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10.1371/journal.pone.0138833 http://scihub22266oqcxt.onion/10.1371/journal.pone.0138833 C4593585!4593585 !26436544     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26436544 &cmd=llinks): Failed to open stream: HTTP request failed! 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Arterial Expression of the Calcium-Sensing Receptor Is Maintained by Physiological Pulsation and Protects against Calcification |pdf=|usr=}}{{26436544 }} gab.com Text Arterial Expression of the Calcium-Sensing Receptor Is Maintained by Physiological Pulsation and Protects against Calcification JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26436544 #FOAvip Vascular calcification (VC) is common in chronic kidney disease (CKD) and contributes to cardiovascular mortality. The calcium-sensing receptor (CaSR) is present in human artery, senses extracellular calcium and may directly modulate VC. OBJECTIVE: to investigate the association between arterial cyclic strain, CaSR expression and VC. METHODS AND RESULTS: human aortic smooth muscle cells (HAoSMC) were cultured under static or strained conditions, with exposure to CaSR agonists, the calcimimetic R568, and after CaSR silencing and over-expression. High extracellular calcium reduced CaSR expression and promoted osteochondrogenic transformation and calcium deposition. This was partially prevented by cyclic strain and exposure to R568. CaSR silencing enhanced calcification and osteochondrogenic transformation, whereas CaSR over-expression attenuated this procalcific response, demonstrating a central role for the CaSR in the response to cyclic strain and regulation of VC. In arterial explants from CKD patients (n = 11) and controls (n = 9), exposure to R568 did not significantly alter calcium deposition, osteochondrogenic markers or total artery calcium content. CONCLUSIONS: physiological mechanical strain is important for arterial homeostasis and may protect arteries from VC. The beneficial effects of cyclic strain may be mediated via the CaSR. Twit Text FOAVip Arterial Expression of the Calcium-Sensing Receptor Is Maintained by Physiological Pulsation and Protects against Calcification ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26436544 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26436544 #FOAvip English Wikipedia <ref>{{Cite pmid|26436544 }}</ref> Arterial Expression of the Calcium-Sensing Receptor Is Maintained by Physiological Pulsation and Protects against Calcification #MMPMID26436544 Molostvov G ; Hiemstra TF ; Fletcher S ; Bland R ; Zehnder D PLoS One 2015[]; 10 (10 ): e0138833 PMID26436544 show ga Vascular calcification (VC) is common in chronic kidney disease (CKD) and contributes to cardiovascular mortality. The calcium-sensing receptor (CaSR) is present in human artery, senses extracellular calcium and may directly modulate VC. OBJECTIVE: to investigate the association between arterial cyclic strain, CaSR expression and VC. METHODS AND RESULTS: human aortic smooth muscle cells (HAoSMC) were cultured under static or strained conditions, with exposure to CaSR agonists, the calcimimetic R568, and after CaSR silencing and over-expression. High extracellular calcium reduced CaSR expression and promoted osteochondrogenic transformation and calcium deposition. This was partially prevented by cyclic strain and exposure to R568. CaSR silencing enhanced calcification and osteochondrogenic transformation, whereas CaSR over-expression attenuated this procalcific response, demonstrating a central role for the CaSR in the response to cyclic strain and regulation of VC. In arterial explants from CKD patients (n = 11) and controls (n = 9), exposure to R568 did not significantly alter calcium deposition, osteochondrogenic markers or total artery calcium content. CONCLUSIONS: physiological mechanical strain is important for arterial homeostasis and may protect arteries from VC. The beneficial effects of cyclic strain may be mediated via the CaSR. |Adult [MESH] |Aged [MESH] |Aorta/cytology/*metabolism [MESH] |Calcium/metabolism/*pharmacology [MESH] |Cells, Cultured [MESH] |Chondrogenesis/drug effects [MESH] |Core Binding Factor Alpha 1 Subunit/biosynthesis/genetics [MESH] |Extracellular Matrix Proteins/biosynthesis/genetics [MESH] |Female [MESH] |Gene Expression Regulation/drug effects [MESH] |Humans [MESH] |Male [MESH] |Middle Aged [MESH] |Muscle, Smooth, Vascular/cytology/*metabolism [MESH] |Myocytes, Smooth Muscle/drug effects/*metabolism [MESH] |Osteoblasts/cytology [MESH] |Osteogenesis/drug effects [MESH] |Phenethylamines/pharmacology [MESH] |Phosphoproteins/biosynthesis/genetics [MESH] |Propylamines/pharmacology [MESH] |Pulsatile Flow/*physiology [MESH] |Receptors, Calcium-Sensing/agonists/antagonists & inhibitors/genetics/*physiology [MESH] |Recombinant Fusion Proteins/biosynthesis [MESH] |Stress, Mechanical [MESH] |Transfection [MESH] |Vascular Calcification/physiopathology/*prevention & control [MESH]Arterial Expression of the Calcium-Sensing Receptor Is Maintained by (epmc).pdf DeepDyve Pubget Overpricing