Inhibition of adipogenic differentiation by myostatin is alleviated by arginine supplementation in porcine-muscle-derived mesenchymal stem cells

Lei, Hulong; Yu, Bing; Yang, Xuerong; Liu, ZeHui; Huang, Zhiqing; Mao, Xiangbing; Tian, Gang; He, Jun; Han, Guang; Chen, Hong; Mao, Qian; Chen, Shuai

doi:10.1007/s11427-011-4227-1

Cited by 17 publications

(6 citation statements)

References 33 publications

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“…In the present study, we found that myostatin notably suppressed the expression of the lipid synthesis enzymes Gpdh, Dgat, and Acs1, whereas it promoted the expression of the lipolytic enzyme Cpt1 in fully differentiated 3T3-L1 adipocytes, which indicates that myostatin decreased the intracellular lipid contents by inhibiting lipogenesis and promoting lipolysis. Similar results were obtained in porcine muscle-derived mesenchymal stem cells, which indicated that myostatin inhibited adipogenesis by suppressing the expression of lipid synthesis enzymes (Lei et al 2011). Although myostatin also reduced the expression of the lipolysis enzymes Atgl and Hsl, the total effect of myostatin was a decrease in the lipid accumulation in 3T3-L1 adipocytes.…”

Section: Discussionsupporting

confidence: 79%

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

Zhu¹,

Pan²,

Zhang³

et al. 2015

Journal of Molecular Endocrinology

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Myostatin is a critical negative regulator of skeletal muscle development, and has been reported to be involved in the progression of obesity and diabetes. In the present study, we explored the effects of myostatin on the proliferation and differentiation of 3T3-L1 preadipocytes by using 3-[4,5-dimethylthiazol-2-yl] 2,5-diphenyl tetrazolium bromide spectrophotometry, intracellular triglyceride (TG) assays, and real-time quantitative RT-PCR methods. The results indicated that recombinant myostatin significantly promoted the proliferation of 3T3-L1 preadipocytes and the expression of proliferation-related genes, including Cyclin B2, Cyclin D1, Cyclin E1, Pcna, and c-Myc, and IGF1 levels in the medium of 3T3-L1 were notably upregulated by 35.2, 30.5, 20.5, 33.4, 51.2, and 179% respectively (all P!0.01) in myostatin-treated 3T3-L1 cells. Meanwhile, the intracellular lipid content of myostatin-treated cells was notably reduced as compared with the non-treated cells. Additionally, the mRNA levels of Pparg, Cebpa, Gpdh, Dgat, Acs1, Atgl, and Hsl were significantly downregulated by 22-76% in fully differentiated myostatin-treated adipocytes. Finally, myostatin regulated the mRNA levels and secretion of adipokines, including Adiponectin, Resistin, Visfatin, and plasminogen activator inhibitor-1 (PAI-1) in 3T3-L1 adipocytes (all P!0.001). Above all, myostatin promoted 3T3-L1 proliferation by increasing the expression of cell-proliferation-related genes and by stimulating IGF1 secretion. Myostatin inhibited 3T3-L1 adipocyte differentiation by suppressing Pparg and Cebpa expression, which consequently deceased lipid accumulation in 3T3-L1 cells by inhibiting the expression of critical lipogenic enzymes and by promoting the expression of lipolytic enzymes. Finally, myostatin modulated the expression and secretion of adipokines in fully differentiated 3T3-L1 adipocytes.

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Section: Discussionsupporting

confidence: 79%

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

Zhu¹,

Pan²,

Zhang³

et al. 2015

Journal of Molecular Endocrinology

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“…At the forefront of treatment options are a family of stem cells, known as mesenchymal stem cells (MSCs), which hold the potential for differentiation into multiple lineages, such as bone, fat, cartilage, tendon and ligament, muscle, and marrow stroma [10,11]. Since the beginning of this field of research, MSCs have been isolated from a variety of sources, including bone marrow, adipose, periosteum, muscle, perichondrium, and synovium [12,13,14,15,16,17,18]. Along with their multipotent capabilities, MSCs also display an amazing ability to self-replicate [19].…”

Section: Introductionmentioning

confidence: 99%

Surface Markers for Chondrogenic Determination: A Highlight of Synovium-Derived Stem Cells

