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Secretion of interleukin-1 by dedifferentiated melanoma cells inhibits JAK1-STAT3-driven actomyosin contractility of lymph node fibroblastic reticular cells

ABSTRACT: Secretion of interleukin-1 by dedifferentiated melanoma cells inhibits JAK1-STAT3-driven actomyosin contractility of lymph node fibroblastic reticular cells

PROVIDER: PRJNA661045 | ENA |

REPOSITORIES: ENA

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Secretion of interleukin-1 by dedifferentiated melanoma cells inhibits JAK1-STAT3-driven actomyosin contractility of lymph node fibroblastic reticular cells

Project description:Fibroblastic reticular cells (FRC) are immunologically specialized myofibroblasts that control the elasticity of the lymph node (LN), in part through their contractile properties. Swelling of tumor-draining LN is a hallmark of lymphophilic cancers such as cutaneous melanoma. Melanoma displays high intratumoral heterogeneity with the coexistence of melanoma cells with variable differentiation phenotypes, from melanocytic to dedifferentiated states. Factors secreted by melanoma cells promote pre-metastatic LN reprograming and tumor spreading. Elucidating the impact of the melanoma secretome on FRC could help identify approaches to prevent metastasis. Here we show that melanocytic and dedifferentiated melanoma cells differentially impact the FRC contractile phenotype. Factors secreted by dedifferentiated cells, but not by melanocytic cells, strongly inhibited actomyosin-dependent contractile forces of FRC by decreasing the activity of the RHOA-ROCK pathway and the mechano-responsive transcriptional co-activator YAP. Transcriptional profiling and biochemical analyses indicated that actomyosin cytoskeleton relaxation in FRC is driven by inhibition of the JAK1-STAT3 pathway. This FRC relaxation was associated with increased FRC proliferation and activation and with elevated tumor invasion in vitro. The secretome of dedifferentiated melanoma cells also modulated the biomechanical properties of distant LN in pre-metastatic mouse models. Lastly, interleukin-1 produced by dedifferentiated cells was involved in the inhibition of FRC contractility. These data highlight the role of the JAK1-STAT3 and YAP pathways in spontaneous contractility of resting FRC. They also suggest that dedifferentiated melanoma cells specifically target FRC biomechanical properties to favor tumor spreading in the pre-metastatic LN niche. Targeting this remote communication could be an effective strategy to prevent metastatic spread of the disease.

2022-02-16 | GSE157355 | GEO

Expression data from actomyosin contractility regulated genes

Project description:Actomyosin contractility regulates cell morphology and movement. The objective of this study was to identify whether actomyosin contractility regulates gene expression in tumour cells and whether such genes are involved in cell morphology and movement. Gene expression analysis was carried out on highly contractile melanoma cell line A375M2 plated on a deformable collagen matrix under conditions where actomyosin contractility could be altered following treatment with blebbistatin, a direct inhibitor of myosin II, or Rho-kinase inhibitors Y27632 or H1152 that interfere with signalling to myosin II. 18 samples (6 x 3 biological replicates). Cells were plated on rigid or deformable matrices. Rounded cells (A375M2 melanoma cells) plated on deformable matrices were left untreated or treated with Rho-kinase inhibitors Y27632, H1152 or blebbistatin an inhibitor of mysoin II.

2010-08-24 | E-GEOD-23764 | biostudies-arrayexpress

Expression data from actomyosin contractility regulated genes

2010-08-24 | GSE23764 | GEO

Bulk RNA-seq of Fibroblastic Reticular Cells

Project description:Fibroblastic reticular cells (FRCs) (CD45- Ter119-MADCAM1- CD21/35- CD31- PDPN-) from skin draining lymph nodes of Grem1-Cre-ERT2.cki; Rosa26-LSL-EYFP mice were sorted and subjected to bulk RNA-seq of Grem1 reporter + and Grem1 reporter - cells.

