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MYH9 facilitates autoregulation of adipose tissue depot development
Sin Ying Cheung, … , Liang Li, Brian J. Feldman
Sin Ying Cheung, … , Liang Li, Brian J. Feldman
Published May 10, 2021
Citation Information: JCI Insight. 2021;6(9):e136233. https://doi.org/10.1172/jci.insight.136233.
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Research Article Development Endocrinology

MYH9 facilitates autoregulation of adipose tissue depot development

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Abstract

White adipose tissue not only serves as a reservoir for energy storage but also secretes a variety of hormonal signals and modulates systemic metabolism. A substantial amount of adipose tissue develops in early postnatal life, providing exceptional access to the formation of this important tissue. Although a number of factors have been identified that can modulate the differentiation of progenitor cells into mature adipocytes in cell-autonomous assays, it remains unclear which are connected to physiological extracellular inputs and are most relevant to tissue formation in vivo. Here, we elucidate that mature adipocytes themselves signal to adipose depot–resident progenitor cells to direct depot formation in early postnatal life and gate adipogenesis when the tissue matures. Our studies revealed that as the adipose depot matures, a signal generated in mature adipocytes is produced, converges on progenitor cells to regulate the cytoskeletal protein MYH9, and attenuates the rate of adipogenesis in vivo.

Authors

Sin Ying Cheung, Mohd Sayeed, Krishnamurthy Nakuluri, Liang Li, Brian J. Feldman

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Figure 4

Adamts1/Wnt/Myh9 pathway regulates adipogenesis.

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Adamts1/Wnt/Myh9 pathway regulates adipogenesis.
(A) (Left) Representati...
(A) (Left) Representative images from light-phase microscopy of APCs isolated from wild-type mice 8 days after the induction of adipogenesis (with dexamethasone, insulin, and 3-Isobutyl-1-methylxanthine) and stained with oil red O and (right) quantification of oil red O levels using spectroscopy. Original magnification, ×100. (B) RT-qPCR quantifying the expression levels of markers of adipogenesis (Pparγ, C/ebpα, and Ap2) in APCs treated with rADAMTS1 or Myh9 or both (n = 5). (C) RT-qPCR monitoring the expression levels of markers of adipogenesis (Pparγ, C/ebpα, and Adipoq) after treatment with rADAMTS1 or rADAMTS1 rescued with Myh9 siRNA (n = 4). (D) Measurements of the calcium influx stimulated by rADAMTS1 exposure (n = 6). (E) Images of male wild-type, Adamts1-transgenic (Adamts1Tg), and Adamts1Tg mice treated with Bleb (Adamts1Tg + Bleb) mice. (F) Quantification of the whole-body weights of wild-type, Adamts1Tg, and Adamts1Tg + Bleb mice (n = 6). (G) Representative images of gross dissected epididymal (eWAT) and subcutaneous (scWAT) white adipose tissue depots from wild-type, Adamts1Tg, and Adamts1Tg + Bleb mice. (H) Quantification of the wet weights of scWAT and eWAT of wild-type, Adamts1Tg, and Adamts1Tg + Bleb mice (n = 6 mice for each type). (I) Quantification of the percentage of EdU+ adipocytes in eWAT and scWAT of wild-type, Adamts1Tg, and Adamts1Tg + Bleb mice by cytometry. Error bars represent mean ± SD. P values were calculated using t test (4D) or 1-way ANOVA with Tukey’s multiple comparisons post hoc test (A–C, F, H, and I). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

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