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Article Open Access

LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression

  • Authors:
    • Xiang Yin
    • Peng Liu
    • Yao‑Yao Liu
    • Ming‑Yong Liu
    • Wei‑Li Fan
    • Bai‑Yi Liu
    • Jian‑Hua Zhao
  • View Affiliations / Copyright

    Affiliations: Department of Spinal Surgery, Institute of Surgery Research, Daping Hospital, Army Medical University, Chongqing 400042, P.R. China
    Copyright: © Yin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 269-277
    |
    Published online on: May 10, 2019
       https://doi.org/10.3892/etm.2019.7571
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Abstract

Platelets primarily participate in hemostasis and antimicrobial host defense. The present study aimed to investigate the effects of leucine‑rich repeat flightless‑interacting protein‑1 (LRRFIP1) on platelet agglutination. The bacterial strain of LRRFIP1 was used to synthesize the recombinant protein and a mouse model of LRRFIP1 gene knockout was established. Platelets were isolated from the mice and divided into the different trial groups according to their treatment with collagen, thrombin receptor SFLLRN, anti‑wild‑type (w)LRRFIP1monoclonal antibodies and the model of LRRFIP1 gene knockout. The platelets were prepared and platelet agglutination was examined using platelet aggregation apparatus. The active αIIbβ3 integrin was examined by flow cytometry. The results revealed that the combined wLRRFIP1 protein was successfully expressed. wLRRFIP1 treatment significantly triggered platelet agglutination of collagen, thrombin and monoclonal antibody treated platelets. wLRRFIP1 knockout significantly decreased αIIbβ3 levels compared with the wild‑type. Platelet agglutination was also significantly inhibited in the LRRFIP1‑/‑mouse model compared with the wild‑type. LRRFIP1 knockout significantly decreased the αIIbβ3 levels in platelets undergoing convulxin treatment. In conclusion, LRRFIP1 treatment triggered platelet agglutination and LRRFIP1 gene knockout inhibited platelet agglutination. In addition, LRRFIP1 gene knockout significantly decreased the levels of αIIbβ3. This suggests that LRRFIP1 my be applied to patients in a clinical setting to trigger platelet agglutination in inflammatory diseases and atherothrombotic diseases.
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Copy and paste a formatted citation
Spandidos Publications style
Yin X, Liu P, Liu YY, Liu MY, Fan WL, Liu BY and Zhao JH: LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression. Exp Ther Med 18: 269-277, 2019.
APA
Yin, X., Liu, P., Liu, Y., Liu, M., Fan, W., Liu, B., & Zhao, J. (2019). LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression. Experimental and Therapeutic Medicine, 18, 269-277. https://doi.org/10.3892/etm.2019.7571
MLA
Yin, X., Liu, P., Liu, Y., Liu, M., Fan, W., Liu, B., Zhao, J."LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression". Experimental and Therapeutic Medicine 18.1 (2019): 269-277.
Chicago
Yin, X., Liu, P., Liu, Y., Liu, M., Fan, W., Liu, B., Zhao, J."LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression". Experimental and Therapeutic Medicine 18, no. 1 (2019): 269-277. https://doi.org/10.3892/etm.2019.7571
Copy and paste a formatted citation
x
Spandidos Publications style
Yin X, Liu P, Liu YY, Liu MY, Fan WL, Liu BY and Zhao JH: LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression. Exp Ther Med 18: 269-277, 2019.
APA
Yin, X., Liu, P., Liu, Y., Liu, M., Fan, W., Liu, B., & Zhao, J. (2019). LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression. Experimental and Therapeutic Medicine, 18, 269-277. https://doi.org/10.3892/etm.2019.7571
MLA
Yin, X., Liu, P., Liu, Y., Liu, M., Fan, W., Liu, B., Zhao, J."LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression". Experimental and Therapeutic Medicine 18.1 (2019): 269-277.
Chicago
Yin, X., Liu, P., Liu, Y., Liu, M., Fan, W., Liu, B., Zhao, J."LRRFIP1 expression triggers platelet agglutination by enhancing αIIbβ3 expression". Experimental and Therapeutic Medicine 18, no. 1 (2019): 269-277. https://doi.org/10.3892/etm.2019.7571
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