HPGD
HPGD (15-hydroxyprostaglandin dehydrogenase, also known as SDR36C1) is a cytoplasmic NAD-dependent enzyme that oxidises prostaglandins and related lipid mediators to their keto metabolites. It is the key enzyme in prostaglandin inactivation and a member of the short-chain dehydrogenase/reductase superfamily. Browse Assay Genie's current range of HPGD research reagents below, or read on for the biology behind the target.
HPGD catalyses the NAD-dependent dehydrogenation (oxidation) of a broad array of hydroxylated polyunsaturated fatty acids, mainly eicosanoids and docosanoids. Its substrates include prostaglandins, lipoxins and resolvins, and the products are the corresponding keto (oxo) metabolites. By lowering levels of pro-proliferative prostaglandins such as prostaglandin E2, whose activity is raised in cancer because of increased cyclooxygenase 2 expression, the enzyme opposes a signal that favours cell proliferation. The oxo-fatty acid products it generates can also influence cell function profoundly, in part by abrogating pro-inflammatory cytokine expression.
HPGD also acts on specialised pro-resolving mediators. It converts resolvins E1, D1 and D2 to their oxo products, which represents a mode of resolvin inactivation. Resolvin E1 plays important roles during the resolution phase of acute inflammation, while resolvins D1 and D2 have a unique role in obesity-induced adipose inflammation. The enzyme therefore sits at a point where prostaglandin and resolvin signalling are both controlled.
The HPGD gene encodes a member of the short-chain nonmetalloenzyme alcohol dehydrogenase family, classed in the SDR superfamily; the protein is localised to the cytoplasm. Its HGNC previous name was hydroxyprostaglandin dehydrogenase 15-(NAD), and SDR36C1 is a recorded alias. Mutations in the gene result in primary autosomal recessive hypertrophic osteoarthropathy and cranioosteoarthropathy. Multiple transcript variants encoding different isoforms have been reported. Mouse and rat both have an orthologous Hpgd gene.
HPGD is responsible for the metabolism of prostaglandins, making it a central enzyme for studying how these lipid mediators are inactivated.
By oxidising resolvins E1, D1 and D2 to oxo products, HPGD inactivates mediators that act in the resolution phase of acute inflammation.
HPGD lowers pro-proliferative prostaglandin E2, whose activity rises in cancer with increased cyclooxygenase 2 expression.
Mutations in HPGD cause primary autosomal recessive hypertrophic osteoarthropathy and cranioosteoarthropathy, linking the enzyme to skeletal disease.
HPGD catalyses the NAD-dependent oxidation of hydroxylated eicosanoids and docosanoids, including prostaglandins, lipoxins and resolvins, to keto metabolites. This lowers prostaglandin E2 levels and inactivates resolvins E1, D1 and D2, so it shapes both pro-proliferative and inflammation-resolving signals.
The gene is also known as SDR36C1, and its previous HGNC name was hydroxyprostaglandin dehydrogenase 15-(NAD). UniProt names the protein 15-hydroxyprostaglandin dehydrogenase [NAD(+)], EC 1.1.1.141. Multiple transcript variants encoding different isoforms have been described for the gene.
Mutations in HPGD result in primary autosomal recessive hypertrophic osteoarthropathy and cranioosteoarthropathy. Its enzymatic activity is also relevant to cancer and inflammation through prostaglandin E2 and resolvin handling. Mouse and rat have an orthologous Hpgd gene; check the datasheet of any product for its validated reactivity.
Other prostaglandin pathway enzymes with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P15428; product specifications from Assay Genie datasheets.