bims-aditis Biomed News
on Adipose tissue, inflammation, immunometabolism
Issue of 2022–04–17
seven papers selected by
Matthew C. Sinton, University of Glasgow
  1. Immune Cell Regulation of White Adipose Progenitor Cell Fate.
  2. Three Layers of Intestinal γδ T Cells Talk Different Languages With the Microbiota.
  3. Plin5 Bidirectionally Regulates Lipid Metabolism in Oxidative Tissues.
  4. Preventing White Adipocyte Browning during Differentiation In Vitro: The Effect of Differentiation Protocols on Metabolic and Mitochondrial Phenotypes.
  5. Intravital lipid droplet labeling and imaging reveals the phenotypes and functions of individual macrophages in vivo.
  6. Phenotypical Conversions of Dermal Adipocytes as Pathophysiological Steps in Inflammatory Cutaneous Disorders.
  7. Nutrition, metabolism, and epigenetics: pathways of circadian reprogramming.
  1. Front Endocrinol (Lausanne). 2022 ;13 859044
    Immune Cell Regulation of White Adipose Progenitor Cell Fate.
    Irem Altun, Xiaocheng Yan, Siegfried Ussar.
      Adipose tissue is essential for energy storage and endocrine regulation of metabolism. Imbalance in energy intake and expenditure result in obesity causing adipose tissue dysfunction. This alters cellular composition of the stromal cell populations and their function. Moreover, the individual cellular composition of each adipose tissue depot, regulated by environmental factors and genetics, determines the ability of the depots to expand and maintain its endocrine and storage function. Thus, stromal cells modulate adipocyte function and vice versa. In this mini-review we discuss heterogeneity in terms of composition and fate of adipose progenitor subtypes and their interactions with and regulation by different immune cell populations. Immune cells are the most diverse cell populations in adipose tissue and play essential roles in regulating adipose tissue function via interaction with adipocytes but also with adipocyte progenitors. We specifically discuss the role of macrophages, mast cells, innate lymphoid cells and T cells in the regulation of adipocyte progenitor proliferation, differentiation and lineage commitment. Understanding the factors and cellular interactions regulating preadipocyte expansion and fate decision will allow the identification of novel mechanisms and therapeutic strategies to promote healthy adipose tissue expansion without systemic metabolic impairment.
    Keywords:  adipose precursor cells; adipose tissue expansion; differentiation; immune cells; obesity; preadipocyte; proliferation
    DOI:  https://doi.org/10.3389/fendo.2022.859044
  2. Front Immunol. 2022 ;13 849954
    Three Layers of Intestinal γδ T Cells Talk Different Languages With the Microbiota.
    Francesca Rampoldi, Immo Prinz.
      The mucosal surfaces of our body are the main contact site where the immune system encounters non-self molecules from food-derived antigens, pathogens, and symbiotic bacteria. γδ T cells are one of the most abundant populations in the gut. Firstly, they include intestinal intraepithelial lymphocytes, which screen and maintain the intestinal barrier integrity in close contact with the epithelium. A second layer of intestinal γδ T cells is found among lamina propria lymphocytes (LPL)s. These γδ LPLs are able to produce IL-17 and likely have functional overlap with local Th17 cells and innate lymphoid cells. In addition, a third population of γδ T cells resides within the Peyer´s patches, where it is probably involved in antigen presentation and supports the mucosal humoral immunity. Current obstacles in understanding γδ T cells in the gut include the lack of information on cognate ligands of the γδ TCR and an incomplete understanding of their physiological role. In this review, we summarize and discuss what is known about different subpopulations of γδ T cells in the murine and human gut and we discuss their interactions with the gut microbiota in the context of homeostasis and pathogenic infections.
    Keywords:  IEL intra-epithelial lymphocyte; Peyer’s patch; gut epithelia; lamina propria (LP); γδ T cells
    DOI:  https://doi.org/10.3389/fimmu.2022.849954
  3. Oxid Med Cell Longev. 2022 ;2022 4594956
    Plin5 Bidirectionally Regulates Lipid Metabolism in Oxidative Tissues.
    Xinqing Zhang, Wu Xu, Rui Xu, Zhen Wang, Xinyan Zhang, Peng Wang, Ke Peng, Meiling Li, Jing Li, Yanfei Tan, Xiong Wang, Haifeng Pei.
