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Translational Research
Published in Goh Cheng Soon, Gerard Bodeker, Kishan Kariippanon, Healthy Ageing in Asia, 2022
Whereas DOI at 0.01 μM significantly enhanced steroidogenic acute regulatory protein (StAR) expression, DOI-like protein from D. alata at 0.01 μM, that from D. zingiberensis at 0.1 μM, that from D. collettii at 0.01 μM, and that from D. collettii at 0.1 μM slightly upregulated expression of StAR. DOI-like protein from D. alata at 0.01 μM, that from D. zingiberensis at 0.1 μM, and that from D. oppositifolia at 0.01 μM significantly increased the expression of Erβ (estrogen receptor agonist β). Our data demonstrate that the protein from D. opposita (D. oppositifolia) was the most active protein (Lu et al., 2016; Zhang et al., 2019).
Testosterone signaling in spermatogenesis, male fertility and infertility
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
Arijit Chakraborty, Vertika Singh, Kiran Singh, Rajender Singh
Testicular Leydig cells synthesize the male sex steroid hormones, which are low molecular weight compounds derived from cholesterol, under the regulation of LH. While Leydig cells are capable of de novo synthesis of cholesterol from acetyl coenzyme A, the main source of cholesterol comes from lipoprotein particles transported through the blood into the Leydig cells. Steroid synthesis commences with the transportation of cytosolic cholesterol from the outer membrane to the inner membrane of the mitochondria, which also serves as the rate-limiting step in the process of steroidogenesis. A number of proteins assist in the transportation of the hydrophobic cholesterol, which is unable to simply diffuse through the membrane on its own. The most important of these proteins is the steroidogenic acute regulatory protein StAR (4), consisting of a family of 37 kDa (precursor) and 30 kDa (mature) mitochondrial proteins (5). It mainly detects the response of Leydig cells against tropic hormones and other external stimuli and helps in transporting free cholesterol inside mitochondria of the Leydig cells, stimulating steroidogenesis.
Environmental toxicants on Leydig cell function
Published in C. Yan Cheng, Spermatogenesis, 2018
Leping Ye, Xiaoheng Li, Xiaomin Chen, Qingquan Lian, Ren-Shan Ge
The second cholesterol-transporting protein is the steroidogenic acute regulatory protein (StAR) (Figure 20.1). StAR is encoded by human STAR and rat Star.52 StAR mobilizes cytosolic cholesterol into the inner membrane of the mitochondria. The mechanism by which StAR helps cholesterol movement remains unclear but possible mechanisms are as a cholesterol-transporting shuttle53 or by binding to cholesterol.54 Star is the rate-limiting step for androgen production in Leydig cells, and thus the protein is critical for androgen production.
Cadmium-induced preeclampsia-like phenotype in the rat is related to decreased progesterone synthesis in the placenta
Published in Xenobiotica, 2022
Xiaojie Zhang, Kai Chen, Zhu Meng, Ru Jia, Feifei Lian, Feng Lin
As is well known, the placenta plays an important role during pregnancy, which transports nutrients and oxygen to the foetus while removes of metabolic wastes and carbon dioxide from the embryos to guarantee healthy growth and development. As one of the major endocrine organs, the placenta also participates in the biosynthesis and transport of steroid hormones during pregnancy condition (Guibourdenche et al. 2009). Progesterone (P4) is a cholesterol-derived hormone critical for establishing and maintaining pregnancy and is synthesised mainly by the placenta. The rat placenta utilises maternal cholesterol as the original substrate to produce progesterone in mitochondria. There are three critical synthases in the process of progesterone production. Steroidogenic acute regulatory protein (StAR) is a rate-limiting enzyme in the transporting of cholesterol to the inner mitochondrial membrane where CYP11A1 converts it into pregnenolone. Finally, progesterone is generated from pregnenolone catalysed by 3β-HSD1 (Wu et al. 2012; Furukawa et al. 2019).
24 hour patterning in gene expression of pineal neurosteroid biosynthesis in young chickens (Gallus gallus domesticus L.)
