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Specialty: Endocrinology
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Total 29 results found since Jan 2013.

Involvement of CREB-regulated transcription coactivators (CRTC) in transcriptional activation of steroidogenic acute regulatory protein (Star) by ACTH
Publication date: Available online 8 October 2019Source: Molecular and Cellular EndocrinologyAuthor(s): Lorna I.F. Smith, Victoria Huang, Mark Olah, Loc Trinh, Ying Liu, Georgina Hazell, Becky Conway-Campbell, Zidong Zhao, Antoine Martinez, Anne-Marie Lefrançois-Martinez, Stafford Lightman, Francesca Spiga, Greti AguileraAbstractStudies in vivo have suggested the involvement of CREB-regulated transcription coactivator (CRTC)2 on ACTH-induced transcription of the key steroidogenic protein, Steroidogenic Acute Regulatory (StAR). The present study uses two ACTH-responsive adrenocortical cell-lines, to examine the role of CRT...
Source: Molecular and Cellular Endocrinology - October 9, 2019 Category: Endocrinology Source Type: research

Endocytosis and degradation of pegvisomant and a potential new mechanism that inhibits the nuclear translocation of GHR.
Conclusion: Our study showed that pegvisomant is a "moonlighting" antagonist. In addition, we revealed the mechanisms of the endocytosis, post-endocytic sorting, and degradation of pegvisomant. PMID: 30602026 [PubMed - as supplied by publisher]
Source: The Journal of Clinical Endocrinology and Metabolism - December 31, 2018 Category: Endocrinology Authors: Hainan L, Li W, Li R, Zheng X, Luo G Tags: J Clin Endocrinol Metab Source Type: research

cGMP/PKG-I pathway-mediated GLUT1/4 regulation by NO (nitric oxide) in female rat granulosa cells.
The objective of the present study was to determine the cellular and molecular mechanism by which NO regulates GLUT expression and glucose uptake in granulosa cells. Our results indicated that NO increased GLUT1/GLUT4 expression and translocation in cells, as well as glucose uptake. These changes were accompanied by upregulation of cGMP level and PKG-I protein content. The results of siRNA analysis showed that knockdown of PKG-I significantly attenuated gene expression, translocation and glucose uptake. Moreover, the PKG-I inhibitor also blocked the above processes. Furthermore, NO induced CREB phosphorylation, and CREB si...
Source: Endocrinology - December 28, 2017 Category: Endocrinology Authors: Tian Y, Heng D, Xu K, Liu W, Weng X, Hu X, Zhang C Tags: Endocrinology Source Type: research

Electrical pulse stimulation induces GLUT4 glucose transporter translocation in C2C12 myotubes that depends on Rab8A, Rab13 and Rab14.
In conclusion, EPS involves Rab8a, Rab13 and Rab14 to elicit GLUT4 translocation but not Rab10; moreover, Rab10 and Rab13 are not engaged by AMPK activation alone. C2C12-GLUT4HA cultures constitute a valuable in vitro model to investigate molecular mechanisms of contraction-stimulated GLUT4 translocation. PMID: 29089333 [PubMed - as supplied by publisher]
Source: Am J Physiol Endocri... - October 31, 2017 Category: Endocrinology Authors: Li Z, Yue Y, Hu F, Zhang C, Ma X, Li N, Qiu L, Fu M, Chen L, Yao Z, Bilan PJ, Klip A, Niu W Tags: Am J Physiol Endocrinol Metab Source Type: research

Importin α-importin β complex mediated nuclear translocation of insulin-like growth factor binding protein-5.
In this study, we further investigated the pathway mediating IGFBP-5 nuclear import after it retro-translocation. Importin-α5 was identified as an IGFBP-5-interacting protein with a yeast two-hybrid system, and its interaction with IGFBP-5 was further confirmed by GST pull down and co-immunoprecipitation. Binding affinity of IGFBP-5 and importins were determined by surface plasmon resonance (IGFBP-5/importin-β: KD=2.44e-7, IGFBP-5/importin-α5: KD=3.4e-7). Blocking the importin-α5/importin-β nuclear import pathway using SiRNA or dominant negative impotin-β dramatically inhibited IGFBP-5-EGFP nuclear import, though imp...
Source: Endocrine Journal - August 26, 2017 Category: Endocrinology Tags: Endocr J Source Type: research

