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X-ORIGINAL-URL:https://www.biomed.cas.cz
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TZID:Europe/Prague
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TZOFFSETFROM:+0100
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TZNAME:CEST
DTSTART:20260329T010000
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DTSTART:20261025T010000
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DTSTART;TZID=Europe/Prague:20260318T150000
DTEND;TZID=Europe/Prague:20260318T160000
DTSTAMP:20260603T002418
CREATED:20260305T070841Z
LAST-MODIFIED:20260408T101238Z
UID:2499-1773846000-1773849600@www.biomed.cas.cz
SUMMARY:Seminář Srikant Ojha
DESCRIPTION:“Plectin Loss Disrupts Mechanotransduction and Attenuates\nHepatic Stellate Cell Activation” \nLiver fibrosis\, a hallmark of fibroproliferative disorders that contribute to nearly 45% of global mortality\, is primarily driven by the activation of hepatic stellate cells (HSCs). In response to injury-induced tissue stiffening\, HSCs undergo mechanosignaling-dependent activation and deposit excessive extracellular matrix (ECM)\, perpetuating a self-sustaining fibrotic loop. We sought to disrupt this process by targeting plectin\, a cytolinker protein central to mechanotransduction. Using an HSC-specific plectin knockout (KO) mouse model\, we observed significantly reduced ECM accumulation following carbon tetrachloride–induced injury. In vitro\, plectin-deficient HSCs displayed impaired proliferation\, migration\, and focal adhesion formation. Single-cell transcriptomics further revealed attenuated activation signatures in KO HSCs. Together\, our findings establish plectin as a key regulator of HSC mechanosignaling and highlight its potential as a therapeutic target to alleviate liver fibrosis.
URL:https://www.biomed.cas.cz/event/seminar-srikant-ojha/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
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