Published in Chronobiology International, 2021
Magdalena Chustecka, Natalia Blügental, Pawel Marek Majewski, Iwona Adamska
Neurosteroid biosynthesis is strongly conserved in all vertebrates, following similar pathways to those in the steroidogenic organs (Tsutsui 2019). Biosynthesis begins with translocation of cholesterol across the mitochondrial membrane by a complex transport mechanism involving several proteins. These include the steroidogenic acute regulatory protein (STAR, synonym STARD1), the translocator protein (TSPO, synonyms PBR, MBR), the adenine nucleotide transporter protein (ANT), and voltage-dependent anion channel protein (VDAC) (Morohaku et al. 2014; Papadopoulos et al. 2018; Selvaraj and Stocco 2015). Pregnenolone (PREG) is then formed by cleavage of the cholesterol side-chain by cytochrome P450scc (E.C 1.14.15.6) encoded by Cyp11a1. PREG is further metabolized in two ways. The first is by hydroxylation to 7α-OH PREG or 7β-hydroxypregnenolone (7β-OH PREG) catalyzed by cytochrome P4507α (E.C 1.14.14.29) encoded by Cyp7b1 (Spg5a). The second is dehydrogenation and isomerization to progesterone (PRO) by 3β-hydroxysteroid dehydrogenase (3β-HSD, E.C 1.1.1.145) encoded by Hsd3b2 (Sdr11e2). PRO can be reduced in two-steps catalyzed by 5α-reductase (E.C 1.3.99.5) encoded by Srd5a1 and 3α-hydroxysteroid dehydrogenase (3α-HSD, E.C 1.3.99.6) encoded by Akr1d1 (Srd5b1) to ALLO. PRO can also be converted to epipregnanolone (EPI) in two steps catalyzed by 3β-HSD and 5β-reductase (E.C 1.3.1.94) encoded by Srd5a3 (Srd5a2l) gene (Figure 1) (Do Rego et al. 2009).
Molecular diagnostics of disorders of sexual development: an Indian survey and systems biology perspective
Published in Systems Biology in Reproductive Medicine, 2019
MR Nagaraja, Satya Prakash Gubbala, C. R. Wilma Delphine Silvia, Ramars Amanchy
Mutations in steroidogenic acute regulatory protein gene (STAR), NR5A1, desert hedgehog gene (DHH), MAMLD1, DAX1, DMRT1, and WT1 accounts for a small percent of 46,XY DSD cases (Table 3). Mitogen-activated protein kinase kinase kinase 1 gene (MAP3K1) mutation/polymorphisms, viz., p.D806N, p.Q1028Q, p.T428T, and p.942insT, were also reported in the cohort of 10 Indian subjects with 46,XY DSD. Also, Polyphen analysis (in silico approach) revealed p.D806N missense mutation might be a cause for hypospadias (in four patients of the cohort) (Das et al. 2013). Hypospadias was also documented as one of the dysmorphic features in patients with defective AR (Nagaraja et al. 2010; Sharma et al. 2014a), SRD5A2 (Eunice et al. 2008; Sahu et al. 2009; Kulshreshtha et al. 2009a; Nagaraja et al. 2010; Shabir et al. 2015), MAMLD1 (Ratan et al. 2016), and partial deletion of chromosome 1q (Paliwal et al. 2011). Intriguingly, Verma et al. (2012) described the clinical course of an Indian girl from birth to 16 years. Briefly, she was characterized by obesity, tall stature, delayed bone age, osteoporosis, hyperinsulinemia with acanthosis nigricans, and hypergonadotropic hypogonadism with cystic ovaries and estrogen replacement therapy (ERT) begun at 13.5 years. Albeit, plateauing of height, improvement of bone maturation, and pubertal progression with the disappearance of ovarian cysts but hyperinsulinemia and acanthosis nigricans persisted despite ERT and metformin regimen. Mutational analysis showed a point mutation in cytochrome P450 family 19 subfamily A member 1 gene (CYP19A1) signified aromatase deficiency (causing 46,XX DSD) and the only Indian report to date (Table 3).