Restoration of Nrf2 Signaling Normalizes the Regenerative Niche
We report that chronic hyperglycemia weakens the endogenous antioxidant response, and the consequences of this defect are manifested by intracellular redox dysregulation, which can be restored by Keap1 inhibition. Targeted siRNA-based therapy represents a novel, efficacious strategy to reestablish redox homeostasis and accelerate diabetic cutaneous tissue regeneration.
Source: Diabetes - February 23, 2016 Category: Endocrinology Authors: Soares, M. A.; Cohen, O. D.; Low, Y. C.; Sartor, R. A.; Ellison, T.; Anil, U.; Anzai, L.; Chang, J. B.; Saadeh, P. B.; Rabbani, P. S.; Ceradini, D. J. Tags: Signal Transduction Source Type: research

Molecular mechanisms underlying oxytocin-induced cardiomyocyte protection from simulated ischemia–reperfusion
In conclusion, the OTR protected H9c2 cells against I–R, especially if activated at the onset of ischemia or reperfusion. The OTR-transduced signals include pro-survival kinases, such as Akt and PKG.
Source: Molecular and Cellular Endocrinology - July 24, 2015 Category: Endocrinology Source Type: research

Testosterone stimulates glucose uptake and GLUT4 translocation through LKB1/AMPK signaling in 3T3-L1 adipocytes
This study was designed to determine the effects of testosterone on glucose uptake in adipocytes. Glucose uptake was assessed with 2-[3H] deoxyglucose in 3T3-L1 adipocytes. GLUT4 translocation was evaluated in plasma membrane (PM) sheets and PM fractions by immunofluorescence and immunoblotting, respectively. Activation of GLUT4 translocation-related protein kinases, including Akt, AMPK, LKB1, CaMKI, CaMKII, and Cbl was followed by immunoblotting. Expression levels of androgen receptor (AR) mRNA and AR translocation to the PM were assessed by real-time RT-PCR and immunoblotting, respectively. The results showed that both h...
Source: Endocrine - June 23, 2015 Category: Endocrinology Source Type: research

Transmembrane tumor necrosis factor-alpha sensitizes adipocytes to insulin
Publication date: 5 May 2015 Source:Molecular and Cellular Endocrinology, Volume 406 Author(s): Wenjing Zhou , Peng Yang , Li Liu , Shan Zheng , Qingling Zeng , Huifang Liang , Yazhen Zhu , Zunyue Zhang , Jing Wang , Bingjiao Yin , Feili Gong , Yiping Wu , Zhuoya Li Transmembrane TNF-α (tmTNF-α) acts both as a ligand, delivering ‘forward signaling’ via TNFR, and as a receptor, transducing ‘reverse signaling’. The contradiction of available data regarding the effect of tmTNF-α on insulin resistance may be due to imbalance in both signals. Here, we demonstrated that high glucose-induced impairment of insulin-sti...
Source: Molecular and Cellular Endocrinology - March 10, 2015 Category: Endocrinology Source Type: research

Oxytocin activates NF-κB-mediated inflammatory pathways in human gestational tissues
Publication date: Available online 14 November 2014 Source:Molecular and Cellular Endocrinology Author(s): Sung Hye Kim , David A. MacIntyre , Maria Firmino Da Silva , Andrew M. Blanks , Yun S Lee , Steven Thornton , Phillip R. Bennett , Vasso Terzidou Human labor, both at term and preterm, is preceded by NF-κB-mediated inflammatory activation within the uterus leading to myometrial activation, fetal membrane remodelling and cervical ripening. The stimuli triggering inflammatory activation in normal human parturition are not fully understood. We show that the neurohypophyseal peptide, oxytocin (OT), activates NF-κB and...
Source: Molecular and Cellular Endocrinology - November 14, 2014 Category: Endocrinology Source Type: research

