Enter your email address
Submit
Write your message
International Journal of Medical Laboratory
Shahid Sadoughi University of Medical Sciences
Fri, Apr 26, 2024
[Archive]
Volume 5, Issue 3 (August 2018)
IJML 2018, 5(3): 195-207 |
Back to browse issues page
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Goodarzi A, Yari F, Mohammadipour M, Deyhim M R, Timori Naghadeh H. Capability of Platelet Factor 4 to Induce Apoptosis in the Cancerous Cell Lines in Vitro. IJML 2018; 5 (3) :195-207
URL: http://ijml.ssu.ac.ir/article-1-221-en.html
URL: http://ijml.ssu.ac.ir/article-1-221-en.html
Alireza Goodarzi 
, Fatemeh Yari * , Mahshid Mohammadipour , Mohammad Reza Deyhim , Hossin Timori Naghadeh
, Fatemeh Yari * , Mahshid Mohammadipour , Mohammad Reza Deyhim , Hossin Timori Naghadeh
Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran
Abstract: (1650 Views)
Background and Aims: Platelet factor 4 (PF4) or CXCL4 is a member of CXC chemokine family which is stored in alpha granules of platelets. The main function known for PF4 is angiostasis which may contribute to prevent tumor metastasis. This feature is mediated by CXCR3 on the endothelial cells. Our principal aim was to study the apoptosis induction in three cell lines treated with PF4 and obtained from human platelet concentrates.
Materials and Methods: We evaluated the apoptotic effect of platelet-derived PF4 on the U266B1 and K562 cell lines expressing CXCR3, compared with Daudi as a CXCR3-negative cell line. PF4 was purified from human platelet concentrates by immunoaffinity chromatography and was concentrated. The quantity and molecular weight of the obtained PF4 was determined by enzyme-linked immunosorbent assay and sodium dodecyl sulfate polyacrylamide gel electrophoresis methods respectively. Cell lines were treated for 72 and 96 h with 90 μg/ml of PF4. Apoptosis was assayed by using CD95, WST-1, active caspase-3, and cell count.
Results: Platelet-derived PF4 was a weak agent to induce apoptosis in U266B1 and K562 cell lines. Our data showed in terms of WST-1 and cell count had a significant difference between control and experiment groups (p≤0.05), while CD95, LDH, and active caspase-3 did not show such a difference (p>0.05).
Conclusions: We observed that PF4 released from platelets has a weak potential to induce apoptosis in cancerous cell lines. Other factors may also contribute to this process including the applied dose, purification method, cell line type, and its proteoglycan carrier.
Materials and Methods: We evaluated the apoptotic effect of platelet-derived PF4 on the U266B1 and K562 cell lines expressing CXCR3, compared with Daudi as a CXCR3-negative cell line. PF4 was purified from human platelet concentrates by immunoaffinity chromatography and was concentrated. The quantity and molecular weight of the obtained PF4 was determined by enzyme-linked immunosorbent assay and sodium dodecyl sulfate polyacrylamide gel electrophoresis methods respectively. Cell lines were treated for 72 and 96 h with 90 μg/ml of PF4. Apoptosis was assayed by using CD95, WST-1, active caspase-3, and cell count.
Results: Platelet-derived PF4 was a weak agent to induce apoptosis in U266B1 and K562 cell lines. Our data showed in terms of WST-1 and cell count had a significant difference between control and experiment groups (p≤0.05), while CD95, LDH, and active caspase-3 did not show such a difference (p>0.05).
Conclusions: We observed that PF4 released from platelets has a weak potential to induce apoptosis in cancerous cell lines. Other factors may also contribute to this process including the applied dose, purification method, cell line type, and its proteoglycan carrier.
Type of Study: Research |
Subject:
Hematology & Blood Banking
Received: 2018/03/7 | Accepted: 2018/06/10 | Published: 2018/08/15
Received: 2018/03/7 | Accepted: 2018/06/10 | Published: 2018/08/15
| Rights and permissions | |
 |
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
