A homozygous TET2 knock-out hiPSC line was generated, modeling loss-of-function mutations for studying CHIP-associated cardiovascular disease mechanisms.
The generation of a TET2 knock-out hiPSC line provides a novel in vitro model for studying the cellular mechanisms of CHIP-associated atherosclerotic cardiovascular diseases.
Absolute Event Rate: 0% vs 0%
Atherosclerotic cardiovascular diseases (CVD) have been linked to mutations related to clonal hematopoiesis of indeterminate potential (CHIP), with Tet methylcytosine dioxygenase 2 (TET2) being the second most often altered gene. ( Jaiswal et al., 2017 , Abplanalp et al., 2021 ) We produced a genome-edited human induced pluripotent stem cell (hiPSC) line with a homozygous knock-out (KO) of TET2, simulating loss-of-function mutations, and a control line. We evaluated the pluripotency status of these lines and their capacity to differentiate into mesoderm, ectodem and endoderm. Analysis of the cellular pathomechanisms of TET2-related, CHIP-associated CVDs is made possible by the generation of these cell lines.
Triantafyllou et al. (Sun,) reported a other. A homozygous TET2 knock-out hiPSC line was generated, modeling loss-of-function mutations for studying CHIP-associated cardiovascular disease mechanisms.