Noggin Is Novel Inducer of Mesenchymal Stem Cell Adipogenesis

Sawant, Anandi; Chanda, Diptiman; Isayeva, Tatyana; Tsuladze, George; Garvey, W. Timothy; Ponnazhagan, Selvarangan

doi:10.1074/jbc.m111.293613

Cited by 23 publications

(19 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The few studies available suggest that the effect on adipogenic differentiation of Noggin varies from cell to cell. In bone marrow MSCs, Noggin treatment promoted adipogenesis, whereas in human stromal cells, Noggin had an inhibitory effect on adipogenic differentiation if added prior to full differentiation . It has also been found that expression of Noggin is reduced or eliminated in differentiated cells, whether they are adipocytes or cardiac/skeletal myocytes, which suggests that modulation by Noggin may be most important during the early cell differentiation.…”

Section: Introductionmentioning

confidence: 99%

Beyond the bone: Bone morphogenetic protein signaling in adipose tissue

Blázquez‐Medela

Jumabay

Boström³

2019

Obesity Reviews

View full text Add to dashboard Cite

Summary The bone morphogenetic proteins (BMPs) belong to the same superfamily as related to transforming growth factor β (TGFβ), growth and differentiation factors (GDFs), and activins. They were initially described as inducers of bone formation but are now known to be involved in morphogenetic activities and cell differentiation throughout the body, including the development of adipose tissue and adipogenic differentiation. BMP4 and BMP7 are the most studied BMPs in adipose tissue, with major roles in white adipogenesis and brown adipogenesis, respectively, but other BMPs such as BMP2, BMP6, and BMP8b as well as some inhibitors and modulators have been shown to also affect adipogenesis. It has become ever more important to understand adipose regulation, including the BMP pathways, in light of the strong links between obesity and metabolic and cardiovascular disease. In this review, we summarize the available information on BMP signaling in adipose tissue using preferentially articles that have appeared in the last decade, which together demonstrate the importance of BMP signaling in adipose biology.

show abstract

Section: Introductionmentioning

confidence: 99%

Beyond the bone: Bone morphogenetic protein signaling in adipose tissue

Blázquez‐Medela

Jumabay

Boström³

2019

Obesity Reviews

View full text Add to dashboard Cite

show abstract

“…Interestingly, this effect has been reported to be independent of BMP activity, raising the question as to whether Noggin can regulate additional cell signaling pathways (Sawant et al, 2012).…”

Section: Nogginmentioning

confidence: 98%

The Bone Morphogenetic Proteins and Their Antagonists

Rider

2015

Vitamins &Amp; Hormones

View full text Add to dashboard Cite

“…Adipose-derived stem cells (ASCs) are mesenchymal stem cells (MSCs) that are obtained from abundant adipose tissue [8,9]. High fat mass is caused by an increase in the size (hypertrophy) and number (hyperplasia) of adipocytes.…”

Section: Introductionmentioning

confidence: 99%

Novel Neohesperidin Dihydrochalcone Analogue Inhibits Adipogenic Differentiation of Human Adipose-Derived Stem Cells through the Nrf2 Pathway

Han

Kang

Chung

et al. 2018

IJMS

View full text Add to dashboard Cite

Obesity, characterized by excess lipid accumulation, has emerged as a leading public health problem. Excessive, adipocyte-induced lipid accumulation raises the risk of metabolic disorders. Adipose-derived stem cells (ASCs) are mesenchymal stem cells (MSCs) that can be obtained from abundant adipose tissue. High fat mass could be caused by an increase in the size (hypertrophy) and number (hyperplasia) of adipocytes. Reactive oxygen species (ROS) are involved in the adipogenic differentiation of human adipose-derived stem cells (hASCs). Lowering the level of ROS is important to blocking or retarding the adipogenic differentiation of hASCs. Nuclear factor erythroid 2-related factor-2 (Nrf2) is a transcription factor that mediates various antioxidant enzymes and regulates cellular ROS levels. Neohesperidin dihydrochalcone (NHDC), widely used as artificial sweetener, has been shown to have significant free radical scavenging activity. In the present study, (E)-3-(4-chlorophenyl)-1-(2,4,6-trimethoxyphenyl)prop-2-en-1-one (CTP), a novel NHDC analogue, was synthesized and examined to determine whether it could inhibit adipogenic differentiation. The inhibition of adipogenic differentiation in hASCs was tested using NHDC and CTP. In the CTP group, reduced Oil Red O staining was observed compared with the differentiation group. CTP treatment also downregulated the expression of PPAR-γ and C/EBP-α, adipogenic differentiation markers in hASCs, compared to the adipogenic differentiation group. The expression of FAS and SREBP-1 decreased in the CTP group, along with the fluorescent intensity (amount) of ROS. Expression of the Nrf2 protein was slightly decreased in the differentiation group. Meanwhile, in both the NHDC and CTP groups, Nrf2 expression was restored to the level of the control group. Moreover, the expression of HO-1 and NQO-1 increased significantly in the CTP group. Taken together, these results suggest that CTP treatment suppresses the adipogenic differentiation of hASCs by decreasing intracellular ROS, possibly through activation of the Nrf2 cytoprotective pathway. Thus, the use of bioactive substances such as CTP, which activates Nrf2 to reduce the cellular level of ROS and inhibit the adipogenic differentiation of hASCs, could be a new strategy for overcoming obesity.

show abstract

Noggin Is Novel Inducer of Mesenchymal Stem Cell Adipogenesis

Cited by 23 publications

References 36 publications

Beyond the bone: Bone morphogenetic protein signaling in adipose tissue

Beyond the bone: Bone morphogenetic protein signaling in adipose tissue

The Bone Morphogenetic Proteins and Their Antagonists

Novel Neohesperidin Dihydrochalcone Analogue Inhibits Adipogenic Differentiation of Human Adipose-Derived Stem Cells through the Nrf2 Pathway

Contact Info

Product

Resources

About