Vimentin Is Involved in Peptidylarginine Deiminase 2-Induced Apoptosis of Activated Jurkat Cells

Hsu, Pei-Chen,Liao, Ya-Fan,Lin, Chin-Li,Lin, Wen-Hao,Liu, Guang-Yaw,Hung, Hui-Chih Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.5

Peptidylarginine deiminase type 2 (PADI2) deiminates (or citrullinates) arginine residues in protein to citrulline residues in a $Ca^{2+}$-dependent manner, and is found in lymphocytes and macrophages. Vimentin is an intermediate filament protein and a well-known substrate of PADI2. Citrullinated vimentin is found in ionomycin-induced macrophage apoptosis. Citrullinated vimentin is the target of anti-Sa antibodies, which are specific to rheumatoid arthritis, and play a critical role in the pathogenesis of the disease. To investigate the role of PADI2 in apoptosis, we generated a Jurkat cell line that overexpressed the PADI2 transgene from a tetracycline-inducible promoter, and used a combination of 12-O-tetradecanoylphorbol-13-acetate and ionomycin to activate Jurkat cells. We found that PADI2 overexpression reduced the cell viability of activated Jurkat cells in1a dose- and time-dependent manner. The PADI2-overexpressed and -activated Jurkat cells presented typical manifestations of apoptosis, and exhibited greater levels of citrullinated proteins, including citrullinated vimentin. Vimentin overexpression rescued a portion of the cells from apoptosis. In conclusion, PADI2 overexpression induces apoptosis in activated Jurkat cells. Vimentin is involved in PADI2-induced apoptosis. Moreover, PADI2-overexpressed Jurkat cells secreted greater levels of vimentin after activation, and expressed more vimentin on their cell surfaces when undergoing apoptosis. Through artificially highlighting PADI2 and vimentin, we demonstrated that PADI2 and vimentin participate in the apoptotic mechanisms of activated T lymphocytes. The secretion and surface expression of vimentin are possible ways of autoantigen presentation to the immune system.

The Effect of Response Shift and Adaptation in Cancer Patients

Chao Li-Fen,Wu Hsu-Hui,Kuo Yi-Shuan,Lin Chia-Yu,Liu Hsueh-Erh 한국간호과학회 2009 한국간호과학회 학술대회 Vol.2009 No.10

Breastfeeding Experiences of Taiwanese Mothers of Infants with Breastfeeding or Breast Milk Jaundice in Certified Baby-Friendly Hospitals

Kuei-Hui Chu,Shuh-Jen Sheu,Mei-Hwa Hsu,Jillian Liao,Li-Yin Chien 한국간호과학회 2019 Asian Nursing Research Vol.13 No.2

Purpose: The purpose was to explore the breastfeeding experiences of mothers of infants with breastfeeding or breast milk jaundice. Methods: In-depth qualitative interviews and content analysis were conducted with nine mothers of newborns with breastfeeding and/or breast milk jaundice who breastfed their babies during the first year postpartum. Results: Mothers' experiences can be described in four phases and six themes. (1) Prenatal stage: build breastfeeding belief, i.e., breastfeeding is best and a natural behavior, without awareness of neonatal jaundice; (2) stage after neonatal jaundice started to appear: include two themes, questioning beliefs in breastfeeding and happiness in being a mother. Mothers lacked knowledge and ignored the threat of neonatal jaundice, mainly focused on their physical discomforts and worried about insufficient breast milk; they also felt an intimate mothereinfant bond through breastfeeding; (3) stage when newborns had confirmed diagnosis of breastfeeding or breast milk jaundice that required medical attention: include two themes, diagnosis of breastfeeding or breast milk jaundice and phototherapy caused negative emotions and regaining original beliefs about breastfeeding. They struggled through emotional swings and inconsistent advices about whether phototherapy and formula supplementation are needed. Then, they decided breastfeeding or breast milk jaundice is only temporary and retrieved initial beliefs of breastfeeding. (4) Stage after neonatal jaundice faded and mothers continued breastfeeding: insisting and adapting. Conclusion: Breastfeeding mothers were unaware of neonatal jaundice until medical attention was required; they experienced physical and mental distress and gradually learned to manage jaundice while insisting on breastfeeding through their breastfeeding beliefs and happiness in being mothers.

