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10.1016/j.bbrc.2019.04.030 http://scihub22266oqcxt.onion/10.1016/j.bbrc.2019.04.030 31003774!ä!31003774 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochem+Biophys+Res+Commun 2019 ; 513 (4): 883-890 Nephropedia Template TP {{tp|p=31003774|t=2019. NIPA2 regulates osteoblast function via its effect on apoptosis pathways in type 2 diabetes osteoporosis |pdf=|usr=}}{{31003774}} gab.com Text NIPA2 regulates osteoblast function via its effect on apoptosis pathways in type 2 diabetes osteoporosis JO: Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=31003774 #FOAvip Type 2 diabetes osteoporosis has recently become a hot topic in the study of diabetic complications, but the specific mechanism of its development remains unclear. Non-imprinted in Prader-Willi/Angelman syndrome region protein 2 (NIPA2), a highly-selective magnesium ion transporter, has been found to be associated with type 2 diabetes. In this study we aimed to investigate the specific role and mechanism of NIPA2 in the pathogenesis of type 2 diabetes osteoporosis. We first used western blotting, PCR, immunofluorescence, and magnesium ion probes to detect changes of NIPA2 and intracellular magnesium levels in osteoblasts at different concentrations of advanced glycation end products (AGEs). We then up- or down-regulated NIPA2 using a lentivirus and analyzed apoptotic biomarkers as well as the osteogenic ability of osteoblasts. We found that AGEs dose-dependently down-regulated the expression of NIPA2 in osteoblasts. NIPA2 also regulated osteoblast apoptosis by affecting the intracellular magnesium level and further affecting the osteogenic capacity of osteoblasts. Our study revealed the changes of NIPA2 in response to AGEs in the environment, as well as its function and mechanism in osteoblasts, demonstrating its important role in the pathogenesis of type 2 diabetes osteoporosis. The study suggests that NIPA2 is a potential target for the treatment of type 2 diabetes osteoporosis. Twit Text FOAVip NIPA2 regulates osteoblast function via its effect on apoptosis pathways in type 2 diabetes osteoporosis ????Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=31003774 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31003774 #FOAvip English Wikipedia <ref>{{Cite pmid|31003774}}</ref> NIPA2 regulates osteoblast function via its effect on apoptosis pathways in type 2 diabetes osteoporosis #MMPMID31003774 Zhao W; Zhang WL; Yang B; Sun J; Yang MW Biochem Biophys Res Commun 2019[Jun]; 513 (4): 883-890 PMID31003774show ga Type 2 diabetes osteoporosis has recently become a hot topic in the study of diabetic complications, but the specific mechanism of its development remains unclear. Non-imprinted in Prader-Willi/Angelman syndrome region protein 2 (NIPA2), a highly-selective magnesium ion transporter, has been found to be associated with type 2 diabetes. In this study we aimed to investigate the specific role and mechanism of NIPA2 in the pathogenesis of type 2 diabetes osteoporosis. We first used western blotting, PCR, immunofluorescence, and magnesium ion probes to detect changes of NIPA2 and intracellular magnesium levels in osteoblasts at different concentrations of advanced glycation end products (AGEs). We then up- or down-regulated NIPA2 using a lentivirus and analyzed apoptotic biomarkers as well as the osteogenic ability of osteoblasts. We found that AGEs dose-dependently down-regulated the expression of NIPA2 in osteoblasts. NIPA2 also regulated osteoblast apoptosis by affecting the intracellular magnesium level and further affecting the osteogenic capacity of osteoblasts. Our study revealed the changes of NIPA2 in response to AGEs in the environment, as well as its function and mechanism in osteoblasts, demonstrating its important role in the pathogenesis of type 2 diabetes osteoporosis. The study suggests that NIPA2 is a potential target for the treatment of type 2 diabetes osteoporosis. |*Apoptosis[MESH] |Cation Transport Proteins/metabolism/*physiology[MESH] |Cells, Cultured[MESH] |Diabetes Mellitus, Type 2/*complications[MESH] |Down-Regulation/drug effects[MESH] |Glycation End Products, Advanced/pharmacology[MESH] |Humans[MESH] |Magnesium/metabolism[MESH] |Osteoblasts/*metabolism/pathology[MESH]NIPA2 regulates osteoblast function via its effect on apoptosis pathwa(epmc).pdf DeepDyve Pubget Overpricing