Matrix Gla protein regulates adipogenesis and is serum marker of visceral adiposity

Li, Chaomin; Li, Jing; He, Fang; Li, Kun; Xu, Li; Zhang, Yan

doi:10.1080/21623945.2020.1721692

Cited by 29 publications

(27 citation statements)

References 31 publications

(42 reference statements)

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“…Obesity is linked with vitamin K deficiency [ 167 , 168 , 169 ]. Vitamin K deficiency results in decreased vitamin K-dependent carboxylation and phosphorylation of Gla-proteins and, as a consequence, into elevated levels of circulating desphosphorylated-uncarboxylated matrix Gla protein (dp-ucMGP).…”

Section: Underlying Mechanisms Linking Obesity To Major Complications As a Results Of Sars-cov-2 Infectionmentioning

confidence: 99%

“…Recent research studied the relationship between obesity and serum dp-ucMGP in a cohort of 278 Chinese Han people. The results demonstrated that serum dp-ucMGP level was positively associated with visceral fat index, waist height ratio, but not BMI [ 167 ]. In addition, lower vitamin K2 levels were observed in obese hemodialysis patients compared to non-obese patients [ 168 ].…”

Section: Underlying Mechanisms Linking Obesity To Major Complications As a Results Of Sars-cov-2 Infectionmentioning

confidence: 99%

See 1 more Smart Citation

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Demeulemeester¹,

Punder²,

Heijningen³

et al. 2021

Cells

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Emerging data suggest that obesity is a major risk factor for the progression of major complications such as acute respiratory distress syndrome (ARDS), cytokine storm and coagulopathy in COVID-19. Understanding the mechanisms underlying the link between obesity and disease severity as a result of SARS-CoV-2 infection is crucial for the development of new therapeutic interventions and preventive measures in this high-risk group. We propose that multiple features of obesity contribute to the prevalence of severe COVID-19 and complications. First, viral entry can be facilitated by the upregulation of viral entry receptors, like angiotensin-converting enzyme 2 (ACE2), among others. Second, obesity-induced chronic inflammation and disruptions of insulin and leptin signaling can result in impaired viral clearance and a disproportionate or hyper-inflammatory response, which together with elevated ferritin levels can be a direct cause for ARDS and cytokine storm. Third, the negative consequences of obesity on blood coagulation can contribute to the progression of thrombus formation and hemorrhage. In this review we first summarize clinical findings on the relationship between obesity and COVID-19 disease severity and then further discuss potential mechanisms that could explain the risk for major complications in patients suffering from obesity.

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Section: Underlying Mechanisms Linking Obesity To Major Complications As a Results Of Sars-cov-2 Infectionmentioning

confidence: 99%

Section: Underlying Mechanisms Linking Obesity To Major Complications As a Results Of Sars-cov-2 Infectionmentioning

confidence: 99%

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Demeulemeester¹,

Punder²,

Heijningen³

et al. 2021

Cells

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“…The resulting transcriptome represented the early response elements that potentially initiated MSC's early lineage commitment as a result of the on-cell-tethered biomaterial's mechanical properties. Notably, cells tethered in soft microgels were enriched in expression of pro-adipogenic factors including LGALS1, [37] MGP, [38] ADIRF, [39] and COX7A1, [40] while cells tethered in stiff microgels expressed more pro-osteogenic factors such as FOSB, [41] STC1, [42] BMP2, and BMP6. [43] Gene ontology (GO) enrichment analysis of the differentially expressed genes suggested that early stem cell commitment associates at the genetic level with altered TGFB/SMAD signaling and metabolic (i.e., mitochondrial) behavior (Figure 3j,k; Tables S5 and S6, Supporting Information).…”

