Disease relevance of LIPI

• Topical ALA-PDT was performed on 24 patients with actinic keratoses (AK) on the head (n = 200) after incubation with a 20% ALA emulsion and irradiation by either an incoherent light source (160 mW/cm(2), 60-160 J/cm(2)) or the LPDL (585 nm, 18 J/cm(2)) [1].

High impact information on LIPI

• We next sequenced the human LPDL gene exons in hypertriglyceridemic subjects and normal controls, and identified seven SNPs within the gene exons and six SNPs in the adjacent introns [2].
• Using bioinformatics, we identified another novel lipase designated LPDLR (for 'LPDL related lipase'), which had 44% protein sequence identity with LPDL [2].
• Together with the phospholipase gene PSPLA1, LPDL and LPDLR form a new lipase gene subfamily, which is characterized by shortened lid motif [2].
• Control lesions (LPDL without ALA) did not clear [1].
• STUDY DESIGN/MATERIALS AND METHODS: HaCaT human keratinocytes were incubated with ALA (3 mmol/l) and irradiated (0-50 J/cm(2)) using the LPDL at 585 nm, 595 nm, or 600 nm vs. an incoherent light source (580-740 nm) [1].

Biological context of LIPI

• These findings indicate that the extent of lipid radical formation in response to oxidative stress can be influenced by changes in the polyunsaturated fatty acid composition of the cell lipids and suggest the possibility that carbon-centered lipi radicals may interact with extracellular structures [3].

Anatomical context of LIPI

• Histologic evaluation demonstrated an increase in activated fibroblasts with positive procollagen staining on the LPDL-treated cheek [4].

References