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Artikel ; Online: New Insights Into the Long Non-coding RNA SRA

Liang Sheng / Lan Ye / Dong Zhang / William P. Cawthorn / Bin Xu

Frontiers in Medicine, Vol

Physiological Functions and Mechanisms of Action

2018 Band 5

Abstract: Long non-coding RNAs (lncRNA) are emerging as new genetic/epigenetic regulators that can impact almost all physiological functions. Here, we focus on the long non-coding steroid receptor RNA activator (SRA), including new insights into its effects on ... ...

Abstract	Long non-coding RNAs (lncRNA) are emerging as new genetic/epigenetic regulators that can impact almost all physiological functions. Here, we focus on the long non-coding steroid receptor RNA activator (SRA), including new insights into its effects on gene expression, the cell cycle, and differentiation; how these relate to physiology and disease; and the mechanisms underlying these effects. We discuss how SRA acts as an RNA coactivator in nuclear receptor signaling; its effects on steroidogenesis, adipogenesis, and myocyte differentiation; the impact on breast and prostate cancer tumorigenesis; and, finally, its ability to modulate hepatic steatosis through several signaling pathways. Genome-wide analysis reveals that SRA regulates hundreds of target genes in adipocytes and breast cancer cells and binds to thousands of genomic sites in human pluripotent stem cells. Recent studies indicate that SRA acts as a molecular scaffold and forms networks with numerous coregulators and chromatin-modifying regulators in both activating and repressive complexes. We discuss how modifications to SRA's unique stem-loop secondary structure are important for SRA function, and highlight the various SRA isoforms and mutations that have clinical implications. Finally, we discuss the future directions for better understanding the molecular mechanisms of SRA action and how this might lead to new diagnostic and therapeutic approaches.
Schlagwörter	long non-coding RNA (lncRNA) ; steroid receptor RNA activator (SRA) ; physiological functions ; regulation of gene expression ; differentiation ; Medicine (General) ; R5-920
Sprache	Englisch
Erscheinungsdatum	2018-09-01T00:00:00Z
Verlag	Frontiers Media S.A.
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: Bone marrow adipose tissue does not express UCP1 during development or adrenergic-induced remodeling

Clarissa S. Craft / Hero Robles / Madelyn R. Lorenz / Eric D. Hilker / Kristann L. Magee / Thomas L. Andersen / William P. Cawthorn / Ormond A. MacDougald / Charles A. Harris / Erica L. Scheller

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Band 14

Abstract: Abstract Adipocytes within the skeleton are collectively termed bone marrow adipose tissue (BMAT). BMAT contributes to peripheral and local metabolism, however, its capacity for cell-autonomous expression of uncoupling protein 1 (UCP1), a biomarker of ... ...

Abstract	Abstract Adipocytes within the skeleton are collectively termed bone marrow adipose tissue (BMAT). BMAT contributes to peripheral and local metabolism, however, its capacity for cell-autonomous expression of uncoupling protein 1 (UCP1), a biomarker of beige and brown adipogenesis, remains unclear. To overcome this, Ucp1-Cre was used to drive diphtheria toxin expression in cells expressing UCP1 (Ucp1 Cre+/DTA+). Despite loss of brown adipose tissue, BMAT volume was not reduced in Ucp1 Cre+/DTA+ mice. Comparably, in mTmG reporter mice (Ucp1 Cre+/mTmG+), Ucp1-Cre expression was absent from BMAT in young (3-weeks) and mature (16-weeks) male and female mice. Further, β3-agonist stimulation failed to induce Ucp1-Cre expression in BMAT. This demonstrates that BMAT adipocytes are not UCP1-expressing beige/brown adipocytes. Thus, to identify novel and emerging roles for BMAT adipocytes in skeletal and whole-body homeostasis, we performed gene enrichment analysis of microarray data from adipose tissues of adult rabbits. Pathway analysis revealed genetic evidence for differences in BMAT including insulin resistance, decreased fatty acid metabolism, and enhanced contributions to local processes including bone mineral density through candidate genes such as osteopontin. In sum, this supports a paradigm by which BMAT adipocytes are a unique subpopulation that is specialized to support cells within the skeletal and hematopoietic niche.
Schlagwörter	Medicine ; R ; Science ; Q
Thema/Rubrik (Code)	616
Sprache	Englisch
Erscheinungsdatum	2019-11-01T00:00:00Z
Verlag	Nature Publishing Group
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: Adipose specific disruption of seipin causes early-onset generalised lipodystrophy and altered fuel utilisation without severe metabolic disease

George D. Mcilroy / Karla Suchacki / Anke J. Roelofs / Wulin Yang / Yanyun Fu / Bo Bai / Robert J. Wallace / Cosimo De Bari / William P. Cawthorn / Weiping Han / Mirela Delibegović / Justin J. Rochford

Molecular Metabolism, Vol 10, Iss , Pp 55-

2018 Band 65

Abstract: Objective: Mutations to the BSCL2 gene disrupt the protein seipin and cause the most severe form of congenital generalised lipodystrophy (CGL). Affected individuals exhibit a near complete loss of white adipose tissue (WAT) and suffer from metabolic ... ...

