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Expression patterns of intermediate filament proteins desmin and lamin A in the developing conduction system of early human embryonic hearts
Author(s) -
Liu HuiXia,
Jing YiXin,
Wang JingJing,
Yang YanPing,
Wang YunXiu,
Li HaiRong,
Song Li,
Li AiHong,
Cui HuiLin,
Jing Ya
Publication year - 2020
Publication title -
journal of anatomy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 118
eISSN - 1469-7580
pISSN - 0021-8782
DOI - 10.1111/joa.13108
Subject(s) - desmin , lamin , embryonic stem cell , microbiology and biotechnology , biology , intermediate filament , lmna , cytoskeleton , transcription factor , embryonic heart , intermediate filament protein , anatomy , genetics , immunohistochemistry , nucleus , gene , vimentin , immunology , cell
Since embryonic heart development is a complex process and acquisition of human embryonic specimens is challenging, the mechanism by which the embryonic conduction system develops remains unclear. Herein, we attempt to gain insights into this developmental process through immunohistochemical staining and 3D reconstructions. Expression analysis of T‐box transcription factor 3, cytoskeleton desmin, and nucleoskeleton lamin A protein in human embryos in Carnegie stages 11–20 showed that desmin is preferentially expressed in the myocardium of the central conduction system compared with the peripheral conduction system, and is co‐expressed with T‐box transcription factor 3 in the central conduction system. Further, lamin A was first expressed in the embryonic ventricular trabeculations, where the terminal ramifications of the peripheral conduction system develop, and extended progressively to all parts of the central conduction system. The uncoupled spatiotemporal distribution pattern of lamin A and desmin indicated that the association of cytoskeleton desmin and nucleoskeleton lamin A may be a late event in human embryonic heart development. Compared with model animals, our data provide a direct morphological basis for understanding the arrhythmogenesis caused by mutations in human DES and LMNA genes.