1,1-Dichloroethylene-Induced Mitochondrial Damage Precedes Apoptotic Cell Death of Bronchiolar Epithelial Cells in Murine Lung

Chinese giant salamander iridovirus (GSIV) is the causative pathogen of Chinese giant salamander (Andrias davidianus) iridovirosis, leading to severe infectious disease and huge economic losses. However, the infection mechanism by GSIV is far from clear. In this study, a Chinese giant salamander muscle (GSM) cell line is used to investigate the mechanism of cell death during GSIV infection. Microscopy observation and DNA ladder analysis revealed that DNA fragmentation happens during GSIV infection. Flow cytometry analysis showed that apoptotic cells in GSIV-infected cells were significantly higher than that in control cells. Caspase 8, 9, and 3 were activated in GSIV-infected cells compared with the uninfected cells. Consistently, mitochondria membrane potential (MMP) was significantly reduced, and cytochrome c was released into cytosol during GSIV infection. p53 expression increased at an early stage of GSIV infection and then slightly decreased late in infection. Furthermore, mRNA expression levels of pro-apoptotic genes participating in the extrinsic and intrinsic pathway were significantly up-regulated during GSIV infection, while those of anti-apoptotic genes were restrained in early infection and then rose in late infection. These results collectively indicate that GSIV induces GSM apoptotic cell death involving mitochondrial damage, caspases activation, p53 expression, and pro-apoptotic molecules up-regulation.

Download Full-text

Autophagic and apoptotic cell death in amniotic epithelial cells

Journal of Structural Biology ◽

10.1016/j.jsb.2006.10.012 ◽

2006 ◽

Author(s):

Z SHEN ◽

E LI ◽

S LU ◽

L XU ◽

J SHEN ◽

...

Keyword(s):

Cell Death ◽

Epithelial Cells ◽

Apoptotic Cell ◽

Apoptotic Cell Death ◽

Amniotic Epithelial Cells

Download Full-text

Methylisothiazolinone induces apoptotic cell death via matrix metalloproteinase activation in human bronchial epithelial cells

Toxicology in Vitro ◽

10.1016/j.tiv.2019.104661 ◽

2020 ◽

Vol 62 ◽

pp. 104661 ◽

Cited By ~ 3

Author(s):

Eun-Jung Park ◽

Eunsol Seong

Keyword(s):

Cell Death ◽

Epithelial Cells ◽

Matrix Metalloproteinase ◽

Apoptotic Cell ◽

Bronchial Epithelial Cells ◽

Apoptotic Cell Death ◽

Human Bronchial Epithelial Cells ◽

Bronchial Epithelial

Download Full-text

Uterine epithelial expression of the tumor necrosis factor superfamily: a strategy for immune privilege during pregnancy in a true epitheliochorial placentation species

Biology of Reproduction ◽

10.1093/biolre/ioz233 ◽

2020 ◽

Vol 102 (4) ◽

pp. 828-842 ◽

Cited By ~ 1

Author(s):

Inkyu Yoo ◽

Yoon Chul Kye ◽

Jisoo Han ◽

Minjeong Kim ◽

Soohyung Lee ◽

...

Keyword(s):

Cell Death ◽

Tumor Necrosis Factor ◽

Epithelial Cells ◽

Tumor Necrosis ◽

Fas Ligand ◽

Apoptotic Cell ◽

Apoptotic Cell Death ◽

Immune Privilege ◽

Tumor Necrosis Factor Superfamily ◽

Necrosis Factor

Abstract The maternal immune system tolerates semi-allogeneic placental tissues during pregnancy. Fas ligand (FASLG) and tumor necrosis factor superfamily 10 (TNFSF10) are known to be components of maternal immune tolerance in humans and mice. However, the role of FASLG and TNFSF10 in the tolerance process has not been studied in pigs, which form a true epitheliochorial type placenta. Thus, the present study examined the expression and function of FASLG and TNFSF10 and their receptors at the maternal-conceptus interface in pigs. The endometrium and conceptus tissues expressed FASLG and TNFSF10 and their receptor mRNAs during pregnancy in a stage-specific manner. During pregnancy, FASLG and TNFSF10 proteins were localized predominantly to endometrial luminal epithelial cells with strong signals on Day 30 to term and on Day 15, respectively, and receptors for TNFSF10 were localized to some stromal cells. Interferon-γ (IFNG) increased the expression of TNFSF10 and FAS in endometrial tissues. Co-culture of porcine endometrial epithelial cells over-expressing TNFSF10 with peripheral blood mononuclear cells yielded increased apoptotic cell death of lymphocytes and myeloid cells. In addition, many apoptotic T cells were found in the endometrium on Day 15 of pregnancy. The present study demonstrated that FASLG and TNFSF10 were expressed at the maternal-conceptus interface and conceptus-derived IFNG increased endometrial epithelial TNFSF10, which, in turn, induced apoptotic cell death of immune cells. These results suggest that endometrial epithelial FASLG and TNFSF10 may be critical for the formation of micro-environmental immune privilege at the maternal-conceptus interface for the establishment and maintenance of pregnancy in pigs.

Download Full-text