Obesity has increased at an alarming rate over the past three decades. It is likely caused by increased caloric intake combined with genetic predisposing factors and is a major risk factor for type 2 diabetes (T2D). Obesity is linked to chronic inflammation, which was proposed as a cause for insulin resistance and T2D. The obese state creates a microenvironment within the adipose tissue that is susceptible to accumulation of reactive oxygen species (ROS). Accumulated ROS leads to DNA damage and activation of DNA damage response. When DNA is severely damaged and can't be repaired, the cell undergoes senescence, an irreversible cell cycle arrest. Senescence has been linked to aging illnesses and even to obesity with accumulation of senescent pre-adipocytes. A major player in detecting and defending against oxidative stress is PARP-1. PARP-1 activation has been shown to be associated to melanoma senescence, inflammation, obesity and diabetes. The role of PARP-1 in ROS-induced senescence and inflammation of pre-adipocytes has not yet been investigated. Therefore, to study PARP-1 function in pre-adipocytes senescence, we generated and characterized an in vitro experimental model for cellular senescence in primary human and mice pre-adipocytes using hydrogen peroxide (H2O2) as a source of ROS. Our preliminary data shows PARP-1 induction in ROS-treated pre-adipocytes. We are currently using this senescence model to characterize the function of PARP-1 by using gene-silencing approaches.


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