| pubmed-article:14734049 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C0040704 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C0687129 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C0070876 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C0001122 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C2004454 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C0599702 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:14734049 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:14734049 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:14734049 | pubmed:dateCreated | 2004-1-21 | lld:pubmed |
| pubmed-article:14734049 | pubmed:abstractText | Initially during acidosis, Ca transient amplitude (Delta[Ca]i) and the rate constant of [Ca]i decline (k(Ca)) are decreased, but later during acidosis Delta[Ca]i and k(Ca) partially recover. This recovery in rat myocytes could be inhibited by KN-93 suggesting that CaMKII-dependent protein phosphorylation (and enhanced SR Ca uptake) may be responsible. To test whether phospholamban (PLB) is required for the Delta[Ca]i and k(Ca) recovery during acidosis, we used isolated myocytes from PLB knockout (PLB-KO) vs. wild-type (WT) mice. [Ca]i was measured using fluo-3. During the initial phase of acidosis (1-4 min), Delta[Ca]i decreased in WT myocytes (n = 8) from 1.75 +/- 0.19 to 1.10 +/- 0.13 DeltaF/F0 (P < 0.05) and k(Ca) decreased from 3.20 +/- 0.22 to 2.38 +/- 0.18 s(-1) (P < 0.05). Later during acidosis (6-12 min), Delta[Ca]i partially recovered to 1.41 +/- 0.18 DeltaF/F0 and k(Ca) to 2.78 +/- 0.22 s(-1) (i.e. both recovered by approximately 50%). CaMKII inhibition using KN-93 completely prevented this recovery of Delta[Ca]i and k(Ca) during late acidosis in WT myocytes. In PLB-KO myocytes (n = 11) Delta[Ca]i decreased during early acidosis from 2.92 +/- 0.31 to 1.33 +/- 0.17 DeltaF/F0 (P < 0.05) and k(Ca) decreased from 10.45 +/- 0.56 to 7.58 +/- 0.68 s(-1) (P < 0.05). However, Delta[Ca]i did not recover during late acidosis and k(Ca) decreased even more (6.59 +/- 0.65 s(-1)). Parallel results were seen for contractile parameters. We conclude that PLB is crucial to the recovery of Delta[Ca]i and k(Ca) during acidosis. Moreover, PLB phosphorylation by CaMKII plays an important role in limiting the decline in Ca transients (and contraction) during acidosis. | lld:pubmed |
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| pubmed-article:14734049 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:14734049 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:14734049 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14734049 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:14734049 | pubmed:issn | 0022-2828 | lld:pubmed |
| pubmed-article:14734049 | pubmed:author | pubmed-author:BersD MDM | lld:pubmed |
| pubmed-article:14734049 | pubmed:author | pubmed-author:DeSantiagoJJ | lld:pubmed |
| pubmed-article:14734049 | pubmed:author | pubmed-author:MaierL SLS | lld:pubmed |
| pubmed-article:14734049 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14734049 | pubmed:volume | 36 | lld:pubmed |
| pubmed-article:14734049 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14734049 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14734049 | pubmed:pagination | 67-74 | lld:pubmed |
| pubmed-article:14734049 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:14734049 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14734049 | pubmed:articleTitle | Phospholamban is required for CaMKII-dependent recovery of Ca transients and SR Ca reuptake during acidosis in cardiac myocytes. | lld:pubmed |
| pubmed-article:14734049 | pubmed:affiliation | Department of Physiology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA. | lld:pubmed |
| pubmed-article:14734049 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:14734049 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:14734049 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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