The Effect of Lipocalin 2 Deficiency on Nutrient-Induced Cellular Senescence in Adipose Tissue
Cellular senescence is described as the permanent arrest of cell proliferation in response to the accumulation of gene mutation and DNA damage. Senescent cells produce and release factors called senescence-associated secretory phenotype (SASP), and these factors can have a significant impact on healthy cells within the tissue. SASP also promotes the expressions of many pro-inflammatory molecules that are often over-expressed in metabolic diseases, one of which is obesity which is highly prevalent in the United States. Obesity is thought to be greatly associated with chronic inflammation in the adipose tissue, and an unbalanced diet may potentially aggravate inflammation. The stromal vascular (SV) cells of LCN2 wild-type (WT) and knockout (KO) mice were used, which are isolated from adipose tissues via collagenase. The SV cells were cultured at 37 degrees celsius in Dulbecco’s modified Eagle’s medium (DMEM) and 10% fetal bovine serum (FBS). The WT and LCN2 KO SV cells were divided into control and experimental groups, where control groups received no arachidonic acid (AA) treatment, and experimental groups received a six-hour intermittent treatment for seven days. The mRNA gene expression of several senescence (p16, p21, p53) and SASP markers (IL-1β, IL-8, TGF-β) were analyzed via qPCR and beta-galactosidase staining. The objective of this study is to associate LCN2 deficiency and metabolic inflammation with cellular senescence.