Ask about this productRelated genes to: HPGD antibody
- Gene:
- HPGD NIH gene
- Name:
- 15-hydroxyprostaglandin dehydrogenase
- Previous symbol:
- -
- Synonyms:
- SDR36C1
- Chromosome:
- 4q34.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-16
- Date modifiied:
- 2017-08-04
Related products to: HPGD antibody
Related articles to: HPGD antibody
- Clear cell renal cell carcinoma (ccRCC), the most common subtype of kidney cancer, exhibits high molecular heterogeneity and poor clinical prognosis. Current prognostic models often lack functional relevance and fail to reflect the immunometabolic complexity of ccRCC. This study aimed to identify robust, functionally relevant prognostic biomarkers through integrative multi-omics analysis and to develop a clinically applicable risk stratification model. - Source: PubMed
Publication date: 2026/02/27
Du YuelinZheng YanghuangZhang XiaojunWang HongboZhang HelinShang Panfeng - The novel per- and polyfluoroalkyl substance (PFAS) alternative, 6:2 chlorinated polyfluorinated ether sulfonic acid (F-53B), has emerged as a major replacement for perfluorooctane sulfonate (PFOS) in China. Its widespread detection in the environment and human matrices, including umbilical cord blood, poses a potential public health threat. This study investigated how early-life F-53B exposure affects offspring lung development and asthma susceptibility using an ovalbumin (OVA)-sensitized mouse model. Pregnant dams were exposed to environmentally relevant concentrations of F-53B (0, 0.015, 0.15, and 1.5 mg/kg/day) in drinking water starting from gestation day 7. An OVA-induced asthma was initiated in the offspring mice at postnatal day 22. RNA sequencing and bioinformatics analysis were used to identify the potential targets and pathogenic mechanisms of F-53B. Our results demonstrated that early-life F-53B exposure not only directly impaired the pulmonary epithelial barrier and pulmonary surfactant homeostasis but also reprogrammed the lung immune microenvironment. Following a subsequent allergen challenge, this reprogramming induced a more severe asthma phenotype characterized by prominent neutrophilic infiltration. Transcriptomic analysis highlighted the upregulation of Alox12e and the downregulation of Hpgd, suggesting their potential roles in F-53B-induced asthma susceptibility and phenotype switching. Furthermore, pathways enrichment analysis revealed the activation of the arachidonic acid metabolism signaling pathway as a key driver of the altered asthma susceptibility. These findings provide crucial toxicological evidence for the risk assessment of F-53B and offer a scientific basis for developing public health protection strategies concerning childhood asthma. - Source: PubMed
Publication date: 2026/03/20
Zeng DeruiHu LiehaiRen KeLi YichangLi DongmeiShi Bin - Ovulatory defects are the leading cause of female infertility. Widespread exposure to endocrine-disrupting chemicals, such as phthalates, may contribute to the high prevalence of failed ovulation among infertile women. Using primary ovarian granulosa cells obtained from women, we tested the hypothesis that exposure to an environmentally relevant mixture of phthalate metabolites (MPTmix) impairs essential mediators of the ovulatory process, including progesterone (P4), progesterone receptor (PGR), and prostaglandins (PGs). The composition of the MPTmix was derived from urinary phthalate levels in women. Ovarian granulosa cells, obtained from in vitro fertilization patients, were acclimated in culture to regain responsiveness to hCG (human chorionic gonadotropin, clinical luteinizing hormone analogue). Following acclimation, cells were treated for 0.5-36hr with media containing DMSO (dimethyl sulfoxide, vehicle control), ± hCG (to initiate the ovulatory cascade), and ± MPTmix (1-500 µg/ml). Compared to hCG controls, treatment with hCG + MPTmix reduced active ovulatory PG levels by up to 77%, likely via decreased synthesis (lower PTGS2 and PTGES levels/activity), enhanced catabolism of PGE to PGF (elevated AKR1C1 and AKR1C3 levels), and increased metabolism (elevated HPGD levels/activity). MPTmix exposure further impaired PG function by altering the levels of PG transporters (ABCC4 and SLCO2A1) and receptors (PTGER1-4 and PTGFR). These MPTmix-induced disruptions were accompanied by upstream defects in LH/hCG receptor signaling (cAMP/PKA, ERK1/2), P4 steroidogenesis, and PGR expression. Together, these findings demonstrate that exposure to phthalates impairs P4/PGR-driven PG production/function in human ovarian cells and advances our mechanistic understanding of how phthalate exposure may contribute to ovulatory dysfunction in women. - Source: PubMed
Publication date: 2026/03/06
Land Katie LXu HongAkin James WHannon Patrick R - To review ophthalmic manifestations, histopathological features, and pathophysiology of primary hypertrophic osteoarthropathy (PHOA). - Source: PubMed
Publication date: 2026/02/20
Magazin MajaAhluwalia AneeshaCharoenkijkajorn ChaowKossler Andrea L - Loss of function of the Krüppel-like zinc finger transcription factor GLI-similar 3 (GLIS3) causes polycystic kidney disease (PKD) indicating that it plays a critical role in regulating normal kidney functions. The first postnatal month is accompanied with significant changes in gene expression and represents a key period in kidney development as well as the progression of PKD. In the current study, we examined the role of GLIS3 in the regulation of eicosanoid gene expression and metabolism during this period of kidney development. Transcriptome analysis showed that several eicosanoid metabolic genes are temporally regulated with the expression of some genes decreasing (lipoxygenase and cyclooxygenase arm) and others increasing (the cytochrome P450 pathways), suggesting that these changes are part of part of normal kidney maturation. Many of these temporal changes in eicosanoid gene expression are suppressed in GLIS3-deficient kidneys, consistent with our hypothesis that loss of GLIS3 function inhibits postnatal kidney maturation. Cistrome analyses revealed that several of these eicosanoid genes are directly regulated by GLIS3 and in coordination with hepatocyte nuclear factor 1 beta (HNF1B). Additionally, LC-MS-based eicosanoid metabolomics showed increased levels of PGD, PGE, TXB, and LTB in PND28 GLIS3-deficient polycystic kidneys, consistent with elevated mRNA expression of Ptgs1/2, Alox5ap, Lta4h, and Tbxas1. The increased urinary excretion of PGE and its metabolite PGEM in GLIS3-deficient mice correlates with increased renal production and metabolism of PGE and higher Slco2a1 and Hpgd mRNA expression. Elevated levels of these eicosanoid metabolites might contribute to cystogenesis, altered osmoregulation, inflammation, and fibrosis in GLIS3-deficient kidneys. - Source: PubMed
Publication date: 2026/02/11
Srivastava ChitrangdaKang Hong SoonEdin Matthew LMukherjee TanushreeLih Fred BGrimm Sara ACollier Justin BZeldin Darryl CJetten Anton M