Abstract	Objective: Mutations to the BSCL2 gene disrupt the protein seipin and cause the most severe form of congenital generalised lipodystrophy (CGL). Affected individuals exhibit a near complete loss of white adipose tissue (WAT) and suffer from metabolic disease. Seipin is critical for adipocyte development in culture and mice with germline disruption to Bscl2 recapitulate the effects of BSCL2 disruption in humans. Here we examined whether loss of Bscl2 specifically in developing adipocytes in vivo is sufficient to prevent adipose tissue development and cause all features observed with congenital BSCL2 disruption. Methods: We generated and characterised a novel mouse model of Bscl2 deficiency in developing adipocytes (Ad-B2(−/−)) using the adipose-specific Adiponectin-Cre line. Results: We demonstrate that Ad-B2(−/−) mice display early onset lipodystrophy, in common with congenital Bscl2 null mice and CGL2 patients. However, glucose intolerance, insulin resistance, and severe hepatic steatosis are not apparent. Food intake and energy expenditure are unchanged, but Ad-B2(−/−) mice exhibit significantly altered substrate utilisation. We also find differential effects of seipin loss between specific adipose depots revealing new insights regarding their varied characteristics. When fed a high-fat diet, Ad-B2(−/−) mice entirely fail to expand adipose mass but remain glucose tolerant. Conclusions: Our findings demonstrate that disruption of Bscl2 specifically in developing adipocytes is sufficient to cause the early-onset generalised lipodystrophy observed in patients with mutations in BSCL2. However, this significant reduction in adipose mass does not cause the overt metabolic dysfunction seen in Bscl2 knockout mice, even following a high-fat diet challenge. Keywords: BSCL2, Seipin, CGL2, Lipodystrophy, Adipose tissue, Browning
Schlagwörter	Internal medicine ; RC31-1245
Thema/Rubrik (Code)	610
Sprache	Englisch
Erscheinungsdatum	2018-04-01T00:00:00Z
Verlag	Elsevier
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: PHOSPHO1 is a skeletal regulator of insulin resistance and obesity

BMC Biology, Vol 18, Iss 1, Pp 1-

2020 Band 20

Abstract: Abstract Background The classical functions of the skeleton encompass locomotion, protection and mineral homeostasis. However, cell-specific gene deletions in the mouse and human genetic studies have identified the skeleton as a key endocrine regulator ... ...

Abstract	Abstract Background The classical functions of the skeleton encompass locomotion, protection and mineral homeostasis. However, cell-specific gene deletions in the mouse and human genetic studies have identified the skeleton as a key endocrine regulator of metabolism. The bone-specific phosphatase, Phosphatase, Orphan 1 (PHOSPHO1), which is indispensable for bone mineralisation, has been recently implicated in the regulation of energy metabolism in humans, but its role in systemic metabolism remains unclear. Here, we probe the mechanism underlying metabolic regulation by analysing Phospho1 mutant mice. Results Phospho1 −/− mice exhibited improved basal glucose homeostasis and resisted high-fat-diet-induced weight gain and diabetes. The metabolic protection in Phospho1 −/− mice was manifested in the absence of altered levels of osteocalcin. Osteoblasts isolated from Phospho1 −/− mice were enriched for genes associated with energy metabolism and diabetes; Phospho1 both directly and indirectly interacted with genes associated with glucose transport and insulin receptor signalling. Canonical thermogenesis via brown adipose tissue did not underlie the metabolic protection observed in adult Phospho1 −/− mice. However, the decreased serum choline levels in Phospho1 −/− mice were normalised by feeding a 2% choline rich diet resulting in a normalisation in insulin sensitivity and fat mass. Conclusion We show that mice lacking the bone mineralisation enzyme PHOSPHO1 exhibit improved basal glucose homeostasis and resist high-fat-diet-induced weight gain and diabetes. This study identifies PHOSPHO1 as a potential bone-derived therapeutic target for the treatment of obesity and diabetes.
Schlagwörter	PHOSPHO1 ; Osteocalcin ; Choline ; Bone ; Energy metabolism ; Insulin ; Biology (General) ; QH301-705.5
Thema/Rubrik (Code)	616
Sprache	Englisch
Erscheinungsdatum	2020-10-01T00:00:00Z
Verlag	BMC
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: Sweet taste receptor deficient mice have decreased adiposity and increased bone mass.

