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10.1152/ajprenal.00323.2015 http://scihub22266oqcxt.onion/10.1152/ajprenal.00323.2015 26608788!4719045!26608788     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 310 (2): F144-51 Nephropedia Template TP {{tp|p=26608788|t=2016. PTH modulation of NCC activity regulates TRPV5 Ca2+ reabsorption |pdf=|usr=}}{{26608788}} gab.com Text PTH modulation of NCC activity regulates TRPV5 Ca2+ reabsorption JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26608788 #FOAvip Since parathyroid hormone (PTH) is known to increase transient receptor potential vanilloid (TRPV)5 activity and decrease Na(+)-Cl(-) cotransporter (NCC) activity, we hypothesized that decreased NCC-mediated Na(+) reabsorption contributes to the enhanced TRPV5 Ca(2+) reabsorption seen with PTH. To test this, we used mDCT15 cells expressing functional TRPV5 and ruthenium red-sensitive (45)Ca(2+) uptake. PTH increased (45)Ca(2+) uptake to 8.8 +/- 0.7 nmol.mg(-1).min(-1) (n = 4, P < 0.01) and decreased NCC activity from 75.4 +/- 2.7 to 20.3 +/- 1.3 nmol.mg(-1).min(-1) (n = 4, P < 0.01). Knockdown of Ras guanyl-releasing protein (RasGRP)1 had no baseline effect on (45)Ca(2+) uptake but significantly attenuated the response to PTH from a 45% increase (6.0 +/- 0.2 to 8.7 +/- 0.4 nmol.mg(-1).min(-1)) in control cells to only 20% in knockdown cells (6.1 +/- 0.1 to 7.3 +/- 0.2 nmol.mg(-1).min(-1), n = 4, P < 0.01). Inhibition of PKC and PKA resulted in further attenuation of the PTH effect. RasGRP1 knockdown decreased the magnitude of the TRPV5 response to PTH (7.9 +/- 0.1 nmol.mg(-1).min(-1) for knockdown compared with 9.1 +/- 0.1 nmol.mg(-1).min(-1) in control), and the addition of thiazide eliminated this effect (a nearly identical 9.0 +/- 0.1 nmol.mg(-1).min(-1)). This indicates that functionally active NCC is required for RasGRP1 knockdown to impact the PTH effect on TRPV5 activity. Knockdown of with no lysine kinase (WNK)4 resulted in an attenuation of the increase in PTH-mediated TRPV5 activity. TRPV5 activity increased by 36% compared with 45% in control (n = 4, P < 0.01 between PTH-treated groups). PKC blockade further attenuated the PTH effect, whereas combined PKC and PKA blockade in WNK4KD cells abolished the effect. We conclude that modulation of NCC activity contributes to the response to PTH, implying a role for hormonal modulation of NCC activity in distal Ca(2+) handling. Twit Text FOAVip PTH modulation of NCC activity regulates TRPV5 Ca2+ reabsorption ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26608788 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26608788 #FOAvip English Wikipedia <ref>{{Cite pmid|26608788}}</ref> PTH modulation of NCC activity regulates TRPV5 Ca2+ reabsorption #MMPMID26608788 Hoover RS; Tomilin V; Hanson L; Pochynyuk O; Ko B Am J Physiol Renal Physiol 2016[Jan]; 310 (2): F144-51 PMID26608788show ga Since parathyroid hormone (PTH) is known to increase transient receptor potential vanilloid (TRPV)5 activity and decrease Na(+)-Cl(-) cotransporter (NCC) activity, we hypothesized that decreased NCC-mediated Na(+) reabsorption contributes to the enhanced TRPV5 Ca(2+) reabsorption seen with PTH. To test this, we used mDCT15 cells expressing functional TRPV5 and ruthenium red-sensitive (45)Ca(2+) uptake. PTH increased (45)Ca(2+) uptake to 8.8 +/- 0.7 nmol.mg(-1).min(-1) (n = 4, P < 0.01) and decreased NCC activity from 75.4 +/- 2.7 to 20.3 +/- 1.3 nmol.mg(-1).min(-1) (n = 4, P < 0.01). Knockdown of Ras guanyl-releasing protein (RasGRP)1 had no baseline effect on (45)Ca(2+) uptake but significantly attenuated the response to PTH from a 45% increase (6.0 +/- 0.2 to 8.7 +/- 0.4 nmol.mg(-1).min(-1)) in control cells to only 20% in knockdown cells (6.1 +/- 0.1 to 7.3 +/- 0.2 nmol.mg(-1).min(-1), n = 4, P < 0.01). Inhibition of PKC and PKA resulted in further attenuation of the PTH effect. RasGRP1 knockdown decreased the magnitude of the TRPV5 response to PTH (7.9 +/- 0.1 nmol.mg(-1).min(-1) for knockdown compared with 9.1 +/- 0.1 nmol.mg(-1).min(-1) in control), and the addition of thiazide eliminated this effect (a nearly identical 9.0 +/- 0.1 nmol.mg(-1).min(-1)). This indicates that functionally active NCC is required for RasGRP1 knockdown to impact the PTH effect on TRPV5 activity. Knockdown of with no lysine kinase (WNK)4 resulted in an attenuation of the increase in PTH-mediated TRPV5 activity. TRPV5 activity increased by 36% compared with 45% in control (n = 4, P < 0.01 between PTH-treated groups). PKC blockade further attenuated the PTH effect, whereas combined PKC and PKA blockade in WNK4KD cells abolished the effect. We conclude that modulation of NCC activity contributes to the response to PTH, implying a role for hormonal modulation of NCC activity in distal Ca(2+) handling. |Animals[MESH] |Calcium Channels/*metabolism[MESH] |Calcium/*metabolism[MESH] |Cell Line[MESH] |Kidney Tubules, Distal/cytology/drug effects/*metabolism[MESH] |Mice[MESH] |Parathyroid Hormone/*pharmacology[MESH] |Receptors, Cytoplasmic and Nuclear/metabolism[MESH] |Solute Carrier Family 12, Member 3/metabolism[MESH]PTH modulation of NCC activity regulates TRPV5 Ca2+ reabsorption (epmc).pdf DeepDyve Pubget Overpricing