Epidermal and Dermal Hallmarks of Photoaging are Prevented by Treatment with Night Serum Containing Melatonin, Bakuchiol, and Ascorbyl Tetraisopalmitate: In Vitro and Ex Vivo Studies.

Introduction: Photoaging is a complex process that is chiefly the result of oxidative stress caused by ultraviolet (UV)-generated reactive oxygen species. To counter this process, we developed a 3-in-1 night facial serum (3-in-1 NFS) containing a combination of direct and indirect antioxidants and polyphenols that is designed to attenuate UV-generated free radicals and stimulate dermal protein synthesis. In clinical trials 3-in-1 NFS improved the appearance of photoaged skin.

The release of pro-inflammatory cytokines is mediated via mitogen-activated protein kinases rather than by the inflammasome signalling pathway in keratinocytes.

Toll-like receptors (TLRs) are expressed in the skin and airway epithelial tissues, which are the most important sites of host-pathogen interactions. TLRs recognize the 3-D structures of pathogen-associated molecules and are therefore useful markers of the innate immune response. Here, we investigated the role of lipopolysaccharides and monosodium urate (MSU) crystals in the activation of the TLR and NOD-like receptor (NLR) pathways in human keratinocytes.

Cross-talk between the VEGF-A and HGF signalling pathways in endothelial cells.

Background Information: Endothelial cells play a major role in angiogenesis, the process by which new blood vessels arise from a pre-existing vascular bed. VEGF-A (vascular endothelial growth factor-A) is a key regulator of angiogenesis during both development and in adults. HGF (hepatocyte growth factor) is a pleiotropic cytokine that may promote VEGF-A-driven angiogenesis, although the signalling mechanisms underlying this co-operation are not completely understood.

Proteomic analysis of ischemia-reperfusion injury upon human liver transplantation reveals the protective role of IQGAP1.

Ischemia-reperfusion injury (IRI) represents a major determinant of liver transplantation. IRI-induced graft dysfunction is related to biliary damage, partly due to a loss of bile canaliculi (BC) integrity associated with a dramatic remodeling of actin cytoskeleton. However, the molecular mechanisms associated with these events remain poorly characterized.

Vascular smooth muscle cell endovascular therapy stabilizes already developed aneurysms in a model of aortic injury elicited by inflammation and proteolysis.

Objective: To investigate the efficiency of endovascular smooth muscle cell (VSMC) seeding in promoting healing and stability in already-developed aneurysms obtained by matrix metalloproteases (MMPs)-driven injury.

Summary Background Data: VSMCs are instrumental in arterial healing after injury and are in decreased number in arterial aneurysms. This cellular deficiency may account for poor healing capabilities and ongoing expansion of aneurysms.