2021-04-10 | E-MTAB-10205 | biostudies-arrayexpress

Bulk RNA-seq of Fibroblastic Reticular Cells

Project description:Bulk RNA-seq of Fibroblastic Reticular Cells

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The CLEC-2-podoplanin axis controls the contractility of fibroblastic reticular cells and lymph node microarchitecture.

Project description: Not available

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Activation of TLR9 signaling suppresses the immuno modulating functions of CD55lo fibroblastic reticular cells during bacterial peritonitis

Project description:Fibroblastic reticular cells (FRCs) are heterogeneous. We use single cell RNA sequencing to identify subsets of FRCs in fat-associated lymphoid clusters (FALC) in the mesenteric adipose tissue

2024-04-18 | GSE250571 | GEO

Gene array data of tumour draining lymph node fibroblastic reticular cells (FRCs)

Project description:Lymph node (LN) stromal cells, particularly fibroblastic reticular cells (FRCs), provide critical structural support and regulate immunity, tolerance and transport properties of LNs. In many tumors, LN metastasis is predictive of poor prognosis, however, stromal contribution to the evolving microenvironment of tumor draining LNs (TDLN) remains poorly understood. Here we present comparative transcriptional data of resting and TDLN FRCs after different time points of tumor drainage. FRCs were isolated from lymph nodes and FACS sorted based on the expression of CD45-, CD31- and PDPN+

2016-07-11 | GSE73728 | GEO

Fibroblastic reticular cells in the spleen - bulk RNAseq

Project description:Splenic white pulp (WP) structures are underpinned by fibroblastic stromal cells (FSCs) to facilitate splenic compartmentalization and execute efficient immune responses. Although distinct WP FSCs exhibit various molecular traits, the origin and the hierarchical differentiation of different cell subsets are not characterized. Here we showed, the organization of splenic WP and the differentiation of WP FSCs were governed by lymphotoxin beta receptor (LTβR) signaling pathway. Cell fate mapping analysis revealed that different WP fibroblastic stromal cells descend from a common perivascular LTβR-sensitive mesenchymal lymphoid organizer cells (mLTo) at prenatal stage. Moreover, embryonic mLTo cells required LTβR signaling to give rise to different WP stromal cell subsets, while the proliferation of these cells was devoid of LTβR signaling but followed the development of WP during ontogeny. Moreover, cell fate mapping from different time point indicated a consecutive commitment of mLTo cells initiated from the proximal region around the splenic artery. RNAseq and differentiation trajectory analysis of distinct FSCs showed that Ltbr-deficient cells and perivascular reticular cells (PRCs) from adult spleen exhibited a progenitor phenotype and revealed a closer hierarchical lineage with embryonic mLTo cells. Taken together, our results unveil that embryonic mLTo cells residing in the perivascular niches can give rise to different FSC populations in a LTβR-dependent manner during development.

2019-03-27 | E-MTAB-7097 | biostudies-arrayexpress

Single cell RNAseq analysis of fibroblastic reticular cells from murine brachial lymph nodes during inflamed and resting states

Project description:The lymph node is home to resident macrophage populations that are essential for healthy immune function and homeostasis. They are involved in multiple processes including the initiation of the local response to pathogens, halting viral and bacterial spread, and clearance of apoptotic cells, but the macrophage niche and factors that create it are largely undefined. Here we analyse fibroblastic reticular cells (FRCs) as an essential component of the lymph node macrophage niche using single-cell RNA-sequencing. Our analysis revealed that most reticular cell subsets within lymph nodes expressed master macrophage regulator CSF1. We further show that signalling through CSF1R was sufficient to support macrophage development, while in the presence of LPS, FRCs underwent a mechanistic switch and maintained support through CSF1R-independent mechanisms. Our data reveal a critically important role for FRCs in the creation of the parenchymal macrophage niche within LNs.

2023-05-01 | E-MTAB-10908 | biostudies-arrayexpress

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