Contribution of protein kinase Cα in the stimulation of insulin by the down-regulation of Ca v β subunits
We examined whether other types of Cavβ subunits also have similar properties. In this regard, we used small interfering RNA (siRNA) of these subunits (20 μg each) to down-regulate them and examined blood glucose, serum insulin and PKC translocation in isolated pancreatic β cells of mice. While the down-regulation of Cavβ2 and β3 subunits increased serum insulin levels and caused efficient glucose homeostasis, the down-regulation of Cavβ1 and β4 subunits failed to affect both these parameters. Examination of PKC isozymes in the pancreatic β-cells of Cavβ2- or β3 siRNA-injected mice showed that three PKC isozymes...
Source: Endocrine - October 23, 2014 Category: Endocrinology Source Type: research

SUMOylation protects against IL-1{beta}-induced apoptosis in INS-1 832/13 cells and human islets
We examined insulin secretion, intracellular Ca2+ responses, induction of endoplasmic reticulum stress markers and inducible nitric oxide synthase (iNOS) expression, and apoptosis by TUNEL and caspase 3 cleavage. Surprisingly, upregulation of SENP1 reduces insulin secretion and impairs intracellular Ca2+ handling. This secretory dysfunction is due to SENP1-induced cell death. Indeed, the detrimental effect of SENP1 on secretory function is diminished when two mediators of β-cell death, iNOS and NF-B, are pharmacologically inhibited. Conversely, enhanced SUMOylation protects against IL-1β-induced cell death. This ...
Source: AJP: Endocrinology and Metabolism - October 15, 2014 Category: Endocrinology Authors: Hajmrle, C., Ferdaoussi, M., Plummer, G., Spigelman, A. F., Lai, K., Manning Fox, J. E., MacDonald, P. E. Tags: Articles Source Type: research

Progesterone induces RhoA inactivation in male rat aortic smooth muscle cells through up-regulation of p27(kip1.)
Abstract Previously, we showed that progesterone (P4) at physiologic concentrations (5-500 nM) inhibits proliferation and migration of rat aortic smooth muscle cells (RASMC). The P4-induced migration inhibition in RASMC was resulted from Ras homolog gene family, member A (RhoA) inactivation induced by activating the cSrc/AKT/ERK 2/p38-mediated signaling pathway. We also demonstrated that up-regulation of p27(kip1) is involved in the P4-induced migration inhibition in RASMC. Since P4 can increase formation of the p27(kip1)-RhoA complex in RASMC, this finding led us to hypothesize that the P4-induced inactivation in...
Source: Endocrinology - August 19, 2014 Category: Endocrinology Authors: Wang HC, Lee WS Tags: Endocrinology Source Type: research

Depression of type I diacylglycerol kinases in pancreatic β-cells from male mice results in impaired insulin secretion.
This study investigated the expression and function of DGK in pancreatic β-cells. mRNA expression of type I DGK isoforms (α, β, γ) was detected in mouse pancreatic islets and the β-cell line MIN6. Protein expression of DGKα and γ was also detected in mouse β-cells and MIN6 cells. The type I DGK inhibitor R59949 inhibited high K(+)- and glucose-induced insulin secretion in MIN6 cells. Moreover, single knockdown of DGKα or γ by siRNA slightly but significantly decreased glucose- and high K(+)-induced insulin secretions, and the double knockdown further decreased them to the levels comparable to those induced by R59...
Source: Endocrinology - September 13, 2013 Category: Endocrinology Authors: Kurohane Kaneko Y, Kobayashi Y, Motoki K, Nakata K, Miyagawa S, Yamamoto M, Hayashi D, Shirai Y, Sakane F, Ishikawa T Tags: Endocrinology Source Type: research