus Infection

Uchide

Obatake

Yamada

et al. 2016

Biological & Pharmaceutical Bulletin

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“…1) Chromosomal DNA in chorion cells is fragmented into oligonucleosomes by IV infection at MOIϭ4 and 40, occurring from 24 h after infection. 1) As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…1) Chromosomal DNA in chorion cells is fragmented into oligonucleosomes by IV infection at MOIϭ4 and 40, occurring from 24 h after infection. 1) As shown in Fig. 1, IV induced DNA fragmentation in chorion (lane 1) but not in amnion cells (lane 2) at 48 h after infection at MOIϭ40.…”

Section: Resultsmentioning

confidence: 99%

“…This indicates that transcription and replication of IV genes are required for the induction of apoptosis. 1) Certain viral factors or double-stranded RNA may be involved in the induction of apoptosis in chorion cells. Expression of the bcl-2 gene blocks apoptosis in many systems, and blocked IV-induced cell death in MDCK cells.…”

Section: Expression Of Mrnas For Inflammatory Cytokines and Fas In mentioning

confidence: 99%

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Differential mRNA Expression of Inflammatory Cytokines in Cultured Human Fetal Membrane Cells Responding to Influenza Virus Infection.

Uchide

Ohyama

Yuan

et al. 2002

Biological & Pharmaceutical Bulletin

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When a virus encounters a susceptible cell, the virus enters and initiates cytocidal, persistent, latent or abortive infection. We recently reported that influenza virus (IV) induces persistent infection accompanied by cell survival and virus production in cultured amnion cells. In addition, cytocidal infection accompanied by apoptotic cell death and virus production occurred in cultured chorion cells. Both cell cultures were prepared from human fetal membranes. 1)IV induces cytocidal infection in a variety of cultures, such as HeLa and Madin-Darby canine kidney (MDCK) cell lines and human peripheral blood monocytes in vitro, all of which die through the mechanism of apoptosis.2-5) Furthermore, IV infection induces gene expression of inflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)-a and interferon (IFN)-a/b, and C-C and C-X-C chemokines such as monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1a, RANTES (regulated on activation, normal T cell expressed and secreted) and IFN-inducible protein (IP)-10, 6,7) and proapoptotic factors such as Fas and Fas ligand,8) which occur in infected host cells undergoing apoptosis. Apoptosis and inducible gene expression of inflammatory mediators therefore seem to be correlated. However, whether IV induces gene expression of inflammatory mediators during persistent infection remains unknown.We therefore extensively examined expression of mRNAs for inflammatory cytokines such as IL-1b, IL-6, TNF-a, IFN-a, IFN-b, IFN-g, macrophage colony-stimulating factor (M-CSF) and granulocyte macrophage colony-stimulating factor (GM-CSF), and Fas during cytocidal and persistent infections by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. Of note is the fact that IV infection induced the gene expression of a set of inflammatory cytokines during cytocidal infection accompanied by apoptotic cell death, but this induction was not present during persistent infection in the absence of apoptosis. In this paper we report a noticeable difference in gene expression of a set of inflammatory cytokines between cytocidal and persistent infections. MATERIALS AND METHODSMaterials PCR primers for IFN-a, IFN-b, IFN-g, M-CSF and GM-CSF were originally designed according to published cDNA sequences. 9-13) PCR primers for Fas were based on the published DNA sequences for the primers. 14)PCR primers for IL-1b, IL-6, TNF-a and glycerol-3-phosphate dehydrogenase (G3PDH) were purchased from CLON-TECH Labs. Inc. (CA, U.S.A.). DNA sequences for the PCR primers are shown in Table 1. Neutralizing antibodies against Fas (Medical & Biological Labs. Co., Ltd., Nagoya, Japan), IFN-b (Yamasa Shoyu Co., Ltd., Tokyo, Japan), TNF-a and IFN-g (Genzyme Diagnostic, MA, U.S.A.) were purchased from the listed suppliers.Cell Culture and Virus Infection Primary cultured chorion and amnion cells were prepared from human fetal membranes obtained by cesarean section during the month of normal parturition as described.15) HeLa cell line was obtained from...

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“…55 Infection with influenza virus type A induces leakage of LDH from cultured chorionic cells; this is accompanied by degradation typical in apoptotic cells, such as fragmentation of oligonucleosomal DNA, and condensation and fragmentation of the nucleus. 56,57 Assessing the release of intracellular LDH, which occurs because of the breakdown and alteration in the permeability of the plasma membrane, is a commonly used marker for estimating cytotoxicity. 58 Therefore, we treated A2780 cells with 50 nM GEM, 50 nM AgNPs, or a combination of 50 nM GEM and 50 nM AgNPs for 24 h and then measured the leakage of LDH.…”

Section: Combined Treatment With Gem and Agnps Enhances Cytotoxicitymentioning

confidence: 99%

Silver nanoparticles enhance the apoptotic potential of gemcitabine in human ovarian cancer cells: combination therapy for effective cancer treatment

Yuan¹,

Peng²,

Gurunathan³

2017

IJN

126

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Background Gemcitabine (GEM) is widely used as an anticancer agent in several types of solid tumors. Silver nanoparticles (AgNPs) possess unique cytotoxic features and can induce apoptosis in a variety of cancer cells. In this study, we investigated whether the combination of GEM and AgNPs can exert synergistic cytotoxic effects in the human ovarian cancer cell line A2780. Methods We synthesized AgNPs using resveratrol as a reducing and stabilizing agent. The synthesized nanomaterials were characterized using various analytical techniques. The anticancer effects of a combined treatment with GEM and AgNPs were evaluated using a series of cellular assays. The expression of pro- and antiapoptotic genes was measured using real-time reverse transcription polymerase chain reaction. Apoptosis was confirmed by TUNEL assay. Results In this study, combined treatment with GEM and AgNPs significantly inhibited viability and proliferation in A2780 cells. Moreover, the levels of apoptosis in cells treated with a combination of GEM and AgNPs were significantly higher compared with those in cells treated with GEM or AgNPs alone. Our data suggest that GEM and AgNPs exhibit potent apoptotic activity in human ovarian cancer cells. Combined treatment with GEM and AgNPs showed a significantly higher cytotoxic effect in ovarian cancer cells compared with that induced by either of these agents alone. Conclusion Our study demonstrated that the interaction between GEM and AgNPs was cytotoxic in ovarian cancer cells. Combined treatment with GEM and AgNPs caused increased cytotoxicity and apoptosis in A2780 cells. This treatment may have therapeutic potential as targeted therapy for the treatment of ovarian cancer. To our knowledge, this study could provide evidence that AgNPs can enhance responsiveness to GEM in ovarian cancer cells and that AgNPs can potentially be used as chemosensitizing agents in ovarian cancer therapy.

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Apoptosis in Cultured Human Fetal Membrane Cells Infected with Influenza Virus.

Cited by 28 publications

References 26 publications

Regulation of Matrix Metalloproteinases-2 and -9 Gene Expression in Cultured Human Fetal Membrane Cells by Influenza Virus Infection

Regulation of Matrix Metalloproteinases-2 and -9 Gene Expression in Cultured Human Fetal Membrane Cells by Influenza Virus Infection

Differential mRNA Expression of Inflammatory Cytokines in Cultured Human Fetal Membrane Cells Responding to Influenza Virus Infection.

Silver nanoparticles enhance the apoptotic potential of gemcitabine in human ovarian cancer cells: combination therapy for effective cancer treatment

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