Interleukin-20 targets podocytes and is upregulated in experimental murine diabetic nephropathy

Yu-Hsiang Hsu,Hsing-Hui Li,Junne-Ming Sung,Wei-Yu Chen,Ya-Chin Hou,Yun-Han Weng,Wei-Ting Lai,Chih-Hsing Wu,Ming-Shi Chang 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-

Interleukin (IL)-20, a proinflammatory cytokine of the IL-10 family, is involved in acute and chronic renal failure. The aim of this study was to elucidate the role of IL-20 during diabetic nephropathy development. We found that IL-20 and its receptor IL-20R1 were upregulated in the kidneys of mice and rats with STZ-induced diabetes. In vitro, IL-20 induced MMP-9, MCP-1, TGF-β1 and VEGF expression in podocytes. IL-20 was upregulated by hydrogen peroxide, high-dose glucose and TGF-β1. In addition, IL-20 induced apoptosis in podocytes by activating caspase-8. In STZ-induced early diabetic nephropathy, IL-20R1-deficient mice had lower blood glucose and serum BUN levels and a smaller glomerular area than did wild-type controls. Anti-IL-20 monoclonal antibody (7E) treatment reduced blood glucose and the glomerular area and improved renal functions in mice in the early stage of STZ-induced diabetic nephropathy. ELISA showed that the serum IL-20 level was higher in patients with diabetes mellitus than in healthy controls. The findings of this study suggest that IL-20 induces cell apoptosis of podocytes and plays a role in the pathogenesis of early diabetic nephropathy.

Family History of Cancer and Head and Neck Cancer Risk in a Chinese Population

Huang, Yu-Hui Jenny,Lee, Yuan-Chin Amy,Li, Qian,Chen, Chien-Jen,Hsu, Wan-Lun,Lou, Pen-Jen,Zhu, Cairong,Pan, Jian,Shen, Hongbing,Ma, Hongxia,Cai, Lin,He, Baochang,Wang, Yu,Zhou, Xiaoyan,Ji, Qinghai,Zho Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.17

Background: The aim of this study was to investigate whether family history of cancer is associated with head and neck cancer risk in a Chinese population. Materials and Methods: This case-control study included 921 cases and 806 controls. Recruitment was from December 2010 to January 2015 in eight centers in East Asia. Controls were matched to cases with reference to sex, 5-year age group, ethnicity, and residence area at each of the centers. Results: We observed an increased risk of head and neck cancer due to first degree family history of head and neck cancer, but after adjustment for tobacco smoking, alcohol drinking and betel quid chewing the association was no longer apparent. The adjusted OR were 1.10 (95% CI=0.80-1.50) for family history of tobacco-related cancer and 0.96 (95%CI=0.75-1.24) for family history of any cancer with adjustment for tobacco, betel quid and alcohol habits. The ORs for having a first-degree relative with HNC were higher in all tobacco/alcohol subgroups. Conclusions: We did not observe a strong association between family history of head and neck cancer and head and neck cancer risk after taking into account lifestyle factors. Our study suggests that an increased risk due to family history of head and neck cancer may be due to shared risk factors. Further studies may be needed to assess the lifestyle factors of the relatives.

Vimentin Is Involved in Peptidylarginine Deiminase 2-Induced Apoptosis of Activated Jurkat Cells

Pei-Chen Hsu,Ya-Fan Liao,Chin-Li Lin,Wen-Hao Lin,Guang-Yaw Liu,Hui-Chih Hung 한국분자세포생물학회 2014 Molecules and cells Vol.37 No.5

Peptidylarginine deiminase type 2 (PADI2) deiminates (or citrullinates) arginine residues in protein to citrulline residues in a Ca2+-dependent manner, and is found in lymphocytes and macrophages. Vimentin is an intermediate filament protein and a well-known substrate of PADI2. Citrullinated vimentin is found in ionomycin-induced macrophage apoptosis. Citrullinated vimentin is the target of anti-Sa antibodies, which are specific to rheumatoid arthritis, and play a critical role in the pathogenesis of the dis-ease. To investigate the role of PADI2 in apoptosis, we generated a Jurkat cell line that overexpressed the PADI2 transgene from a tetracycline-inducible promoter, and used a combination of 12-O-tetradecanoylphorbol-13-acetate and ionomycin to activate Jurkat cells. We found that PADI2 overexpression reduced the cell viability of activated Jurkat cells in a dose- and time-dependent manner. The PADI2-overexpressed and -activated Jurkat cells presented typical manifestations of apoptosis, and exhibited greater levels of citrullinated proteins, including citrullinated vimentin. Vimentin overexpression rescued a portion of the cells from apoptosis. In conclusion, PADI2 overexpression induces apoptosis in activated Jurkat cells. Vimentin is involved in PADI2-induced apoptosis. Moreover, PADI2-overexpressed Jurkat cells secreted greater levels of vimentin after activation, and expressed more vimentin on their cell surfaces when undergoing apoptosis. Through artificially highlighting PADI2 and vimentin, we demonstrated that PADI2 and vimentin participate in the apoptotic mechanisms of activated T lymphocytes. The secretion and surface expression of vimentin are possible ways of autoantigen presentation to the immune system.

