8-Br-Ado - CAS 2946-39-6
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8- Bromoadenosine
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CAS 2946-39-6 8-Br-Ado

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1.Directed mouse embryonic stem cells into leydig-like cells rescue testosterone-deficient male rats in vivo.
Yang Y1, Su Z, Xu W, Luo J, Liang R, Xiang Q, Zhang Q, Ge RS, Huang Y. Stem Cells Dev. 2015 Feb 15;24(4):459-70. doi: 10.1089/scd.2014.0370. Epub 2014 Dec 18.
The primary function of Leydig cells is to secrete testosterone, which is critical in the regulation of male reproduction and development. Low levels of testosterone will lead to male hypogonadism. Stem cell-derived Leydig cell transplantation may be a promising alternative therapy for male hypogonadism. Thus far, others have reported that Leydig-like cells can be derived from mesenchymal stem cells, embryonic stem cells (ESCs), and induced pluripotent stem cells. However, the efficiency of the differentiating Leydig cells remains low, and progress toward generating functional adult Leydig cells (ALCs) is limited. Herein, we describe a robust method of directing differentiation of mouse embryonic stem cells (mESCs) into Leydig-like cells in vitro by overexpression of the transcription factor steroidogenic factor-1 (SF-1) and treatment with a combination of 8-Bromoadenosine-3',5'-cyclic monophosphate and forskolin. These differentiated cells express mRNA encoding the steroidogenic enzymes and produce progesterone and testosterone.
2.Functional characterization of the human facilitative glucose transporter 12 (GLUT12) by electrophysiological methods.
Pujol-Giménez J1, Pérez A2, Reyes AM2, Loo DD3, Lostao MP4. Am J Physiol Cell Physiol. 2015 Jun 15;308(12):C1008-22. doi: 10.1152/ajpcell.00343.2014. Epub 2015 Apr 8.
GLUT12 is a member of the facilitative family of glucose transporters. The goal of this study was to characterize the functional properties of GLUT12, expressed in Xenopus laevis oocytes, using radiotracer and electrophysiological methods. Our results showed that GLUT12 is a facilitative sugar transporter with substrate selectivity: d-glucose ≥ α-methyl-d-glucopyranoside (α-MG) > 2-deoxy-d-glucose(2-DOG) > d-fructose = d-galactose. α-MG is a characteristic substrate of the Na(+)/glucose (SGLT) family and has not been shown to be a substrate of any of the GLUTs. In the absence of sugar, (22)Na(+) was transported through GLUT12 at a higher rate (40%) than noninjected oocytes, indicating that there is a Na(+) leak through GLUT12. Genistein, an inhibitor of GLUT1, also inhibited sugar uptake by GLUT12. Glucose uptake was increased by the PKA activator 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) but not by the PKC activator phorbol-12-myristate-13-acetate (PMA).
3.Prostacyclin regulates bone growth via the Epac/Rap1 pathway.
Hutchison MR1, White PC. Endocrinology. 2015 Feb;156(2):499-510. doi: 10.1210/en.2014-1348. Epub 2014 Nov 18.
Prostaglandins, particularly PGE2, are important to adult bone and joint health, but how prostaglandins act on growth plate cartilage to affect bone growth is unclear. We show that growth plate cartilage is distinct from articular cartilage with respect to cyclooxygenase (COX)-2 mRNA expression; although articular chondrocytes express very little COX-2, COX-2 expression is high in growth plate chondrocytes and is increased by IGF-I. In bovine primary growth plate chondrocytes, ATDC5 cells, and human metatarsal explants, inhibition of COX activity with nonsteroidal antiinflammatory drugs (NSAIDs) inhibits chondrocyte proliferation and ERK activation by IGF-I. This inhibition is reversed by prostaglandin E2 and prostacyclin (PGI2) but not by prostaglandin D2 or thromboxane B2. Inhibition of COX activity in young mice by ip injections of NSAIDs causes dwarfism. In growth plate chondrocytes, inhibition of proliferation and ERK activation by NSAIDs is reversed by forskolin, 8-bromoadenosine, 3',5'-cAMP and a prostacyclin analog, iloprost.
4.Brain Histamine Is Crucial for Selective Serotonin Reuptake Inhibitors' Behavioral and Neurochemical Effects.
Munari L1, Provensi G1, Passani MB1, Galeotti N1, Cassano T1, Benetti F1, Corradetti R1, Blandina P2. Int J Neuropsychopharmacol. 2015 Apr 21;18(10):pyv045. doi: 10.1093/ijnp/pyv045.
BACKGROUND: The neurobiological changes underlying depression resistant to treatments remain poorly understood, and failure to respond to selective serotonin reuptake inhibitors may result from abnormalities of neurotransmitter systems that excite serotonergic neurons, such as histamine.