Lipid phosphate phosphohydrolase type 1 (LPP1) degrades extracellular lysophosphatidic acid in vivo.

摘要: LPA (lysophosphatidic acid) is a lipid mediator that stimulates cell proliferation and growth, involved in physiological pathological processes such as wound healing, platelet activation, angiogenesis the growth of tumours. Therefore defining mechanisms production degradation are interest understanding regulation these processes. Extracellular synthesis relatively well understood, whereas its not. One route dephosphorylation. A candidate enzyme integral membrane exophosphatase LPP1 (lipid phosphate phosphohydrolase type 1). In present paper, we report development mouse wherein gene ( Ppap2a ) was disrupted. The homozygous mice, which phenotypically unremarkable, generally lack mRNA, multiple tissues exhibit substantial (35–95%) reduction phosphatase activity. Compared with wild-type littermates, tr/tr animals have increased levels plasma LPA, injected intravenously metabolized at 4-fold lower rate. Our results demonstrate rapidly bloodstream an important determinant this turnover. These indicate catabolic for vivo .