Lysyl hydroxylase 2 deficiency promotes filopodia formation and fibroblast migration

Lysyl hydroxylase 2 (LH2) regulates the intermolecular cross-linking of collagen molecules. Accumulation of LH2-modified collagen, which is highly stable and resistant to collagenase cleavage, is one of the causes of fibrosis. In this study, we established LH2-deficient fibroblasts and first analyzed morphology of LH2-deficient fibroblasts by microscopy. LH2-deficient fibroblasts showed a dramatic increase in filopodial dynamics and cell migration, which were supported by time-lapse video microscopy and Immunocytochemistry, and gene expression profiling data. Understanding the precise role of phenotype in LH2-deficient cells may be helpful to define the pathogenesis of fibrosis. Data shows the comparison of differentially expressed genes in LH2 cKO TTFs in culture medium with tamoxifen (LH2 cKO_no.1) vs. LH2 cKO TTFs in culture medium without tamoxifen (LH2 cKO_no.2) after 24h tamoxifen treatent.