Site-specific microtubule-associated protein 4 dephosphorylation causes microtubule network densification in pressure overload cardiac hypertrophy.
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| Grant Information: | R01 HL094545 United States HL NHLBI NIH HHS; HL48788 United States HL NHLBI NIH HHS; R01 EY019065 United States EY NEI NIH HHS; HL094545 United States HL NHLBI NIH HHS; HL104287 United States HL NHLBI NIH HHS; P01 HL048788 United States HL NHLBI NIH HHS; R21 HL104287 United States HL NHLBI NIH HHS |
| Substance Nomenclature: | 0 (DNA, Complementary) 0 (Microtubule-Associated Proteins) 452VLY9402 (Serine) |
| Entry Date(s): | Date Created: 20100504 Date Completed: 20100812 Latest Revision: 20221207 |
| Update Code: | 20240829 |
| PubMed Central ID: | PMC2898445 |
| DOI: | 10.1074/jbc.M110.120709 |
| PMID: | 20436166 |
| Autor: | Chinnakkannu P; Cardiology Division, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina 29403, USA., Samanna V, Cheng G, Ablonczy Z, Baicu CF, Bethard JR, Menick DR, Kuppuswamy D, Cooper G 4th |
| Jazyk: | angličtina |
| Zdroj: | The Journal of biological chemistry [J Biol Chem] 2010 Jul 09; Vol. 285 (28), pp. 21837-48. Date of Electronic Publication: 2010 May 01. |
| DOI: | 10.1074/jbc.M110.120709 |
| Abstrakt: | In severe pressure overload-induced cardiac hypertrophy, a dense, stabilized microtubule network forms that interferes with cardiocyte contraction and microtubule-based transport. This is associated with persistent transcriptional up-regulation of cardiac alpha- and beta-tubulin and microtubule-stabilizing microtubule-associated protein 4 (MAP4). There is also extensive microtubule decoration by MAP4, suggesting greater MAP4 affinity for microtubules. Because the major determinant of this affinity is site-specific MAP4 dephosphorylation, we characterized this in hypertrophied myocardium and then assessed the functional significance of each dephosphorylation site found by mimicking it in normal cardiocytes. We first isolated MAP4 from normal and pressure overload-hypertrophied feline myocardium; volume-overloaded myocardium, which has an equal degree and duration of hypertrophy but normal functional and cytoskeletal properties, served as a control for any nonspecific growth-related effects. After cloning cDNA-encoding feline MAP4 and obtaining its deduced amino acid sequence, we characterized by mass spectrometry any site-specific MAP4 dephosphorylation. Solely in pressure overload-hypertrophied myocardium, we identified striking MAP4 dephosphorylation at Ser-472 in the MAP4 N-terminal projection domain and at Ser-924 and Ser-1056 in the assembly-promoting region of the C-terminal microtubule-binding domain. Site-directed mutagenesis of MAP4 cDNA was then used to switch each serine to non-phosphorylatable alanine. Wild-type and mutated cDNAs were used to construct adenoviruses; microtubule network density, stability, and MAP4 decoration were assessed in normal cardiocytes following an equivalent level of MAP4 expression. The Ser-924 --> Ala MAP4 mutant produced a microtubule phenotype indistinguishable from that seen in pressure overload hypertrophy, such that Ser-924 MAP4 dephosphorylation during pressure overload hypertrophy may be central to this cytoskeletal abnormality. |
| Databáze: | MEDLINE |
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