Purinergic signalling-evoked intracellular Ca2+ concentration changes in the regulation of chondrogenesis and skeletal muscle formation

Matta, Csaba; Fodor, János; Csernoch, László; Zákány, Róza

doi:10.1016/j.ceca.2016.01.006

Cited by 8 publications

(11 citation statements)

References 96 publications

(116 reference statements)

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“…There is growing evidence to suggest that extracellular nucleotides play a significant role in the regulation of cartilage physiology [30]. Chondrocytes, for example, employ purinergic signaling as part of the mechanotransduction cascade, which promotes chemical signaling inside the cell.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Nucleotides Selectively Induce Migration of Chondrocytes and Expression of Type II Collagen

Szustak

Gendaszewska‐Darmach

2020

IJMS

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The migration of chondrocytes from healthy to injured tissues is one of the most important challenges during cartilage repair. Additionally, maintenance of the chondrogenic phenotype remains another limitation, especially during monolayer culture in vitro. Using both the differentiated and undifferentiated chondrogenic ATDC5 cell line, we showed that extracellular nucleotides are able to increase the migration rate of chondrocytes without affecting their chondrogenic phenotype. We checked the potency of natural nucleotides (ATP, ADP, UTP, and UDP) as well as their stable phosphorothioate analogs, containing a sulfur atom in the place of one nonbridging oxygen atom in a phosphate group. We also detected P2y1, P2y2, P2y4, P2y6, P2y12, P2y13, and P2y14 mRNA transcripts for nucleotide receptors, demonstrating that P2y1 and P2y13 are highly upregulated in differentiated ATDC5 cells. We showed that ADPβS, UDPβS, and ADP are the best stimulators of migration of differentiated chondrocytes. Additionally, ADP and ADPβS positively affected the expression of type II collagen, a structural component of the cartilage matrix.

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Section: Discussionmentioning

confidence: 99%

Extracellular Nucleotides Selectively Induce Migration of Chondrocytes and Expression of Type II Collagen

Szustak

Gendaszewska‐Darmach

2020

IJMS

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“…Modern pharmacological research showed that puerarin inhibited pulmonary fibrosis via reducing the content of NO in lung tissue, and decreased spontaneous or dexamethasone-induced apoptosis of thymocytes [12,13]. A certain concentration of puerarin has anti-inflammatory properties via inhibiting proliferation of vascular endothelial cell and leukocyte adhesion [14,15]. In addition, puerarin was proved with protecting function on Lysosomes and mitochondria via regulating mitochondrion membrane potential [16,17].…”

Section: Discussionmentioning

confidence: 99%

Puerarin promotes rehabilitation of cartilage injury in juvenile rat model via inhibiting apoptosis: A mechanism study

Zheng¹,

Huang²,

Peng³

et al. 2018

biomedicalresearch

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Objective: Perthes' disease is one of the most common pediatric surgical disease and affects children's health seriously. Pathogenesis of Perthes' disease is associated with pressure overload and inflammation. Puerarin was proved with promising efficacy on adult surgical disease. Our study is aimed explore effect of puerarin on cartilage injury of juvenile rat. Methods: BALB/C rats were randomly assigned into three groups, including control group (A group), saline-treated group (B group) and puerarin-treated group (C group). Every group contains 10 rats. Saline and puerarin were treated with intragastric administration for B group and C group, respectively (2.18 g/kg, twice a day, 4 w). Cartilage injury of juvenile rat model was established with Hulth method for B group and C group. Pathologic change of articular cartilage was assessed for three groups. Cellular activity was examined with MTT assays. Apoptosis was assessed with flow cytometry. Results: Intact and smooth structure integrity of chondrocyte was observed in control group. Compared with saline-treated group, cartilage injury in puerarin-treated group was significantly alleviated, including reduced surface rupture, intact cell structure and relieving inflammation (P<0.05). Puerarin treatment significantly reduced the percentage of apoptosis and enhanced cell activity of chondrocyte (P<0.05). Conclusions: Puerarin promotes rehabilitation of cartilage injury in juvenile rat model. Potential mechanism was that puerarin inhibited apoptosis and enhanced cell activity of chondrocyte.

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“…EMF may activate calcium channels other than voltage-gated calcium channels, and although there are relatively few reports of electromagnetic activation of purinergic receptors and TRP family of cation channels to further influence calcium oscillations, both may play an important role in EMF against inflammation and cartilage in osteoarthritis. Purinergic receptors play a key role in the development of cartilage as important molecular receptors that are widely present on the membranes of mesenchymal stem cells, chondrocytes, skeletal muscle cells, and other cells that receive purinergic signals [ 84 ]. Purinergic receptors can be divided into two major categories, P1 and P2 receptors, and it has been demonstrated that electromagnetic fields can upregulate the expression of Adenosine Receptors, with significant upregulation of A 2A and A 3 , exerting similar effects as adenosine receptor agonists, and can downregulate PGE(2) levels to achieve control of osteoarthritis [ 85 , 86 ].…”

Section: Application Of Emf In Stem Cells and Its Regulation Of Calci...mentioning

confidence: 99%

“…Purinergic receptors can be divided into two major categories, P1 and P2 receptors, and it has been demonstrated that electromagnetic fields can upregulate the expression of Adenosine Receptors, with significant upregulation of A 2A and A 3 , exerting similar effects as adenosine receptor agonists, and can downregulate PGE(2) levels to achieve control of osteoarthritis [ 85 , 86 ]. We found that EMF can upregulate P2X7 receptors in MSCs [ 40 ], and that the adenosine purinergic system acts as a classical regulatory pathway affecting the intracellular calcium ion homeostasis during the process of chondrogenic differentiation of cells [ 84 ].…”

Section: Application Of Emf In Stem Cells and Its Regulation Of Calci...mentioning

confidence: 99%

Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis

Ding

Liu

et al. 2023

Stem Cell Res Ther

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Electromagnetic fields (EMF) are increasing in popularity as a safe and non-invasive therapy. On the one hand, it is widely acknowledged that EMF can regulate the proliferation and differentiation of stem cells, promoting the undifferentiated cells capable of osteogenesis, angiogenesis, and chondroblast differentiation to achieve bone repair purpose. On the other hand, EMF can inhibit tumor stem cells proliferation and promote apoptosis to suppress tumor growth. As an essential second messenger, intracellular calcium plays a role in regulating cell cycle, such as proliferation, differentiation and apoptosis. There is increasing evidence that the modulation of intracellular calcium ion by EMF leads to differential outcomes in different stem cells. This review summarizes the regulation of channels, transporters, and ion pumps by EMF-induced calcium oscillations. It furtherly discusses the role of molecules and pathways activated by EMF-dependent calcium oscillations in promoting bone and cartilage repair and inhibiting tumor stem cells growth.

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Purinergic signalling-evoked intracellular Ca2+ concentration changes in the regulation of chondrogenesis and skeletal muscle formation

Cited by 8 publications

References 96 publications

Extracellular Nucleotides Selectively Induce Migration of Chondrocytes and Expression of Type II Collagen

Extracellular Nucleotides Selectively Induce Migration of Chondrocytes and Expression of Type II Collagen

Puerarin promotes rehabilitation of cartilage injury in juvenile rat model via inhibiting apoptosis: A mechanism study

Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis

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