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10.3892/mmr.2017.7300 http://scihub22266oqcxt.onion/10.3892/mmr.2017.7300 28849029!ä!28849029 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Med+Rep 2017 ; 16 (4): 5699-5705 Nephropedia Template TP {{tp|p=28849029|t=2017. Ca2+/Mg2+ homeostasis?related TRPM7 channel mediates chondrocyte hypertrophy via regulation of the PI3K?Akt signaling pathway |pdf=|usr=}}{{28849029}} gab.com Text Ca2+/Mg2+ homeostasis related TRPM7 channel mediates chondrocyte hypertrophy via regulation of the PI3K Akt signaling pathway JO: Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28849029 #FOAvip Chondrocytes are specialized cells that form cartilage tissue, and are able to respond to their osmotic environment and exercise important roles in endochondral ossification via undergoing proliferation, hypertrophy and apoptosis. The transient receptor melastatin potential 7 (TRPM7) cation channel can modulate the intracellular and extracellular levels of Ca2+ and Mg2+, and therefore the cellular osmotic environment. However, the molecular pathways involved in TRPM7?mediated signal transduction have yet to be elucidated. In the present study, the expression and functionality of TRPM7 were investigated during chondrocyte proliferation and hypertrophy. The ATDC5 mouse cell line was employed and cellular viability was evaluated using the MTT assay, whereas hypertrophy was monitored via evaluating the expression of chondrogenic marker genes and the activity of alkaline phosphatase (ALP). Gene expression of TRPM7 appeared slightly upregulated during the proliferative stages of chondrocyte development, and significantly upregulated during the hypertrophic stages, suggesting the importance of Ca2+/Mg2+ homeostasis for chondrocyte growth. Low extracellular Ca2+/Mg2+ levels significantly reduced the expression of type X collagen, Indian hedgehog homolog (Ihh) and matrix metalloproteinase (MMP)?13 genes, as well as ALP activity; however, cell viability remained unaffected. Conversely, the gene expression levels of TRPM7 appeared upregulated in ATDC5 cells under low extracellular Ca2+ or Mg2+ conditions. Silencing TRPM7 expression during the chondrocyte differentiation period also reduced type X collagen, Ihh and MMP?13 gene expression, and ALP activity. Furthermore, the phosphatidylinositol?4,5?bisphosphate 3?kinase (PI3K)?Akt signaling pathway was activated following TRPM7 overexpression, and inhibited following TRPM7 silencing. Notably, the actions of TRPM7 on chondrocyte hypertrophy were abolished through the inhibition of PI3K?Akt signaling. The present results suggested that TRPM7 may be involved in Ca2+/Mg2+ homeostasis during chondrocyte hypertrophy, and contribute to endochondral ossification via interacting with the PI3K?Akt signaling pathway. Twit Text FOAVip Ca2+/Mg2+ homeostasis related TRPM7 channel mediates chondrocyte hypertrophy via regulation of the PI3K Akt signaling pathway ????Mol Med Rep http://www.kidney.de/pget.php?&tw=1&pmid=28849029 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28849029 #FOAvip English Wikipedia <ref>{{Cite pmid|28849029}}</ref> Ca2+/Mg2+ homeostasis?related TRPM7 channel mediates chondrocyte hypertrophy via regulation of the PI3K?Akt signaling pathway #MMPMID28849029 Lu D; Qu J; Sun L; Li Q; Ling H; Yang N; Ma T; Wang Q; Li M; Zhang K; Li Z Mol Med Rep 2017[Oct]; 16 (4): 5699-5705 PMID28849029show ga Chondrocytes are specialized cells that form cartilage tissue, and are able to respond to their osmotic environment and exercise important roles in endochondral ossification via undergoing proliferation, hypertrophy and apoptosis. The transient receptor melastatin potential 7 (TRPM7) cation channel can modulate the intracellular and extracellular levels of Ca2+ and Mg2+, and therefore the cellular osmotic environment. However, the molecular pathways involved in TRPM7?mediated signal transduction have yet to be elucidated. In the present study, the expression and functionality of TRPM7 were investigated during chondrocyte proliferation and hypertrophy. The ATDC5 mouse cell line was employed and cellular viability was evaluated using the MTT assay, whereas hypertrophy was monitored via evaluating the expression of chondrogenic marker genes and the activity of alkaline phosphatase (ALP). Gene expression of TRPM7 appeared slightly upregulated during the proliferative stages of chondrocyte development, and significantly upregulated during the hypertrophic stages, suggesting the importance of Ca2+/Mg2+ homeostasis for chondrocyte growth. Low extracellular Ca2+/Mg2+ levels significantly reduced the expression of type X collagen, Indian hedgehog homolog (Ihh) and matrix metalloproteinase (MMP)?13 genes, as well as ALP activity; however, cell viability remained unaffected. Conversely, the gene expression levels of TRPM7 appeared upregulated in ATDC5 cells under low extracellular Ca2+ or Mg2+ conditions. Silencing TRPM7 expression during the chondrocyte differentiation period also reduced type X collagen, Ihh and MMP?13 gene expression, and ALP activity. Furthermore, the phosphatidylinositol?4,5?bisphosphate 3?kinase (PI3K)?Akt signaling pathway was activated following TRPM7 overexpression, and inhibited following TRPM7 silencing. Notably, the actions of TRPM7 on chondrocyte hypertrophy were abolished through the inhibition of PI3K?Akt signaling. The present results suggested that TRPM7 may be involved in Ca2+/Mg2+ homeostasis during chondrocyte hypertrophy, and contribute to endochondral ossification via interacting with the PI3K?Akt signaling pathway. |*Chondrogenesis[MESH] |Animals[MESH] |Biomarkers[MESH] |Calcium/*metabolism[MESH] |Cell Line[MESH] |Chondrocytes/cytology/*metabolism[MESH] |Gene Expression Regulation[MESH] |Gene Silencing[MESH] |Hypertrophy[MESH] |Magnesium/*metabolism[MESH] |Mice[MESH] |Phosphatidylinositol 3-Kinases/*metabolism[MESH] |Proto-Oncogene Proteins c-akt/*metabolism[MESH] |RNA Interference[MESH]Ca2+/Mg2+ homeostasis?related TRPM7 channel mediates chondrocyte hyper(epmc).pdf DeepDyve Pubget Overpricing