Campbell

Pei

2012

Cells

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Cartilage tissue engineering is a promising field in regenerative medicine that can provide substantial relief to people suffering from degenerative cartilage disease. Current research shows the greatest chondrogenic potential for healthy articular cartilage growth with minimal hypertrophic differentiation to be from mesenchymal stem cells (MSCs) of synovial origin. These stem cells have the capacity for differentiation into multiple cell lineages related to mesenchymal tissue; however, evidence exists for cell surface markers that specify a greater potential for chondrogenesis than other differentiation fates. This review will examine relevant literature to summarize the chondrogenic differentiation capacities of tested synovium-derived stem cell (SDSC) surface markers, along with a discussion about various other markers that may hold potential, yet require further investigation. With this information, a potential clinical benefit exists to develop a screening system for SDSCs that will produce the healthiest articular cartilage possible.

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“…This is the first comprehensive study, in our knowledge, which reports detailed characterization and comparative analysis of a broad panel of porcine integumentary and connective tissue-derived mesenchymal stromal cells. Indeed, the bulk of literature on pMSCs and their preclinical uses in the porcine model are restricted to bone marrow and adipose-derived cells [ 28 – 32 ], with very few reports on the isolation of multipotent pMSCs from porcine skeletal muscle [ 33 – 35 ], dermis [ 36 , 37 ], and periodontal ligament [ 38 ]. While several reports used decellularized porcine tendon as a biological scaffold to seed human tissue-derived stromal cells [ 39 , 40 ], there exist limited reports on the isolation and characterization of pMSCs derived from porcine tendon tissues.…”

Section: Discussionmentioning

confidence: 99%

Culture and characterization of various porcine integumentary-connective tissue-derived mesenchymal stromal cells to facilitate tissue adhesion to percutaneous metal implants

et al. 2021

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Background Transdermal osseointegrated prosthesis have relatively high infection rates leading to implant revision or failure. A principle cause for this complication is the absence of a durable impervious biomechanical seal at the interface of the hard structure (implant) and adjacent soft tissues. This study explores the possibility of recapitulating an analogous cellular musculoskeletal-connective tissue interface, which is present at naturally occurring integumentary tissues where a hard structure exits the skin, such as the nail bed, hoof, and tooth. Methods Porcine mesenchymal stromal cells (pMSCs) were derived from nine different porcine integumentary and connective tissues: hoof-associated superficial flexor tendon, molar-associated periodontal ligament, Achilles tendon, adipose tissue and skin dermis from the hind limb and abdominal regions, bone marrow and muscle. For all nine pMSCs, the phenotype, multi-lineage differentiation potential and their adhesiveness to clinical grade titanium was characterized. Transcriptomic analysis of 11 common genes encoding cytoskeletal proteins VIM (Vimentin), cell–cell and cell–matrix adhesion genes (Vinculin, Integrin β1, Integrin β2, CD9, CD151), and for ECM genes (Collagen-1a1, Collagen-4a1, Fibronectin, Laminin-α5, Contactin-3) in early passaged cells was performed using qRT-PCR. Results All tissue-derived pMSCs were characterized as mesenchymal origin by adherence to plastic, expression of cell surface markers including CD29, CD44, CD90, and CD105, and lack of hematopoietic (CD11b) and endothelial (CD31) markers. All pMSCs differentiated into osteoblasts, adipocytes and chondrocytes, albeit at varying degrees, under specific culture conditions. Among the eleven adhesion genes evaluated, the cytoskeletal intermediate filament vimentin was found highly expressed in pMSC isolated from all tissues, followed by genes for the extracellular matrix proteins Fibronectin and Collagen-1a1. Expression of Vimentin was the highest in Achilles tendon, while Fibronectin and Col1agen-1a1 were highest in molar and hoof-associated superficial flexor tendon bone marrow, respectively. Achilles tendon ranked the highest in both multilineage differentiation and adhesion assessments to titanium metal. Conclusions These findings support further preclinical research of these tissue specific-derived MSCs in vivo in a transdermal osseointegration implant model.

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Inhibition of adipogenic differentiation by myostatin is alleviated by arginine supplementation in porcine-muscle-derived mesenchymal stem cells

Cited by 17 publications

References 33 publications

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

The effect of myostatin on proliferation and lipid accumulation in 3T3-L1 preadipocytes

Surface Markers for Chondrogenic Determination: A Highlight of Synovium-Derived Stem Cells

Culture and characterization of various porcine integumentary-connective tissue-derived mesenchymal stromal cells to facilitate tissue adhesion to percutaneous metal implants

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