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3 results on '"miR‐424(322)/503"'

1. A microRNA Cluster Controls Fat Cell Differentiation and Adipose Tissue Expansion By Regulating SNCG.

Author

Rodríguez‐Barrueco, Ruth, Latorre, Jessica, Devis‐Jáuregui, Laura, Lluch, Aina, Bonifaci, Nuria, Llobet, Francisco J., Olivan, Mireia, Coll‐Iglesias, Laura, Gassner, Katja, Davis, Meredith L., Moreno‐Navarrete, José M., Castells‐Nobau, Anna, Plata‐Peña, Laura, Dalmau‐Pastor, Miki, Höring, Marcus, Liebisch, Gerhard, Olkkonen, Vesa M., Arnoriaga‐Rodríguez, Maria, Ricart, Wifredo, and Fernández‐Real, José M.

Subjects
*TISSUE differentiation, *ADIPOSE tissues, *FAT cells, *TISSUE expansion, *WEIGHT loss, *CELL physiology
Abstract

The H19X‐encoded miR‐424(322)/503 cluster regulates multiple cellular functions. Here, it is reported for the first time that it is also a critical linchpin of fat mass expansion. Deletion of this miRNA cluster in mice results in obesity, while increasing the pool of early adipocyte progenitors and hypertrophied adipocytes. Complementary loss and gain of function experiments and RNA sequencing demonstrate that miR‐424(322)/503 regulates a conserved genetic program involved in the differentiation and commitment of white adipocytes. Mechanistically, it is demonstrated that miR‐424(322)/503 targets γ‐Synuclein (SNCG), a factor that mediates this program rearrangement by controlling metabolic functions in fat cells, allowing adipocyte differentiation and adipose tissue enlargement. Accordingly, diminished miR‐424(322) in mice and obese humans co‐segregate with increased SNCG in fat and peripheral blood as mutually exclusive features of obesity, being normalized upon weight loss. The data unveil a previously unknown regulatory mechanism of fat mass expansion tightly controlled by the miR‐424(322)/503 through SNCG. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
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2. A microRNA Cluster Controls Fat Cell Differentiation and Adipose Tissue Expansion By Regulating SNCG

Author

Ruth Rodríguez‐Barrueco, Jessica Latorre, Laura Devis‐Jáuregui, Aina Lluch, Nuria Bonifaci, Francisco J. Llobet, Mireia Olivan, Laura Coll‐Iglesias, Katja Gassner, Meredith L. Davis, José M. Moreno‐Navarrete, Anna Castells‐Nobau, Laura Plata‐Peña, Miki Dalmau‐Pastor, Marcus Höring, Gerhard Liebisch, Vesa M. Olkkonen, Maria Arnoriaga‐Rodríguez, Wifredo Ricart, José M. Fernández‐Real, José M. Silva, Francisco J. Ortega, and David Llobet‐Navas

Subjects
γ‐Synuclein, adipocytes, adipose tissue, miR‐424(322)/503, obesity, Science
Abstract

Abstract The H19X‐encoded miR‐424(322)/503 cluster regulates multiple cellular functions. Here, it is reported for the first time that it is also a critical linchpin of fat mass expansion. Deletion of this miRNA cluster in mice results in obesity, while increasing the pool of early adipocyte progenitors and hypertrophied adipocytes. Complementary loss and gain of function experiments and RNA sequencing demonstrate that miR‐424(322)/503 regulates a conserved genetic program involved in the differentiation and commitment of white adipocytes. Mechanistically, it is demonstrated that miR‐424(322)/503 targets γ‐Synuclein (SNCG), a factor that mediates this program rearrangement by controlling metabolic functions in fat cells, allowing adipocyte differentiation and adipose tissue enlargement. Accordingly, diminished miR‐424(322) in mice and obese humans co‐segregate with increased SNCG in fat and peripheral blood as mutually exclusive features of obesity, being normalized upon weight loss. The data unveil a previously unknown regulatory mechanism of fat mass expansion tightly controlled by the miR‐424(322)/503 through SNCG.

Published
2022
Full Text
View/download PDF

3. A microRNA cluster controls fat cell differentiation and adipose tissue expansion by regulating SNCG

Author

Ruth Rodríguez‐Barrueco, Jessica Latorre, Laura Devis‐Jáuregui, Aina Lluch, Nuria Bonifaci, Francisco J. Llobet, Mireia Olivan, Laura Coll‐Iglesias, Katja Gassner, Meredith L. Davis, José M. Moreno‐Navarrete, Anna Castells‐Nobau, Laura Plata‐Peña, Miki Dalmau‐Pastor, Marcus Höring, Gerhard Liebisch, Vesa M. Olkkonen, Maria Arnoriaga‐Rodríguez, Wifredo Ricart, José M. Fernández‐Real, José M. Silva, Francisco J. Ortega, David Llobet‐Navas, Medicum, and Department of Anatomy

Subjects
Male, miR‐424(322)/503, obesity, γ‐Synuclein, General Chemical Engineering, adipocytes, Science, General Physics and Astronomy, Medicine (miscellaneous), ADIPOCYTE PRECURSOR CELLS, Biochemistry, Genetics and Molecular Biology (miscellaneous), Mice, gamma-Synuclein, Cell diferentiation, Animals, Humans, General Materials Science, Obesity, TANDEM MASS-SPECTROMETRY, Experimentació animal, LIPID EXTRACTION, Mice, Inbred BALB C, Adipogenesis, GROWTH-FACTOR-BETA, INSULIN SENSITIVITY, SET ENRICHMENT ANALYSIS, General Engineering, BREAST-CANCER CELLS, Cell Differentiation, Adipose tissues, miR-424(322)/503, HIGH-THROUGHPUT QUANTIFICATION, Neoplasm Proteins, adipose tissue, Mice, Inbred C57BL, TRANSCRIPTION FACTORS, MicroRNAs, Teixit adipós, 3121 General medicine, internal medicine and other clinical medicine, Animal experimentation, 1182 Biochemistry, cell and molecular biology, Obesitat, Female, 3111 Biomedicine, Diferenciació cel·lular, EXPRESSION ANALYSIS
Abstract

The H19X-encoded miR-424(322)/503 cluster regulates multiple cellular functions. Here, it is reported for the first time that it is also a critical linchpin of fat mass expansion. Deletion of this miRNA cluster in mice results in obesity, while increasing the pool of early adipocyte progenitors and hypertrophied adipocytes. Complementary loss and gain of function experiments and RNA sequencing demonstrate that miR-424(322)/503 regulates a conserved genetic program involved in the differentiation and commitment of white adipocytes. Mechanistically, it is demonstrated that miR-424(322)/503 targets gamma-Synuclein (SNCG), a factor that mediates this program rearrangement by controlling metabolic functions in fat cells, allowing adipocyte differentiation and adipose tissue enlargement. Accordingly, diminished miR-424(322) in mice and obese humans co-segregate with increased SNCG in fat and peripheral blood as mutually exclusive features of obesity, being normalized upon weight loss. The data unveil a previously unknown regulatory mechanism offat mass expansion tightly controlled by the miR-424(322)/503 through SNCG.

Published
2021

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