Lipocalin 2 regulation by thermal stresses: Protective role of Lcn2/NGAL against cold and heat stresses

Lipocalin‐2 Promotes M1 Macrophages Polarization in a Mouse Cardiac Ischaemia–Reperfusion Injury Model

“…The field of macrophage polarization has expanded substantially over the past years, which further reflects the importance and relevance of different macrophage populations. A previous study has indicated the protective role of Lcn2/ NGAL against cold and heart stresses [10]. The current study has revealed Lcn2 as the mediator in chemokine expression and granulocyte infiltration during ischaemia and reperfusion [11].…”

Non-healing is associated with persistent stimulation of the innate immune response in chronic venous leg ulcers

“…This small protein was initially postulated to play a part in mediating apoptosis [44] due to its upregulation in renal failure, various forms of cancer and of inflammatory conditions [45][46][47][48]. It is now believed that this robust protein is associated with protection from apoptosis, and may play a role in cell defence and cell survival [49][50][51]. Another antibacterial peptide, the human cathelicidin antimicrobial peptide LL-37, has also recently been shown to suppress apoptosis in keratinocytes [52], and is involved in wound healing [53].…”

Hypothermic renal perfusion during aortic surgery reduces the presence of lipocalin-2 and preserves renal extraction of dimethylarginines in rats

“…It has been suggested that NGAL protects cells and therefore is upregulated during cold stress, when free iron and free radicals are released (31). Induction of NGAL can be observed in reperfusion injury caused by a sudden increase in ROS (31). Our data reveal that cold perfusion of the kidneys did not result in upregulation of NGAL in the tubular epithelial cells.…”

“…NGAL binds low-molecular-weight ligands such as heme and forms a complex with iron-binding siderophores, which may facilitate the removal of excess intracellular iron, thereby limiting oxidant-mediated apoptosis of renal tubular cells (9). Roudkenar et al (31) showed that NGAL may improve cell proliferation and preservation to prevent cold ischemia injury in transplantation surgery. It has been suggested that NGAL protects cells and therefore is upregulated during cold stress, when free iron and free radicals are released (31).…”

“…Roudkenar et al (31) showed that NGAL may improve cell proliferation and preservation to prevent cold ischemia injury in transplantation surgery. It has been suggested that NGAL protects cells and therefore is upregulated during cold stress, when free iron and free radicals are released (31). Induction of NGAL can be observed in reperfusion injury caused by a sudden increase in ROS (31).…”