Author/Authors :
-، - نويسنده Anatomical Sciences Research Center, Kashan University of Medical Sciences, Kashan, Iran Bahmani, Bahareh , -، - نويسنده Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran Amiri, Fatemeh , -، - نويسنده Anatomical Sciences Department, Medicine Faculty, Hamadan University of Medical Sciences, Hamadan, Iran Mohammadi Roushandeh, Amaneh , -، - نويسنده Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran Bahadori, Marzie , -، - نويسنده Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran Dehghan Harati, Mozhgan , -، - نويسنده Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tehran, Iran Habibi Roudkenar, Mehryar
Abstract :
Objective(s): Lipocalin2 (Lcn2) gene is highly expressed in response to various types of cellular stresses. The precise role of Lcn2 has not been fully understood yet. However, it plays a key role in controlling vital cellular processes such as proliferation, apoptosis and metabolism. Recently it was shown that Lcn2 decreases senescence and increases proliferation of mesenchymal stem cells (MSC) with finite life span under either normal or oxidative stress conditions. However, Lcn2 effects on immortal cell line with infinite proliferation are not defined completely. Materials and Material and Methods: HEK-293 cells were transfected with recombinant pcDNA3.1 containing Lcn2 fragment (pcDNA3.1-Lcn2). Expression of lipocalin2 in transfected cells was evaluated by RT-PCR, real time RT-PCR, and ELISA. Different cell groups were treated with H2O2 and WST-1 assay was performed to determine their proliferation rate. Senescence was studied by β-galactosidase and gimsa staining methods as well as evaluation of the expression of senescence-related genes by real time RT-PCR. Results: Lcn2 increased cell proliferation under normal culture condition, while the proliferation slightly decreased under oxidative stress. This decrease was further found to be attributed to senescence. Conclusion: Our findings indicated that under harmful conditions, Lcn2 gene is responsible for the regulation of cell survival through senescence.
