Searchable abstracts of presentations at key conferences in endocrinology

ea0049oc13.3 | Reproduction & Endocrine Disruption | ECE2017

Sertoli cell expressed hydroxysteroid (17beta) dehydrogenase 1 is required for male fertility

Hakkarainen Janne , Jokela Heli , Zhang Fuping , Kotaja Noora , Sipila Petra , Poutanen Matti

: Hydroxysteroid (17beta) dehydrogenase 1 (Hsd17b1) is a steroidogenic enzyme catalyzing the conversion of estrone (E1) to estradiol (E2), and androstenedione (A-dione) to testosterone (T). We have shown that the deletion of Hsd17b1 gene in mice resulted in the failure of ovarian estrogen production and subfertility. In this study, we clarified the role of Hsd17b1 in male reproduction. The data revealed that in mice Hsd17b1 mRNA is highly expressed in the Sertoli cells at the ...

ea0049ep364 | Cardiovascular Endocrinology and Lipid Metabolism | ECE2017

Deleting genomic region of Hsd17b1 in mice results into a hypomorphic Naglu allele, and consequently to a phenotype mimicking a lysosomal storage disease

Jokela Heli , Hakkarainen Janne , Pakarinen Pirjo , Ruohonen Suvi , Zhang Fuping , Poutanen Matti

Hydroxysteroid 17-beta dehydrogenase 1 (HSD17B1) is an enzyme catalyzing the reduction of estrone (E1) to estradiol (E2), as well as androstenedione (Adione) to testosterone (T). To elucidate the physiological function of HSD17B1, we generated knockout mice with disrupted Hsd17b1 gene using targeted ES cells (clone 10231) obtained from KOMP repository (www.komp.org). In these ES cells the whole coding region of Hsd17b1 was replaced with LacZ/Neo cass...

ea0042oc17 | (1) | Androgens2016

miR-32 promotes replicative changes in prostate epithelium in vivo

Latonen Leena , Gillen Andrew , Valkonen Mira , Ruusuvuori Pekka , Zhang Fuping , Poutanen Matti , Visakorpi Tapio

The androgen receptor (AR) signaling pathway is central to the emergence of castration-resistant prostate cancer (CRPC). miR-32 is an androgen regulated miRNA which is differentially expressed in CRPC compared to benign prostatic hyperplasia (BPH) and able to provide a significant growth advantage to LNCaP cells. To study how increased miR-32 expression contributes to prostate cancer formation and/or progression in vivo, we have established transgenic mice expressing ...