Comparative analysis of the secretory proteome of human adipose stromal vascular fraction cells during adipogenesis

Kim, Jaeyoon; Choi, Yoon Sup; Lim, Seyoung; Yea, Kyungmoo; Yoon, Jong Hyuk; Jun, Dong-Jae; Ha, Sung Ho; Kim, Jung-Wook; Kim, Jae Ho; Suh, Pann‐Ghill; Ryu, Sung Ho; Lee, Taehoon G.

doi:10.1002/pmic.200900218

Cited by 67 publications

(62 citation statements)

References 43 publications

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“…22 Proteomics analysis has identified secretory factors associated with adipogenesis in human adipose stromal vascular fraction cells and differentiated adipocytes. 23 Although proteomic methods have been used to characterize drug transporters and receptors at the BBB, 11,[24][25][26] the changes of BBB proteomes after DIO have not been shown previously. The proteins identified in our study are involved in a variety of cellular functions, cytoskeleton stability, stress response, vesicular transport, and energy metabolism ( Table 3).…”

Section: Discussionmentioning

confidence: 99%

Diet-Induced Obesity Suppresses Expression of Many Proteins at the Blood–Brain Barrier

Ouyang

Hsuchou

Kastin

et al. 2013

J Cereb Blood Flow Metab

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The blood-brain barrier (BBB) is a regulatory interface between the central nervous system and the rest of the body. However, BBB changes in obesity and metabolic syndrome have not been fully elucidated. We hypothesized that obesity reduces energy metabolism in the cerebral microvessels composing the BBB, reflected by downregulation of protein expression and function. We performed comparative proteomic analyses in enriched microvessels from the cerebral cortex of mice 2 months after ingestion of a high-fat diet or regular rodent chow. In mice with diet-induced obesity (DIO), there was downregulation of 47 proteins in the cerebral microvessels, including cytoskeletal proteins, chaperons, enzymes, transport-related proteins, and regulators for transcriptional and translational activities. Only two proteins, involved in messenger RNA (mRNA) transport and processing, were upregulated. The changes of these proteins were further validated by quantitative polymerase chain reaction (qPCR), western blotting, and immunofluorescent staining of freshly isolated microvessels, in samples obtained from different batches of mice. The predominant downregulation suggests that DIO suppresses metabolic activity of BBB microvessels. The finding of a hypometabolic state of the BBB in mice at the chronic stage of DIO is unexpected and unprecedented; it may provide novel mechanistic insight into how obesity influences CNS function via regulatory changes of the BBB. Keywords: blood-brain barrier; cerebral microvessels; high-fat diet; mass spectrometry; obesity; proteomics INTRODUCTION Obesity has become one of the most critical problems in human health and is associated with many complications of metabolic diseases. 1,2 Proteomic methods have been used to investigate human and mouse obesity, but most reports have focused on changes in adipose tissue. [3][4][5][6] Recent results suggest that the blood-brain barrier (BBB) is activated in obesity; for example, mice with adult-onset obesity show resistance to leptin transport across the BBB, region-specific astrogliosis, and upregulation of astrocytic leptin receptors. 7,8 The BBB is a regulatory interface between the central nervous system (CNS) and the peripheral circulation. It is a complex threedimensional structure composed of specialized endothelial cells that are reinforced by pericytes, astrocytic endfeet, and extracellular matrix. The tight junctions between the endothelia and the continuous basement membrane prevent diffusion of large non-lipophilic molecules between the CNS parenchyma (brain and spinal cord) and the circulation. The function of the BBB is further reinforced by a high mitochondrial content that ensures sufficient energy, an abundance of enzymes, and metabolically active astrocytes. The functions of the BBB in obesity, however, remain unclear. We predicted that BBB homeostasis is disturbed by metabolic changes in obesity.Although normal transport and secretory functions of the BBB are essential for CNS function, proteomic analyses have shown that BBB activity is ch...

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Section: Discussionmentioning

confidence: 99%

Diet-Induced Obesity Suppresses Expression of Many Proteins at the Blood–Brain Barrier

Ouyang

Hsuchou

Kastin

et al. 2013

J Cereb Blood Flow Metab

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“…However, there is limited information about global expression of potential adipokines in adipocytes and other cells of adipose tissue. Recently, proteomics have been applied to determine the secretion pattern of peptides from human subcutaneous progenitor cells undergoing in vitro differentiation to fat cells (Kim et al, 2010;Zhong et al, 2010). We recently identified 347 proteins in a profiling on concentrated conditioned medium derived from primary human in vitro differentiated adipocytes using SDS-PAGE/LC-ESI-MS/MS…”

Section: Introductionmentioning

confidence: 99%

Functional annotation of the human fat cell secretome

Dahlman

Elsen

Tennagels

et al. 2012

Archives of Physiology and Biochemistry

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“…Adipokines have been shown to influence a wide range of biological functions, such as immunity, insulin sensitivity, inflammation, blood pressure, lipid metabolism, energy homeostasis and appetite (Trayhurn and Wood, 2004). To date, over 100 adipokines have been cataloged and more adipokines continue to be discovered using new technologies and innovative approaches (Shah et al, 2009;Mutch et al, 2009a;Kim et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Fatty acid–gene interactions, adipokines and obesity

Stryjecki

Mutch

2011

Eur J Clin Nutr

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It is now recognized that the low-grade inflammation observed with obesity is associated with the development of a wide range of downstream complications. As such, there is considerable interest in elucidating the regulatory mechanisms underlying the production of inflammatory molecules to improve the prevention and treatment of obesity and its co-morbidities. White adipose tissue is no longer considered a passive reservoir for storing lipids, but rather an important organ influencing energy metabolism, insulin sensitivity and inflammation by the secretion of proteins, commonly referred to as adipokines. Dysregulation of several adipokines, such as tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6) and adiponectin, contributes to the low-grade inflammation that is a hallmark of obesity. Evidence now suggests that fatty acids represent a class of molecules that can modulate adipokine production, thereby influencing inflammatory status. Although the precise molecular mechanisms by which dietary fats regulate adipokine production remain unclear, recent findings indicate that diet-gene interactions may have an important role in the transcriptional and secretory regulation of adipokines. Single-nucleotide polymorphisms in the genes encoding TNF-a, IL-6 and adiponectin can modify circulating levels of these adipokines and, subsequently, obesity-related phenotypes. This genetic variation can also alter the influence of dietary fatty acids on adipokine production. Therefore, the current review will show that it is paramount to consider both genetic information and dietary fat intake to unravel the interindividual variability in inflammatory response observed in intervention protocols targeting obesity.

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Comparative analysis of the secretory proteome of human adipose stromal vascular fraction cells during adipogenesis

Cited by 67 publications

References 43 publications

Diet-Induced Obesity Suppresses Expression of Many Proteins at the Blood–Brain Barrier

Diet-Induced Obesity Suppresses Expression of Many Proteins at the Blood–Brain Barrier

Functional annotation of the human fat cell secretome

Fatty acid–gene interactions, adipokines and obesity

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