HSD17B6

Last update 08 May 2025

Basic Info

Synonyms

17-beta-HSD 6, 17-beta-HSD6, 17-beta-hydroxysteroid dehydrogenase type 6

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Introduction

NAD-dependent oxidoreductase with broad substrate specificity that shows both oxidative and reductive activity (in vitro). Has 17-beta-hydroxysteroid dehydrogenase activity towards various steroids (in vitro). Converts 5-alpha-androstan-3-alpha,17-beta-diol to androsterone and estradiol to estrone (in vitro). Has 3-alpha-hydroxysteroid dehydrogenase activity towards androsterone (in vitro). Has retinol dehydrogenase activity towards all-trans-retinol (in vitro). Can convert androsterone to epi-androsterone. Androsterone is first oxidized to 5-alpha-androstane-3,17-dione and then reduced to epi-andosterone. Can act on both C-19 and C-21 3-alpha-hydroxysteroids.

100 Clinical Results associated with HSD17B6

100 Translational Medicine associated with HSD17B6

0 Patents (Medical) associated with HSD17B6

368

Literatures (Medical) associated with HSD17B6

01 May 2025·Gene

Divergent adaptation to highland and tropical environments in Bolivian Creole cattle

Article

Author: Giovambattista, Guillermo ; Calcaterra, Francisco ; Vega, Ariel Loza ; Peral-García, Pilar ; Fernández, María E ; Olivera, Leónidas H ; Cecco, Paulo Álvarez ; Pereira Rico, Juan A ; Muñoz, Andrés Rogberg ; Marcuzzi, Olivia

Bolivian Creole cattle populations evolved under low levels of breeding management and, during more than 500 years of natural selection, became adapted to various environments such as the contrasting highland and subtropical environments. Recently, highland Creole cattle were crossbred with Holstein to improve dairy production. The aim of this research was to evaluate the divergent adaptation through selection footprints of Bolivian Creole cattle from Andean highland and tropical lowlands, and to evaluate the effect of Holstein introgression in highland Creole. For this purpose, 130 Creole cattle (75 highland, 55 lowland) and 88 Holstein were genotyped using a microarray. The database was used to determine population structure and admixture and detect selection sweeps using F_ST, Rsb, XP-EHH, and ROH. Ancestry inference suggested that selection peaks were not due to Holstein introgression. The NCBI database was used to retrieve genes from the common regions and then perform gene ontology analysis. The most prominent selection peaks were on BTA20 and BTA23 and included the PRLR (slick phenotype) and Class I and IIa BoLA genes. Other windows contained candidate genes for hypoxia (ANXA2, NDUFA4L2), angiogenesis and haematological parameters (ANXA2, CPLANE1, NRP1, NRP2), immune response (IL7R, IL6ST, IL31RA, C6, C7, STAT6, NKG2A, IRAK4, KLR, CLEC), oxidative stress (GSTA, HSD17B6) and morphological traits (PLAG1, CHCHD7, CAP2, ARL15). GO analysis revealed enrichment terms and pathways related to immune response, glutathione and retinol metabolism and reported QTLs for coat characteristics, immune response and tick resistance. The results suggest the complex mechanism in the adaptation of Bolivian Creole cattle to the contrasting highland and subtropical environments.

01 Mar 2025·Biochemistry and Biophysics Reports

Hepatic HSD17B6 is dispensable for diet-induced fatty liver disease in mice

Article

Author: Chen, Yali ; Song, Shaoxuan ; Wang, Jianqing ; Zhu, Qihan ; Yuan, Delong ; He, Anyuan ; Bai, Nan

Metabolic dysfunction-associated fatty liver disease (MAFLD) affects up to a third of the global population, which causes huge both clinical and economic burdens. However, its therapeutic strategy is still limited. Steroid dysregulation plays a pivotal role in the homeostasis of lipid metabolism. 17-beta-hydroxysteroid dehydrogenase type 6 (HSD17B6)-one member of 17β-HSDs, encoded by the gene Hsd17b6, catalyzes the synthesis of androsterone and estrone-steroid hormones. However, whether the manipulation of HSD17B6 could ameliorate diet-induced fatty liver disease remains unknown. Here, we found that the expression of Hsd17b6 is enriched in the liver in both humans and mice. The data of single-cell RNA-seq suggests that Hsd17b6 appears to be exclusively expressed in hepatocytes-the parenchymal cells of the liver. Furthermore, the hepatic expression of Hsd17b6 is correlated with fatty liver disease. A mouse model with Hsd17b6 deletion in the liver (HLKO) is successfully generated via the administration of AAV8 expressing Cre recombinase (driven by TBG-a liver-specific promoter) and sgRNAs of Hsd17b6 to Cre-dependent Cas9 mice. Control and HLKO mice were challenged with the high-fat choline-deficient diet-a diet widely used for the model generation of fatty liver disease. Interestingly, the HLKO liver shows a special proteome signature, with the altered proteins enriched in the Golgi apparatus. However, the deletion of Hsd17b6 does not affect fatty liver disease in terms of fat accumulation, inflammation, and hepatic fibrosis. Taken together, our study suggests that the expression of Hsd17b6 is enriched in the liver and correlated with fatty liver disease but its hepatic deletion does not affect diet-induced fatty liver disease.

01 Mar 2025·Bioengineering & Translational Medicine

Assessing the impact of airborne particulate pollution on human skin utilizing a novel human skin equivalent containing MUTZ‐3‐derived Langerhans cells

Article

Author: Przyborski, Stefan ; Simpson, Amy ; DiColandrea, Teresa

AbstractAir pollution is an exogenous stressor known to have a detrimental impact on skin health through the induction of inflammation; however, the direct effect of topical pollution exposure is still being elucidated. Human skin equivalents (HSE) aim to reproduce in vitro the structure and function of the native skin tissue. However, HSEs typically lack skin‐resident immune cells, which could play a key role in the inflammatory response induced by pollution exposure. We outline the development of a HSE‐containing MUTZ‐3‐derived Langerhans cells (MUTZ‐3‐LCs), which show dendritic morphology and Langerhans cell marker expression. We demonstrated that HSE‐containing MUTZ‐3‐LC have lower basal levels of proinflammatory cytokines, but topical stimulation with allergens and irritant compounds induced a greater inflammatory response in these models compared to HSE without immune cells. To study the effect of pollution, we created a technique to apply diesel particulate matter (DPM) to HSEs. Though our microscopic analysis demonstrated that DPM does not penetrate the stratum corneum, we showed that DPM did induce production of proinflammatory cytokines, but notably only in HSEs containing MUTZ‐3‐LCs. These data suggest that topical exposure to air pollution can induce cutaneous inflammation and that skin‐resident immune cells contribute to this response. This highlights the significance of immune‐competent HSEs to the study of exogenous stressors in vitro.

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HSD17B6

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