      Cytoplasmic lipid droplets (LDs) can store neutral lipids as an energy source when needed and also regulate the key metabolic processes of intracellular lipid accumulation, which is associated with several metabolic diseases. The perilipins (Plins) are a family of proteins that associate with the surface of LDs. As a member of Plins superfamily, perilipin 5 (Plin5) coats LDs in cardiomyocytes, which is significantly related to reactive oxygen species (ROS) production originated from mitochondria in the heart, consequently determining the progression of diabetic cardiomyopathy. Plin5 may play a bidirectional function in lipid metabolism which is in a state of dynamic balance. In the basic state, Plin5 inhibited the binding of comparative gene identification-58 (CGI-58) to adipose triglyceride lipase (ATGL) by binding CGI-58, thus inhibiting lipolysis. However, when the body is under stress (such as cold, fasting, exercise, and other stimuli), protein kinase A (PKA) phosphorylates and activates Plin5, which then causes Plin5 to release the binding site of CGI-58 and ATGL, prompting CGI-58 to bind to ATGL and activate ATGL activity, thus accelerating the lipolysis process, revealing the indispensable role of Plin5 in lipid turnover. Here, the purpose of this review is to summarize the present understanding of the bidirectional regulation role of Plin5 in oxidative tissues and to reveal its potential role in diabetic cardiomyopathy protection.
    DOI:  https://doi.org/10.1155/2022/4594956
  4. Stem Cells Int. 2022 ;2022 3308194
    Preventing White Adipocyte Browning during Differentiation In Vitro: The Effect of Differentiation Protocols on Metabolic and Mitochondrial Phenotypes.
    Elena Herbers, Mimmi Patrikoski, Anita Wagner, Riikka Jokinen, Antti Hassinen, Sini Heinonen, Susanna Miettinen, Hilkka Peltoniemi, Eija Pirinen, Kirsi H Pietiläinen.
      Mitochondrial dysfunction in white adipose tissue is strongly associated with obesity and its metabolic complications, which are important health challenges worldwide. Human adipose-derived stromal/stem cells (hASCs) are a promising tool to investigate the underlying mechanisms of such mitochondrial dysfunction and to subsequently provide knowledge for the development of treatments for obesity-related pathologies. A substantial obstacle in using hASCs is that the key compounds for adipogenic differentiation in vitro increase mitochondrial uncoupling, biogenesis, and activity, which are the signature features of brown adipocytes, thus altering the white adipocyte phenotype towards brown-like cells. Additionally, commonly used protocols for hASC adipogenic differentiation exhibit high variation in their composition of media, and a systematic comparison of their effect on mitochondria is missing. Here, we compared the five widely used adipogenic differentiation protocols for their effect on metabolic and mitochondrial phenotypes to identify a protocol that enables in vitro differentiation of white adipocytes and can more faithfully recapitulate the white adipocyte phenotype observed in human adipose tissue. We developed a workflow that included functional assays and morphological analysis of mitochondria and lipid droplets. We observed that triiodothyronine- or indomethacin-containing media and commercially available adipogenic media induced browning during in vitro differentiation of white adipocytes. However, the differentiation protocol containing 1 μM of the peroxisome proliferator-activated receptor gamma (PPARγ) agonist rosiglitazone prevented the browning effect and would be proposed for adipogenic differentiation protocol for hASCs to induce a white adipocyte phenotype. Preserving the white adipocyte phenotype in vitro is a crucial step for the study of obesity and associated metabolic diseases, adipose tissue pathologies, such as lipodystrophies, possible therapeutic compounds, and basic adipose tissue physiology.
    DOI:  https://doi.org/10.1155/2022/3308194
  5. J Lipid Res. 2022 Apr 06. pii: S0022-2275(22)00040-2. [Epub ahead of print] 100207
    Intravital lipid droplet labeling and imaging reveals the phenotypes and functions of individual macrophages in vivo.
    Yue Li, Yuwei Du, Zhengqing Xu, Yuan He, Ran Yao, Huiran Jiang, Wen Ju, Jianlin Qiao, Kailin Xu, Tzu-Ming Liu, Lingyu Zeng.