Becky R Simon / Brian S Learman / Sebastian D Parlee / Erica L Scheller / Hiroyuki Mori / William P Cawthorn / Xiaomin Ning / Venkatesh Krishnan / Yanfei L Ma / Björn Tyrberg / Ormond A MacDougald

PLoS ONE, Vol 9, Iss 1, p e

2014 Band 86454

Abstract: Functional expression of sweet taste receptors (T1R2 and T1R3) has been reported in numerous metabolic tissues, including the gut, pancreas, and, more recently, in adipose tissue. It has been suggested that sweet taste receptors in these non-gustatory ... ...

Abstract	Functional expression of sweet taste receptors (T1R2 and T1R3) has been reported in numerous metabolic tissues, including the gut, pancreas, and, more recently, in adipose tissue. It has been suggested that sweet taste receptors in these non-gustatory tissues may play a role in systemic energy balance and metabolism. Smaller adipose depots have been reported in T1R3 knockout mice on a high carbohydrate diet, and sweet taste receptors have been reported to regulate adipogenesis in vitro. To assess the potential contribution of sweet taste receptors to adipose tissue biology, we investigated the adipose tissue phenotypes of T1R2 and T1R3 knockout mice. Here we provide data to demonstrate that when fed an obesogenic diet, both T1R2 and T1R3 knockout mice have reduced adiposity and smaller adipocytes. Although a mild glucose intolerance was observed with T1R3 deficiency, other metabolic variables analyzed were similar between genotypes. In addition, food intake, respiratory quotient, oxygen consumption, and physical activity were unchanged in T1R2 knockout mice. Although T1R2 deficiency did not affect adipocyte number in peripheral adipose depots, the number of bone marrow adipocytes is significantly reduced in these knockout animals. Finally, we present data demonstrating that T1R2 and T1R3 knockout mice have increased cortical bone mass and trabecular remodeling. This report identifies novel functions for sweet taste receptors in the regulation of adipose and bone biology, and suggests that in these contexts, T1R2 and T1R3 are either dependent on each other for activity or have common independent effects in vivo.
Schlagwörter	Medicine ; R ; Science ; Q
Thema/Rubrik (Code)	571
Sprache	Englisch
Erscheinungsdatum	2014-01-01T00:00:00Z
Verlag	Public Library of Science (PLoS)
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: SRA regulates adipogenesis by modulating p38/JNK phosphorylation and stimulating insulin receptor gene expression and downstream signaling.

Shannon Liu / Ruichuan Xu / Isabelle Gerin / William P Cawthorn / Ormond A Macdougald / Xiao-Wei Chen / Alan R Saltiel / Ronald J Koenig / Bin Xu

PLoS ONE, Vol 9, Iss 4, p e

2014 Band 95416

Abstract: The Steroid Receptor RNA Activator (SRA) enhances adipogenesis and increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin. To assess the mechanism, we differentiated ST2 mesenchymal precursor cells that did or did not ... ...

Abstract	The Steroid Receptor RNA Activator (SRA) enhances adipogenesis and increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin. To assess the mechanism, we differentiated ST2 mesenchymal precursor cells that did or did not overexpress SRA into adipocytes using combinations of methylisobutylxanthine, dexamethasone and insulin. These studies showed that SRA overexpression promotes full adipogenesis in part by stimulation of insulin/insulin-like growth factor-1 (IGF-1) signaling. SRA overexpression inhibited phosphorylation of p38 mitogen activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) in the early differentiation of ST2 cells. Conversely, knockdown of endogenous SRA in 3T3-L1 cells increased phosphorylation of JNK. Knockdown of SRA in mature 3T3-L1 adipocytes reduced insulin receptor (IR) mRNA and protein levels, which led to decreased autophosphorylation of IRβ and decreased phosphorylation of insulin receptor substrate-1 (IRS-1) and Akt. This likely reflects a stimulatory role of SRA on IR transcription, as transfection studies showed that SRA increased expression of an IR promoter-luciferase reporter construct.
Schlagwörter	Medicine ; R ; Science ; Q
Thema/Rubrik (Code)	571
Sprache	Englisch
Erscheinungsdatum	2014-01-01T00:00:00Z
Verlag	Public Library of Science (PLoS)
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: Correction

Erica L. Scheller / Casey R. Doucette / Brian S. Learman / William P. Cawthorn / Shaima Khandaker / Benjamin Schell / Brent Wu / Shi-Ying Ding / Miriam A. Bredella / Pouneh K. Fazeli / Basma Khoury / Karl J. Jepsen / Paul F. Pilch / Anne Klibanski / Clifford J. Rosen / Ormond A. MacDougald

Nature Communications, Vol 7, Iss 1, Pp 1-

Corrigendum: Region-specific variation in the properties of skeletal adipocytes reveals regulated and constitutive marrow adipose tissues

2016 Band 2

Abstract: Nature Communications 6: Article number: 7808 (2015); Published: 6 August 2015; Updated: 8 December 2016 In Figure 3 of this Article, marrow adipose tissue volumes (in panels b and c) and adipocyte numbers (in panel g) were calculated incorrectly. In Fig. ...

