Reduction of CD147 surface expression on primary T cells leads to enhanced cell proliferation
Background: CD147 is a ubiquitously expressed membrane glycoprotein that has numerous functional associations in health and disease. However, the molecular mechanisms by which CD147 participates in these processes are unclear. Establishing physiologically relevant silencing of CD147 in primary T cel...
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Main Authors: | , |
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Format: | Article |
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The Allergy and Immunology Society of Thailand
2015
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Online Access: | http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84873295544&origin=inward http://cmuir.cmu.ac.th/handle/6653943832/38110 |
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Institution: | Chiang Mai University |
Summary: | Background: CD147 is a ubiquitously expressed membrane glycoprotein that has numerous functional associations in health and disease. However, the molecular mechanisms by which CD147 participates in these processes are unclear. Establishing physiologically relevant silencing of CD147 in primary T cells could provide clues essential for elucidating some aspects of CD147 biology. To date, achieving the knockdown of CD147 in primary T cells has remained elusive. Objective: Utilizing RNA interference and the Nucleofector transfection system, we were able to reduce the expression of CD147 in primary T cells. Comparison of basic functions, such as proliferation and CD25 expression, were then made between control populations and populations with reduced expression. Results: Up-regulation of CD147 was found upon T-cell activation, indicating a role in T-cell responses. To better understand the possible importance of this up-regulation, we knocked down the expression of CD147 using RNA interference. When compared to control populations the CD147 knockdown populations exhibited increased proliferation. This alteration of cell proliferation, however, was not linked to a change in CD25 expression. Conclusions: We achieved reduction of CD147 surface expression in primary T cells by siRNAmediated gene silencing. Our results point to CD147 having a possible negative regulatory role in T cell-mediated immune responses. |
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