Platelet-derived Growth Factor-α and Neuropilin-1 Mediate Lung Fibroblast Response to Rigid Collagen Fibers

McGowan, Stephen E.; Lansakara, Thiranjeewa I.; McCoy, Diann M.; Zhu, Lien; Tivanski, Alexei V.

doi:10.1165/rcmb.2019-0173oc

Cited by 9 publications

(3 citation statements)

References 47 publications

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“…Pathway enrichment analyses showed lots of common significant pathways of pulmonary function using GREAT. The significant enrichment pathway include negative regulation of phospholipid biosynthetic process [ 48 ], platelet-derived growth factor binding [ 49 ], potassium:chloride symporter activity [ 50 ], epithelial-mesenchymal cell signaling [ 51 ], decreased serum estradiol [ 52 ], low voltage-gated calcium channel activity [ 53 ], cAMP response element binding protein binding [ 54 ], activation of Cdc42 GTPase activity [ 55 ], ceramide signaling pathway [ 56 ], transcription regulation by bZIP transcription factor [ 57 ], mitogen-activated protein kinase p38 binding [ 58 ], and notch signaling pathway [ 59 ].…”

Section: Discussionmentioning

confidence: 99%

Genome-wide DNA methylation analysis of pulmonary function in middle and old-aged Chinese monozygotic twins

Wang

et al. 2021

Respir Res

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Background Previous studies have determined the epigenetic association between DNA methylation and pulmonary function among various ethnics, whereas this association is largely unknown in Chinese adults. Thus, we aimed to explore epigenetic relationships between genome-wide DNA methylation levels and pulmonary function among middle-aged Chinese monozygotic twins. Methods The monozygotic twin sample was drawn from the Qingdao Twin Registry. Pulmonary function was measured by three parameters including forced expiratory volume the first second (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio. Linear mixed effect model was used to regress the methylation level of CpG sites on pulmonary function. After that, we applied Genomic Regions Enrichment of Annotations Tool (GREAT) to predict the genomic regions enrichment, and used comb-p python library to detect differentially methylated regions (DMRs). Gene expression analysis was conducted to validate the results of differentially methylated analyses. Results We identified 112 CpG sites with the level of P < 1 × 10–4 which were annotated to 40 genes. We identified 12 common enriched pathways of three pulmonary function parameters. We detected 39 DMRs located at 23 genes, of which PRDM1 was related to decreased pulmonary function, and MPL, LTB4R2, and EPHB3 were related to increased pulmonary function. The gene expression analyses validated DIP2C, ASB2, SLC6A5, and GAS6 related to decreased pulmonary function. Conclusion Our DNA methylation sequencing analysis on identical twins provides new references for the epigenetic regulation on pulmonary function. Several CpG sites, genes, biological pathways and DMRs are considered as possible crucial to pulmonary function.

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Section: Discussionmentioning

confidence: 99%

Genome-wide DNA methylation analysis of pulmonary function in middle and old-aged Chinese monozygotic twins

Wang

et al. 2021

Respir Res

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“…Poisson’s ratios of 0.5 and 0.25 were assumed for the follicles and AFM probe, respectively. The data analysis was carried out as in our previously reported work ( Kruger et al, 2019 ; Bell et al, 2020 ; Kruger et al, 2020 ; McGowan et al, 2020 ).…”

Section: Methodsmentioning

confidence: 99%

Fascin limits Myosin activity within Drosophila border cells to control substrate stiffness and promote migration

Lamb

Kaluarachchi

Lansakara

et al. 2021

eLife

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A key regulator of collective cell migrations, which drive development and cancer metastasis, is substrate stiffness. Increased substrate stiffness promotes migration and is controlled by Myosin. Using Drosophila border cell migration as a model of collective cell migration, we identify, for the first time, that the actin bundling protein Fascin limits Myosin activity in vivo. Loss of Fascin results in: increased activated Myosin on the border cells and their substrate, the nurse cells; decreased border cell Myosin dynamics; and increased nurse cell stiffness as measured by atomic force microscopy. Reducing Myosin restores on-time border cell migration in fascin mutant follicles. Further, Fascin’s actin bundling activity is required to limit Myosin activation. Surprisingly, we find that Fascin regulates Myosin activity in the border cells to control nurse cell stiffness to promote migration. Thus, these data shift the paradigm from a substrate stiffness-centric model of regulating migration, to uncover that collectively migrating cells play a critical role in controlling the mechanical properties of their substrate in order to promote their own migration. This understudied means of mechanical regulation of migration is likely conserved across contexts and organisms, as Fascin and Myosin are common regulators of cell migration.

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“…Poisson's ratios of 0.5 and 0.25 were assumed for the follicles and AFM probe, respectively. The data analysis was carried out as in our previously reported work (Bell et al, 2020;Kruger et al, 2019Kruger et al, , 2020McGowan et al, 2020).…”

Section: Atomic Force Microscopy (Afm) Nanoindentation On Drosophila Folliclesmentioning

confidence: 99%

Fascin limits Myosin activity withinDrosophilaborder cells to control substrate stiffness and promote migration

Lamb

Kaluarachchi

Lansakara

et al. 2021

Preprint

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A key regulator of collective cell migrations, which drive development and cancer metastasis, is substrate stiffness. Increased substrate stiffness promotes migration and is controlled by Myosin. Using Drosophila border cell migration as a model of collective cell migration, we identify, for the first time, that the actin bundling protein Fascin limits Myosin activity in vivo. Loss of Fascin results in: increased activated Myosin on the border cells and their substrate, the nurse cells; decreased border cell Myosin dynamics; and increased nurse cell stiffness as measured by atomic force microscopy. Reducing Myosin restores on-time border cell migration in fascin mutant follicles. Further, Fascin’s actin bundling activity is required to limit Myosin activation. Surprisingly, we find that Fascin regulates Myosin activity in the border cells to control nurse cell stiffness to promote migration. Thus, these data shift the paradigm from a substrate stiffness-centric model of regulating migration, to uncover that collectively migrating cells play a critical role in controlling the mechanical properties of their substrate in order to promote their own migration. This new means of mechanical regulation of migration is likely conserved across contexts and organisms, as Fascin and Myosin are common regulators of cell migration.

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Platelet-derived Growth Factor-α and Neuropilin-1 Mediate Lung Fibroblast Response to Rigid Collagen Fibers

Cited by 9 publications

References 47 publications

Genome-wide DNA methylation analysis of pulmonary function in middle and old-aged Chinese monozygotic twins

Genome-wide DNA methylation analysis of pulmonary function in middle and old-aged Chinese monozygotic twins

Fascin limits Myosin activity within Drosophila border cells to control substrate stiffness and promote migration

Fascin limits Myosin activity withinDrosophilaborder cells to control substrate stiffness and promote migration

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