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MYH9 facilitates autoregulation of adipose tissue depot development
Sin Ying Cheung, Mohd Sayeed, Krishnamurthy Nakuluri, Liang Li, Brian J. Feldman
Sin Ying Cheung, Mohd Sayeed, Krishnamurthy Nakuluri, Liang Li, Brian J. Feldman
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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 1

Adamts1 and Myh9 expression changes during adipose depot development.

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Adamts1 and Myh9 expression changes during adipose depot development.
(A...
(A) RT-qPCR quantifying Adamts1 and Myh9 expression levels in white adipose tissue harvested from 3-week-old and 8-week-old male wild-type mice (n = 6). (B) Immunoblots (left) with quantification (right) of ADAMTS1 and MHY9 from white adipose tissue harvested from 3-week-old and 8-week-old male wild-type mice and their quantification (n = 3). (C) Immunoblots (left) with quantification (right) of MYH9 levels in APCs isolated from male wild-type mice and treated with rADAMTS1 (100 ng/mL), myosin II inhibitor blebbistatin (Bleb) (30 μM), or both rADAMTS1 and Bleb (n = 4). Error bars represent mean ± SD. P values were calculated using t tests. **P < 0.01, ***P < 0.001. Post hoc Bonferroni’s test was performed in C.

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