{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T01:03:46Z","timestamp":1775091826346,"version":"3.50.1"},"reference-count":46,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2013,12,1]]},"abstract":"<jats:p> Mechanical stress causes filament remodeling leading to myocyte hypertrophy and heart failure. The actin capping protein Z (CapZ) tightly binds to the barbed end of actin filaments, thus regulating actin assembly. The hypothesis is that the binding between CapZ and the actin filament is modulated through phosphatidylinositol 4,5-bisphosphate (PIP<jats:sub>2<\/jats:sub>) and how the COOH-terminus of CapZ\u03b21 regulates this binding. Primary neonatal rat ventricular myocytes (NRVMs) were strained at 10% amplitude and 1-Hz frequency. Dot blotting measured the PIP<jats:sub>2<\/jats:sub> amount, and affinity precipitation assay assessed the direct interaction between PIP<jats:sub>2<\/jats:sub> and CapZ\u03b21. Fluorescence recovery after photobleaching of green fluorescent protein-CapZ\u03b21 and actin-green fluorescent protein after 1 h of strain shows the dynamics significantly increased above the unstrained group. The increases in CapZ and actin dynamics were blunted by neomycin, suggesting PIP<jats:sub>2<\/jats:sub> signaling is involved. The amount of PIP<jats:sub>2<\/jats:sub> dramatically increased in NRVMs strained for 1 h. With a ROCK or RhoA inhibitor, changes were markedly reduced. Subcellular fractionation and antibody localization showed PIP<jats:sub>2<\/jats:sub> distributed to the sarcomeres. More PIP<jats:sub>2<\/jats:sub>-bound CapZ\u03b21 was found in strained NRVMs. Less PIP<jats:sub>2<\/jats:sub> bound to the CapZ\u03b21 with its COOH-terminus intact than in the COOH-terminal mutant of CapZ\u03b21, suggesting some inhibitory role for the COOH-terminus. Myocyte hypertrophy normally induced by 48 h of cyclic strain was blunted by dominant negative RhoA or neomycin. This suggests that after many hours of cyclic strain, a possible mechanism for cell hypertrophy is the accumulation of thin filament assembly triggered partially by the increased PIP<jats:sub>2<\/jats:sub> level and its binding to CapZ. <\/jats:p>","DOI":"10.1152\/ajpheart.00477.2013","type":"journal-article","created":{"date-parts":[[2013,9,17]],"date-time":"2013-09-17T04:15:06Z","timestamp":1379391306000},"page":"H1614-H1623","source":"Crossref","is-referenced-by-count":29,"title":["Phosphatidylinositol 4,5-bisphosphate regulates CapZ\u03b21 and actin dynamics in response to mechanical strain"],"prefix":"10.1152","volume":"305","author":[{"given":"Jieli","family":"Li","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brenda","family":"Russell","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, 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