Abstract	Nature Communications 6: Article number: 7808 (2015); Published: 6 August 2015; Updated: 8 December 2016 In Figure 3 of this Article, marrow adipose tissue volumes (in panels b and c) and adipocyte numbers (in panel g) were calculated incorrectly. In Fig. 3b,c, regional MAT volumes in the ‘GP to T/FJ’ group were normalized incorrectly to both regional marrow volume and total marrow volume instead of normalizing to total marrow volume only.
Schlagwörter	Science ; Q
Sprache	Englisch
Erscheinungsdatum	2016-12-01T00:00:00Z
Verlag	Nature Portfolio
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: Bone marrow adipose tissue is a unique adipose subtype with distinct roles in glucose homeostasis

Karla J. Suchacki / Adriana A. S. Tavares / Domenico Mattiucci / Erica L. Scheller / Giorgos Papanastasiou / Calum Gray / Matthew C. Sinton / Lynne E. Ramage / Wendy A. McDougald / Andrea Lovdel / Richard J. Sulston / Benjamin J. Thomas / Bonnie M. Nicholson / Amanda J. Drake / Carlos J. Alcaide-Corral / Diana Said / Antonella Poloni / Saverio Cinti / Gavin J. Macpherson /

Marc R. Dweck / Jack P. M. Andrews / Michelle C. Williams / Robert J. Wallace / Edwin J. R. van Beek / Ormond A. MacDougald / Nicholas M. Morton / Roland H. Stimson / William P. Cawthorn

Nature Communications, Vol 11, Iss 1, Pp 1-

2020 Band 18

Abstract: Bone marrow adipose tissue (BMAT) comprises over 10% of total fat mass but its systemic metabolic role is unclear. Here, the authors show that BMAT glucose uptake is not insulin or cold responsive; however, BMAT basal glucose uptake is higher than in ... ...

Abstract	Bone marrow adipose tissue (BMAT) comprises over 10% of total fat mass but its systemic metabolic role is unclear. Here, the authors show that BMAT glucose uptake is not insulin or cold responsive; however, BMAT basal glucose uptake is higher than in white adipose tissue or skeletal muscle, underscoring BMAT’s potential to influence systemic glucose homeostasis.
Schlagwörter	Science ; Q
Sprache	Englisch
Erscheinungsdatum	2020-06-01T00:00:00Z
Verlag	Nature Portfolio
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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Artikel ; Online: Multiple roles for the non-coding RNA SRA in regulation of adipogenesis and insulin sensitivity.

Bin Xu / Isabelle Gerin / Hongzhi Miao / Dang Vu-Phan / Craig N Johnson / Ruichuan Xu / Xiao-Wei Chen / William P Cawthorn / Ormond A MacDougald / Ronald J Koenig

PLoS ONE, Vol 5, Iss 12, p e

2010 Band 14199

Abstract: Peroxisome proliferator-activated receptor-γ (PPARγ) is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARγ coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and ... ...

Abstract	Peroxisome proliferator-activated receptor-γ (PPARγ) is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARγ coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and physiology. We show that the non-coding RNA, Steroid receptor RNA Activator (SRA), associates with PPARγ and coactivates PPARγ-dependent reporter gene expression. Overexpression of SRA in ST2 mesenchymal precursor cells promotes their differentiation into adipocytes. Conversely, knockdown of endogenous SRA inhibits 3T3-L1 preadipocyte differentiation. Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes involved in the cell cycle, and insulin and TNFα signaling pathways. Some functions of SRA may involve mechanisms other than coactivation of PPARγ. SRA in adipocytes increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin. SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2. SRA also inhibits the expression of adipocyte-related inflammatory genes and TNFα-induced phosphorylation of c-Jun NH(2)-terminal kinase. In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways.
Schlagwörter	Medicine ; R ; Science ; Q
Thema/Rubrik (Code)	571
Sprache	Englisch
Erscheinungsdatum	2010-12-01T00:00:00Z
Verlag	Public Library of Science (PLoS)
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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