MCAM knockdown impairs PPARγ expression and 3T3-L1 fibroblasts differentiation to adipocytes

Gabrielli, Matias; Romero, Damián G.; Martini, Claudia; Iustman, Laura J. Raiger; Vila, María del Carmen

doi:10.1007/s11010-018-3334-8

Cited by 8 publications

(7 citation statements)

References 41 publications

(55 reference statements)

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“…Another study found that CD146+ human placenta‐derived MSCs had identical chondrogenic or adipogenic differentiation potential compared with the CD146− cells . However, CD146 KO impaired adipogenic differentiation in 3T3‐L1 fibroblasts . The level of SSEA4 in human BMSCs or Wharton's Jelly‐derived MSCs did not correlate with either chondrogenic or adipogenic potential .…”

Section: Discussionmentioning

confidence: 99%

Liver Kinase B1 Fine‐Tunes Lineage Commitment of Human Fetal Synovium‐Derived Stem Cells

Zhou

Zhang

et al. 2019

Journal Orthopaedic Research

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Liver kinase B1 (LKB1), a serine/threonine protein, is a key regulator in stem cell function and energy metabolism. Herein, we describe the role of LKB1 in modulating the differentiation of synovium-derived stem cells (SDSCs) toward chondrogenic, adipogenic, and osteogenic lineages. Human fetal SDSCs were transduced with CRISPR associated protein 9 (Cas9)-single-guide RNA vectors to knockout or lentiviral vectors to overexpress the LKB1 gene. Analyses including ICE (Inference of CRISPR Edits) data from Sanger sequencing and quantitative polymerase chain reaction (qPCR) as well as Western blot demonstrated successful knockout (KO) or overexpression (OE) of LKB1 in human fetal SDSCs without any detectable side effects in morphology, proliferation rate, and cell cycle. LKB1 KO increased CD146 expression; interestingly, LKB1 OE increased SSEA4 level. The qPCR data showed that LKB1 KO upregulated the levels of SOX2 and NANOG while LKB1 OE lowered the expression of POU5F1 and KLF4. Furthermore, LKB1 KO enhanced, and LKB1 OE inhibited, chondrogenic and adipogenic differentiation potential. However, perhaps due to the inherent inability to achieve osteogenesis, LKB1 did not obviously affect osteogenic differentiation. These data demonstrate that LKB1 plays a significant role in determining human SDSCs' adipogenic and chondrogenic differentiation, which might provide an approach for fine-tuning the direction of stem cell differentiation in tissue engineering and regeneration.

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Section: Discussionmentioning

confidence: 99%

Liver Kinase B1 Fine‐Tunes Lineage Commitment of Human Fetal Synovium‐Derived Stem Cells

Zhou

Zhang

et al. 2019

Journal Orthopaedic Research

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“…Adipocytes are derived from mesenchymal stromal cells (MSCs), which are precursor cells that can differentiate to several lineages (e.g., osteocytes, chondrocytes, and adipocytes) [30]. 3T3-L1 fibroblasts are precursor cells used as a model to assess adipogenesis.…”

Section: Discussionmentioning

confidence: 99%

The Antiobesity Effects of Buginawa in 3T3-L1 Preadipocytes and in a Mouse Model of High-Fat Diet-Induced Obesity

Park

Seo

et al. 2019

BioMed Research International

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There has been a remarkable interest in finding lipid inhibitors from natural products to replace synthetic compounds, and a variety of oriental medicinal herbs are reported to have biological activity with regard to lipid inhibition. Buginawa (Bugi) is a novel combined formula that contains twelve medicinal herbs with potential for weight loss induction. We hypothesized that Bugi may have antiobesity effects in 3T3-L1 preadipocytes and in a high-fat diet- (HFD-) induced mouse model. In this study, 3T3-L1 cells were treated with varied concentrations of Bugi (62.5, 125, or 250 μg/mL). Bugi treatment inhibited adipocyte differentiation by suppressing adipogenic transcription genes, including peroxisome proliferator-activated receptor γ protein (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), sterol regulatory element-binding protein 1 (SREBP1), and CCAAT/enhancer-binding protein β (C/EBPβ). Mice were fed a normal diet or an HFD for 11 weeks, and Bugi was simultaneously administered at 50 or 100 mg/kg. Bugi administration significantly reduced body weight gain and white adipose tissue (WAT) weight and effectively inhibited lipid droplet accumulation in epididymal white adipose tissue (eWAT) and liver tissue. Further, Bugi treatment suppressed mRNA levels of PPARγ, C/EBPα, and SREBP1 in eWAT and liver tissue. Our findings demonstrate that Bugi could be an effective candidate for preventing obesity and related metabolic disorders.

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“…Here we show loss of Gpr56 decreases 3T3‐L1 cell proliferation. Reduced cell adhesion inhibits adipogenesis (Gabrielli et al, ; Kamiya et al, ; Luo et al, ) and GPR56 is a member of the adhesion GPCR family that is involved in adhesion of various cell types including developing neurons, hemopoietic stem cells, and tumor cells (Koirala et al, ; Shashidhar et al, ; Saito et al, ). Here we show loss of Gpr56 reduces cell adhesion.…”

Section: Discussionmentioning

confidence: 99%

Adhesion G‐protein coupled receptor 56 is required for 3T3‐L1 adipogenesis

Hasan

Roy

Dolan

et al. 2019

Journal Cellular Physiology

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Obesity-associated conditions represent major global health and financial burdens and understanding processes regulating adipogenesis could lead to novel intervention strategies. This study shows that adhesion G-protein coupled receptor 56 (GPR56) gene transcripts are reduced in abdominal visceral white adipose tissue derived from obese Zucker rats versus lean controls. Immunostaining in 3T3-L1 preadipocytes reveals both mitotic cell restricted surface and low level general expression patterns of Gpr56. Gpr56 transcripts are differentially expressed in 3T3-L1 cells during adipogenesis. Transient knockdown (KD) of Gpr56 in 3T3-L1 cells dramatically inhibits differentiation through reducing the accumulation of both neutral cellular lipids (56%) and production of established adipogenesis Pparγ 2 (60-80%), C/ebpα (40-78%) mediator, and Ap2 (56-80%) marker proteins. Furthermore, genome editing of Gpr56 in 3T3-L1 cells created CW2.2.4 and RM4.2.5.5 clones (Gpr56 −/−

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MCAM knockdown impairs PPARγ expression and 3T3-L1 fibroblasts differentiation to adipocytes

Cited by 8 publications

References 41 publications

Liver Kinase B1 Fine‐Tunes Lineage Commitment of Human Fetal Synovium‐Derived Stem Cells

Liver Kinase B1 Fine‐Tunes Lineage Commitment of Human Fetal Synovium‐Derived Stem Cells

The Antiobesity Effects of Buginawa in 3T3-L1 Preadipocytes and in a Mouse Model of High-Fat Diet-Induced Obesity

Adhesion G‐protein coupled receptor 56 is required for 3T3‐L1 adipogenesis

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