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Lysyl hydroxylase 2 deficiency promotes filopodia formation and fibroblast migration

ABSTRACT: Lysyl hydroxylase 2 deficiency promotes filopodia formation and fibroblast migration

PROVIDER: PRJNA772615 | ENA |

REPOSITORIES: ENA

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Lysyl hydroxylase 2 deficiency promotes filopodia formation and fibroblast migration

Project description: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.

2021-10-20 | GSE186100 | GEO

Lysyl hydroxylase 2 deficiency promotes filopodia formation and fibroblast migration.

Project description:Lysyl hydroxylase 2 (LH2) regulates intermolecular cross-linking of collagen molecules. Accumulation of LH2-modified collagen, which is highly stable and resistant to collagenase cleavage, is one cause of fibrosis. We previously demonstrated that conventional LH2 knockout mice showed embryonic lethality. Here we established LH2 conditional knockout mice using a tamoxifen-inducible Cre system. Morphological analysis of LH2-deficient fibroblasts by microscopy showed a dramatic increase in the number of filopodia, the finger-like cell surface projections that enable cell movement. The tips and leading edges of these filopodia exhibited up-regulated expression of Myosin-X (Myo10), a regulator of filopodial integrity. Wound healing assays demonstrated that migration of LH2-deficient cells was significantly faster than that of control cells. Gene expression profiling data also supported this phenotype. Together these findings indicate that LH2 deficiency may prevent fibrosis through decreased accumulation of LH2-cross-linked collagen, and that fibroblasts with faster migration contribute to enhanced wound healing activity. In conclusion, our cellular models provide evidence that LH2 deficiency plays a critical role in cell migration mediated through filopodia formation. Understanding the precise role of this phenotype in LH2-deficient cells may be helpful to define the pathogenesis of fibrosis. As such, detailed analyses of fibrosis and wound healing using LH2-deficient mouse models are needed.

| S-EPMC10020999 | biostudies-literature

Lysyl hydroxylase 1 deficiency exacerbates the alterations of gene transcriptional profile of abdominal aorta in angiotensin II induced abdominal aortic aneurysm

Project description:Lysyl hydroxylase 1 (LH1) plays an important role in hydroxylation of lysyl residuel in Xaa-Lys-Gly. The hydroxylysine residues serve as sites of attachment for carbohydrate units which are essential for the formation of intra- and intermolecular collagen crosslinks. To gain mechanistic insights into the effects of LH1 deficiency on abdominal aortic aneurysm (AAA) formation, a whole transcriptomic analysis of abdominal aorta were performed using RNA-seq. The abdominal aorta of mice for RNA-seq were acquired at day 14 after angiotensin II infusion in order to provide the mechanistic or causal evidence of a direct participatory role of LH1 to the effects of AAA.

2021-08-15 | GSE175683 | GEO

Analysis of proline and lysine post-translational modifications of collagen from prolyl 3-hydroxylase 3 and lysyl hydroxylase 1 null mice

Project description:We performed shotgun proteomic analysis of type V collagens purified from wild-type mice and prolyl 3-hydroxylase 3 or lysyl hydroxylase 1 null mice by LC-MS after trypsin digestion for identification of lysine glycosylation sites.

2021-02-19 | PXD019748 | JPOST Repository

Lysyl hydroxylase 3 mediated post-translational modifications are required for proper biosynthesis of collagen a1a1a2(IV)

Project description:We performed proteomic identification of type IV collagen gel bands from wild-type and lysyl hydroxylase 3 knockout cells by LC-MS after trypsin digestion.

2022-11-21 | PXD035051 | JPOST Repository

N-hydroxylase

Project description:N-hydroxylase

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Lysyl hydroxylase 1 deficiency exacerbates the alterations of gene transcriptional profile of abdominal aorta in angiotensin II induced abdominal aortic aneurysm

Project description:Lysyl hydroxylase 1 deficiency exacerbates the alterations of gene transcriptional profile of abdominal aorta in angiotensin II induced abdominal aortic aneurysm

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Fibroblast-tracks are topographical cues that direct cancer cell migration

Project description:Fibroblasts rely on adhesive structures to migrate. It is generally thought that adhesive structures disassemble once at the rear of the cell to release the cell and allow further movement. However, a significant portion of adhesions is not disassembled and is instead left on the substrate. We observed that virtually all the non-resorbed adhesions remain connected to the substrate by the means of integrin β5. Forward cell migration results in plasma membrane pulling giving rise to tubular structures that are then left on the ground, forming a network of lipid tracks that persist for several days, thus altering substrate’s topography. Cancer cells of different origin exploit fibroblast-tracks as migration railways. The adhesion of cancer cells along tracks is not mediated by focal adhesions, but rather by frustrated clathrin-coated structures (CCSs). Analysis of the composition of track generated by cancer associated fibroblasts allowed to identify integrin αv as the receptor on cancer cells responsible for track recognition. Some cancer cell lines are not able to perform durotaxis (rigidity driven migration), while fibroblasts are very good at it. We thus tested whether, in the presence of fibroblast-tracks, non-durotactic cancer cells would become durotactic by following tracks and this was indeed the case. Hence, fibroblast-tracks are a novel structure capable of physically directing cell migration of different cell types.

2023-09-22 | PXD034091 | Pride

Modifier Genes in 21-hydroxylase Deficiency - GSD 5607

Project description:Modifier Genes in 21-hydroxylase Deficiency - GSD 5607

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Targeting the Epigenome Reduces Keloid Fibroblast Cell Proliferation, Migration and Invasion

Project description:Targeting the Epigenome Reduces Keloid Fibroblast Cell Proliferation, Migration and Invasion

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