Section: Temporal Stiffening Of Tethered Biomaterials Controls Early Onset Stem Cell Lineage Commitmentmentioning

confidence: 99%

Tethering Cells via Enzymatic Oxidative Crosslinking Enables Mechanotransduction in Non‐Cell‐Adhesive Materials

et al. 2021

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proliferation, apoptosis, metabolism, and differentiation. [1,2] However, the variety of strategies to control cell-biomaterial interactions able to transmit mechanical cues from the microenvironment to the cells within engineered tissue constructs has remained limited and near-exclusively relied on cell adhesion. Biomaterials are typically endowed with bioligands that bind to cell adhesion molecules (CAMs; e.g., integrins, cadherins, and selectins). The integrinbinding tripeptide arginine-glycine-aspartic acid (RGD) [3] has been most commonly used as cell-adhesive moiety, but also numerous alternative cell-adhesive nucleotides, [4] peptides, [5] and proteins including antibodies [6] and amyloid-like lysozyme [7] have been explored. However, the constitutively active binding nature of these cell-adhesive bioligands has been associated with adverse effects such as increased fibrous capsule formation and chronic inflammation upon implantation. [8,9] Dynamic material modification strategies that display cell-adhesive bioligands with precise spatial and temporal control have been developed to address this challenge. However, once activated, their cell-adhesive properties are continuously active and can only be annihilated using Cell-matrix interactions govern cell behavior and tissue function by facilitating transduction of biomechanical cues. Engineered tissues often incorporate these interactions by employing cell-adhesive materials. However, using constitutively active cell-adhesive materials impedes control over cell fate and elicits inflammatory responses upon implantation. Here, an alternative cell-material interaction strategy that provides mechanotransducive properties via discrete inducible on-cell crosslinking (DOCKING) of materials, including those that are inherently non-cell-adhesive, is introduced. Specifically, tyramine-functionalized materials are tethered to tyrosines that are naturally present in extracellular protein domains via enzyme-mediated oxidative crosslinking. Temporal control over the stiffness of on-cell tethered 3D microniches reveals that DOCKING uniquely enables lineage programming of stem cells by targeting adhesome-related mechanotransduction pathways acting independently of cell volume changes and spreading. In short, DOCKING represents a bioinspired and cytocompatible cell-tethering strategy that offers new routes to study and engineer cell-material interactions, thereby advancing applications ranging from drug delivery, to cell-based therapy, and cultured meat.The ORCID identification number(s) for the author(s) of this article can be found under https://doi.org/10.1002/adma.202102660.

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“…26 ). Furthermore, these genes were reported to be higher expressed in visceral compared to subcutaneous ASPCs and have as such been associated with the impaired capacity of visceral ASPCs to give rise to in vitro adipocytes (Reichert et al , 2011; Meissburger et al , 2016; Takeda et al , 2016; Li et al , 2020). Further studies will now be required to investigate how this seemingly diverse collection of molecules may cooperate within the retinoic acid signalling pathway to steer the developmental, phenotypic and functional properties of Aregs.…”

Section: Discussionmentioning

confidence: 99%

Mammalian adipogenesis regulators (Aregs) exhibit robust non- and anti-adipogenic properties that arise with age and involve retinoic acid signalling

Zachara

et al. 2021

Preprint

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Adipose stem and precursor cells (ASPCs) give rise to adipocytes and determine the composition and plasticity of adipose tissue. Recently, several studies have demonstrated that ASPCs partition into at least three distinct cell subpopulations: Dpp4+ stem-like cells, Aoc3+ pre-adipocyte-like cells, and the enigmatic CD142+ cells. A great challenge now is to functionally characterize these distinct ASPC populations. Here, we focus on CD142+ ASPCs since discrepant properties have been assigned to this subpopulation, from adipogenic to non- and even anti-adipogenic. To address these inconsistencies, we comprehensively characterized mammalian subcutaneous CD142+ ASPCs across various sampling conditions. Our findings demonstrate that CD142+ ASPCs exhibit high molecular and phenotypic robustness, firmly supporting their non- and anti-adipogenic properties. However, these properties emerge in an age-dependent manner, revealing surprising temporal CD142+ ASPC behavioural alterations. Finally, using multi-omic and functional assays, we show that the inhibitory nature of these adipogenesis-regulatory CD142+ ASPCs (Aregs) is driven by specifically expressed secretory factors that cooperate with the retinoic acid signalling pathway to transform the adipogenic state of CD142- ASPCs into a non-adipogenic, Areg-like one.

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Matrix Gla protein regulates adipogenesis and is serum marker of visceral adiposity

Cited by 29 publications

References 31 publications

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

Tethering Cells via Enzymatic Oxidative Crosslinking Enables Mechanotransduction in Non‐Cell‐Adhesive Materials

Mammalian adipogenesis regulators (Aregs) exhibit robust non- and anti-adipogenic properties that arise with age and involve retinoic acid signalling

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