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Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis

  • Authors:
    • Tingting Fan
    • Changsong Zhang
    • Ming Zong
    • Lieying Fan
  • View Affiliations / Copyright

    Affiliations: Department of Clinical Laboratory, Shanghai East Hospital, Tongji University Medical School, Shanghai 200120, P.R. China, Clinical Oncology Laboratories, Changzhou Tumor Hospital, Medical College of Soochow University, Changzhou, Jiangsu 213032, P.R. China
    Copyright: © Fan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5116-5124
    |
    Published online on: January 26, 2018
       https://doi.org/10.3892/mmr.2018.8501
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Abstract

Impaired apoptosis of rheumatoid arthritis (RA)‑fibroblast‑like synoviocytes (FLS) is pivotal in the process of RA. Peptidyl arginine deiminase type IV (PADI4) is associated with autoantibody regulation via histone citrullination in RA. The present study aimed to investigate the role of PADI4 in the apoptosis of RA‑FLS. FLS were isolated from patients with RA and a rat model. The effects of PADI4 on RA‑FLS were investigated in vitro and in vivo. Hypoxia‑induced autophagy was induced by 1% O2 and was detected by immunohistochemical and immunofluorescence analysis; in addition, apoptosis was detected by flow cytometry. RA‑FLS obtained from RA rat model exhibited significant proliferation under severe hypoxia conditions. Hypoxia also significantly induced autophagy and elevated the expression of PADI4. Subsequently, short hairpin RNA‑mediated PADI4 knockdown was demonstrated to significantly inhibit hypoxia‑induced autophagy and promote apoptosis in RA‑FLS. The results of these in vitro and in vivo studies suggested that PADI4 may be closely associated with hypoxia‑induced autophagy, and the inhibition of hypoxia‑induced autophagy by PADI4 knockdown may contribute to an increase in the apoptosis of RA‑FLS.
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Copy and paste a formatted citation
Spandidos Publications style
Fan T, Zhang C, Zong M and Fan L: Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis. Mol Med Rep 17: 5116-5124, 2018.
APA
Fan, T., Zhang, C., Zong, M., & Fan, L. (2018). Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis. Molecular Medicine Reports, 17, 5116-5124. https://doi.org/10.3892/mmr.2018.8501
MLA
Fan, T., Zhang, C., Zong, M., Fan, L."Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis". Molecular Medicine Reports 17.4 (2018): 5116-5124.
Chicago
Fan, T., Zhang, C., Zong, M., Fan, L."Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis". Molecular Medicine Reports 17, no. 4 (2018): 5116-5124. https://doi.org/10.3892/mmr.2018.8501
Copy and paste a formatted citation
x
Spandidos Publications style
Fan T, Zhang C, Zong M and Fan L: Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis. Mol Med Rep 17: 5116-5124, 2018.
APA
Fan, T., Zhang, C., Zong, M., & Fan, L. (2018). Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis. Molecular Medicine Reports, 17, 5116-5124. https://doi.org/10.3892/mmr.2018.8501
MLA
Fan, T., Zhang, C., Zong, M., Fan, L."Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis". Molecular Medicine Reports 17.4 (2018): 5116-5124.
Chicago
Fan, T., Zhang, C., Zong, M., Fan, L."Hypoxia‑induced autophagy is inhibited by PADI4 knockdown, which promotes apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis". Molecular Medicine Reports 17, no. 4 (2018): 5116-5124. https://doi.org/10.3892/mmr.2018.8501
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