      Macrophages play pivotal roles in the maintenance of tissue homeostasis. However, the re-activation of macrophages toward pro-inflammatory states correlates with a plethora of inflammatory diseases, including atherosclerosis, obesity, neurodegeneration, and bone marrow failure syndromes. However, the lack of methods to reveal macrophage phenotype and function in vivo impedes the translational research of these diseases. Here, we found that pro-inflammatory macrophages accumulate intracellular lipid droplets (LDs) relative to resting or non-inflammatory macrophages both in vitro and in vivo, indicating that LD accumulation serves as a structural biomarker for macrophage phenotyping. To realize the staining and imaging of macrophage LDs in vivo, we developed a fluorescent fatty acid analog-loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticle to label macrophages in mice with high efficiency and specificity. Using these novel nanoparticles, we achieved in situ functional identification of single macrophages in bone marrow, liver, lung, and adipose tissues under conditions of acute or chronic inflammation. Moreover, with this intravital imaging platform, we further realized in vivo phenotyping of individual macrophages in the calvarial bone marrow of mice under systemic inflammation. In conclusion, we established an efficient in vivo LD labeling and imaging system for single macrophage phenotyping, which will aid in the development of diagnostics and therapeutic monitoring. Moreover, this method also provides new avenues for the study of lipid trafficking and dynamics in vivo.
    Keywords:  Macrophage; biomarker; bone marrow; fatty acid analog; in vivo imaging; inflammation; lipid droplet; lipid trafficking; nanoparticle delivery; systemic inflammation
    DOI:  https://doi.org/10.1016/j.jlr.2022.100207
  6. Int J Mol Sci. 2022 Mar 30. pii: 3828. [Epub ahead of print]23(7):
    Phenotypical Conversions of Dermal Adipocytes as Pathophysiological Steps in Inflammatory Cutaneous Disorders.
    Ilja L Kruglikov, Zhuzhen Zhang, Philipp E Scherer.
      Adipocytes from the superficial layer of subcutaneous adipose tissue undergo cyclic de- and re-differentiation, which can significantly influence the development of skin inflammation under different cutaneous conditions. This inflammation can be connected with local loading of the reticular dermis with lipids released due to de-differentiation of adipocytes during the catagen phase of the hair follicle cycle. Alternatively, the inflammation parallels a widespread release of cathelicidin, which typically takes place in the anagen phase (especially in the presence of pathogens). Additionally, trans-differentiation of dermal adipocytes into myofibroblasts, which can occur under some pathological conditions, can be responsible for the development of collateral scarring in acne. Here, we provide an overview of such cellular conversions in the skin and discuss their possible involvement in the pathophysiology of inflammatory skin conditions, such as acne and psoriasis.
    Keywords:  acne; de-differentiation; dermal adipocytes; psoriasis; re-differentiation; trans-differentiation
    DOI:  https://doi.org/10.3390/ijms23073828
  7. EMBO Rep. 2022 Apr 12. e52412
    Nutrition, metabolism, and epigenetics: pathways of circadian reprogramming.
    Tomoki Sato, Paolo Sassone-Corsi.
      Food intake profoundly affects systemic physiology. A large body of evidence has indicated a link between food intake and circadian rhythms, and ~24-h cycles are deemed essential for adapting internal homeostasis to the external environment. Circadian rhythms are controlled by the biological clock, a molecular system remarkably conserved throughout evolution. The circadian clock controls the cyclic expression of numerous genes, a regulatory program common to all mammalian cells, which may lead to various metabolic and physiological disturbances if hindered. Although the circadian clock regulates multiple metabolic pathways, metabolic states also provide feedback on the molecular clock. Therefore, a remarkable feature is reprogramming by nutritional challenges, such as a high-fat diet, fasting, ketogenic diet, and caloric restriction. In addition, various factors such as energy balance, histone modifications, and nuclear receptor activity are involved in the remodeling of the clock. Herein, we review the interaction of dietary components with the circadian system and illustrate the relationships linking the molecular clock to metabolism and critical roles in the remodeling process.
    Keywords:  circadian clock; energy metabolism; epigenetics; nutrition
    DOI:  https://doi.org/10.15252/embr.202152412
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