The Effect of a Scenario-Based Spiritual Care Course on Spiritual Care Competence among Clinical Nurses

Suh-Ing Hsieh,Li-Ling Hsu,Hui-Ling Lin,Chen-Yi Kao,Yi-Ping Tseng,Li-Yun Szu,Ching-Yun Lee,Lun-Hui Ho,Shu-Ling Yeh,Shu-Hua Kao,Yen-Fang Chou,Tzu-Hsin Huang 한국성인간호학회 2021 성인간호학회 학술대회 Vol.2021 No.8

Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis

Hsieh, Wei-Chung,Hsu, Pei-Chen,Liao, Ya-Fan,Young, Shu-Ting,Wang, Zeng-Wei,Lin, Chih-Li,Tsay, Gregory J.,Lee, Huei,Hung, Hui-Chih,Liu, Guang-Yaw Korean Society for Molecular and Cellular Biology 2010 Molecules and cells Vol.30 No.4

Ornithine decarboxylase (ODC), the key enzyme of polyamine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC prevents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/endoplasmic reticulum (ER) $Ca^{2+}$ ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpression of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspse-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homologous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC preserved the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and downstream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-mediated apoptotic pathway, induced by TG. Finally, overexpression of ODC maintains the protein and mRNA expression of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.

SINICA CORPUS; Design Methodology for Balanced Corpora

( Keh Jiann Chen ),( Chu Ren Huang ),( Li Ping Chang ),( Hui Li Hsu ) 한국언어정보학회 1996 국제 워크샵 Vol.1996 No.-

The Academia Sinica Balanced Corpus (Sinica Corpus) is the first balanced Chinese corpus with part-of-speech tagging. The corpus (Sinica 2.0) is open to the research community through the WWW (http://www.sinica.edu.tw/ftms-bin/ kiwi.sh). Current size of the corpus is 3.5 million words, and the immediate expansion target is five million words. Each text In the corpus is classified and marked according to five criteria: genre, style, mode, topic, and source. The feature values of these classifications are assigned in a hierarchy. Subcorpora can be defined with a specific set of attributes to serve different research purposes. Texts in the corpus are segmented according to the word segmentation standard proposed by the ROC Computational Linguistic Society. Each segmented word is tagged with its part-of-speech. Linguistic patterns and language structures can be extracted from the tagged corpus via a corpus inspection program which has the functions of KWIC searching, filtering, statistics, printing, and collocation.

Overexpression of Ornithine Decarboxylase Suppresses Thapsigargin-Induced Apoptosis

Wei-Chung Hsieh,Pei-Chen Hsu,Ya-Fan Liao,Shu-Ting Young,Zeng-Wei Wang,Chih-Li Lin,Gregory J. Tsay,Huei Lee,Hui-Chih Hung,Guang-Yaw Liu 한국분자세포생물학회 2010 Molecules and cells Vol.30 No.4

Ornithine decarboxylase (ODC), the key enzyme of poly-amine biosynthesis, has paradoxical roles in apoptosis. Our published papers show overexpression of ODC pre-vents the apoptosis induced by many cytotoxic drugs. Thapsigargin (TG) is an inhibitor of the sarcoplasmic/en-doplasmic reticulum (ER) Ca2+ ATPase (SERCA) pumps and causes ER stress-induced apoptosis. We used ODC overexpressing cell lines to examine whether overexpres-sion of ODC inhibits TG-induced apoptosis. Our results indicated overexpression of ODC attenuated TG-induced apoptosis. Overexpression of ODC blocked procaspse-4 cleavage and phosphorylation of protein kinase-like ER-resident kinase (PERK), triggered by TG. It also attenuated the increase in CAAT/enhancer binding protein homolo-gous protein (CHOP). Cells with overexpressed ODC had greater Bcl-2 expression. Overexpression of ODC pre-served the expression of Bcl-2, inhibited the increase in Bak and stabilized mitochondrial membrane potential without the influences of TG. Cytochrome c release and downstream caspase activation were blocked. That is, overexpression of ODC inhibits the mitochondria-medi-ated apoptotic pathway, induced by TG. Finally, overex-pression of ODC maintains the protein and mRNA expres-sion of SERCA. In conclusion, overexpression of ODC suppresses TG-induced apoptosis by blocking caspase-4 activation and PERK phosphorylation, attenuating CHOP expression and inhibiting the mitochondria-mediated apoptotic pathway.