Paraquat-Induced Apoptotic Cell Death in Lung Epithelial Cells

2006 ◽  
Vol 61 (4) ◽  
pp. 366 ◽  
Author(s):  
Tak Ho Song ◽  
Joo Yeon Yang ◽  
In Kook Jeong ◽  
Jae Seok Park ◽  
Young Koo Jee ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

Heat Shock Protein 27 Protects Lung Epithelial Cells From Hyperoxia-Induced Apoptotic Cell Death

2009 ◽  
Vol 65 (3) ◽  
pp. 328-333 ◽  
Author(s):  
Lei Shao ◽  
Ricardo E Perez ◽  
William T Gerthoffer ◽  
William E Truog ◽  
Dong Xu
Keyword(s):  
Cell Death ◽  
Heat Shock ◽  
Epithelial Cells ◽  
Heat Shock Protein ◽  
Apoptotic Cell ◽  
Heat Shock Protein 27 ◽  
Apoptotic Cell Death ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

Characterization of Nitric Oxide (NO)-Induced Cell Death in Lung Epithelial Cells

2004 ◽  
Vol 56 (2) ◽  
pp. 187
Author(s):  
Wha Shim Yong ◽  
Youn Seup Kim ◽  
Jae Seuk Park ◽  
Young Koo Jee ◽  
Kye Young Lee
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

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

2020 ◽  
Vol 102 (4) ◽  
pp. 828-842 ◽  
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.

scholarly journals Novel lnc RNA regulated by HIF-1 inhibits apoptotic cell death in the renal tubular epithelial cells under hypoxia

2017 ◽  
Vol 5 (8) ◽  
pp. e13203 ◽  
Author(s):  
Imari Mimura ◽  
Yosuke Hirakawa ◽  
Yasuharu Kanki ◽  
Natsuki Kushida ◽  
Ryo Nakaki ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular

scholarly journals Induction of Cell Death through Alteration of Oxidants and Antioxidants in Lung Epithelial Cells Exposed to High Energy Protons

2010 ◽  
Vol 285 (32) ◽  
pp. 24769-24774 ◽  
Author(s):  
Sudhakar Baluchamy ◽  
Prabakaran Ravichandran ◽  
Adaikkappan Periyakaruppan ◽  
Vani Ramesh ◽  
Joseph C. Hall ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
High Energy ◽  
Lung Epithelial Cells ◽  
Lung Epithelial

scholarly journals F-Box Protein FBXW17-Mediated Proteasomal Degradation of Protein Methyltransferase PRMT6 Exaggerates CSE-Induced Lung Epithelial Inflammation and Apoptosis

2021 ◽  
Vol 9 ◽  
Author(s):  
Tiao Li ◽  
Xue He ◽  
Lijuan Luo ◽  
Huihui Zeng ◽  
Siying Ren ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Cell Apoptosis ◽  
Molecular Mechanisms ◽  
Lung Epithelial Cells ◽  
Chronic Obstructive ◽  
Structural Cell ◽  
Lung Epithelial

Chronic obstructive pulmonary disease (COPD) is a chronic debilitating lung disease, characterized by progressive airway inflammation and lung structural cell death. Cigarette smoke is considered the most common risk factor of COPD pathogenesis. Understanding the molecular mechanisms of persistent inflammation and epithelial apoptosis induced by cigarette smoke would be extremely beneficial for improving the treatment and prevention of COPD. A histone methyl modifier, protein arginine N-methyltransferase 6 (PRMT6), is reported to alleviate cigarette smoke extract (CSE)-induced emphysema through inhibiting inflammation and cell apoptosis. However, few studies have focused on the modulation of PRMT6 in regulating inflammation and cell apoptosis. In this study, we showed that protein expression of PRMT6 was aberrantly decreased in the lung tissue of COPD patients and CSE-treated epithelial cells. FBXW17, a member of the Skp1-Cullin-F-box (SCF) family of E3 ubiquitin ligases, selectively bound to PRMT6 in nuclei to modulate its elimination in the proteasome system. Proteasome inhibitor or silencing of FBXW17 abrogated CSE-induced PRMT6 protein degradation. Furthermore, negative alteration of FBXW17/PRMT6 signaling lessened the proapoptotic and proinflammatory effects of CSE in lung epithelial cells. Our study, therefore, provides a potential therapeutic target against the airway inflammation and cell death in CS-induced COPD.

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