nCounter® Fibrosis Panel

 

Uncover the mechanisms of disease pathogenesis, identify biomarkers of progression, and develop signatures for therapeutic response with the nCounter Fibrosis Panel. This gene expression panel combines hundreds of genes involved in the initial tissue damage response, chronic inflammation, proliferation of pro-fibrotic cells, and tissue modification that leads to fibrotic disease of the lungs, heart, liver, kidney, and skin.

Profile 770 genes across 51 annotated pathways.IM_MK1624_FibrosisWheel_r5_FINAL.png

  • Study pathogenesis and identify biomarkers for fibrotic diseases of the lungs, heart, liver, kidney, and skin
  • Elucidate the mechanism of action behind the four stages of fibrosis: initiation, inflammation, proliferation, and modification
  • Understand the signaling cascade from cell stress to inflammation
  • Quantify the relative abundance of immune cells

IM_MK1625_FibrosisGraphic.png

Stage Description Pathways Number of Human Genes Number of Mouse Genes
Initiation Cell and tissue damage, often specific to an organ or fibrotic disease, initiates a cascade of stress and immune responses. Autophagy, Cholesterol Metabolism, Cytosolic DNA Sensing, De Novo Lipogenesis, Endotoxin Response, Fatty Acid Metabolism, Gluconeogenesis, Insulin Resistance/Signaling, MAPK Cell Stress, mTOR, Oxidative Stress, PPAR Signaling, Proteotoxic Stress, SASP 369 369
Inflammation Inflammation is one of many responses to the initial damage, involving multiple immune cell types and signaling pathways. Chronic inflammation drives the proliferation of pro-fibrotic cells and tissue modification. Adenosine Pathway, Chemokine Signaling, Complement Activation, Cytokine Signaling, Granulocyte Activity, Inflammasome, M1/M2 Activation, MHC Class II Antigen Presentation, Neutrophil Degranulation, NF-kB, Phagocytic Cell Function, Platelet Degranulation, Th1/Th2/Th17 Differentiation, TLR Signaling, Type I/Type II Interferon 297 297
Proliferation Differentiation and proliferation of myofibroblasts are driven by upstream inflammation. These cells drive the wound-healing response that results in fibrotic damage. Cell Cycle, ECM Synthesis, EMT, Focal Adhesion Kinase, Hedgehog Signaling, Hypoxia, Myofibroblast Regulation, Notch, PDGF Signaling, PI3K-Akt, Tgf-Beta, Wnt 159 161
Modification Immune and myofibroblast cells contribute to extracellular matrix modification and tissue alterations that are characteristic of fibrotic disease. Angiogenesis, Apoptosis, Collagen Biosynthesis & Modification, ECM Degradation, Epigenetic Modification, Hippo Pathway, Regulated Necrosis 287 287

 

 

   Pathway Number of Human Genes Number of Mouse Genes
Adenosine Pathway 51 53
Angiogenesis 37 37
Autophagy 39 39
Cell Cycle 49 49
Chemokine Signaling 23 22
Cholesterol Metabolism 26 24
Collagen Biosynthesis & Modification 27 27
Complement Activation 22 19
Cytokine Signaling 60 58
De Novo Lipogenesis 20 20
ECM Degradation 42 44
ECM Synthesis 38 38
EMT 88 88
Endotoxin Response 42 41
Epigenetic Modification 24 24
Fatty Acid Metabolism 55 57
Focal Adhesion Kinase 49 49
Gluconeogenesis 20 19
Granulocyte Activity 34 34
Hedgehog Signaling 24 24
Hippo Pathway 13 13
Hypoxia 16 16
Inflammasome 32 32
Insulin Resistance 38 38
Insulin Signaling 16 16
Internal Reference Gene 10 10
M1 Activation 12 12
M2 Activation 12 12
MAPK Cell Stress 67 67
MHC Class II Antigen Presentation 16 15
mTOR 36 36
Myofibroblast Regulation 25 25
Neutrophil Degranulation 67 73
NF-kb 41 40
Notch 20 20
Oxidative Stress 18 18
PDGF Signaling 29 29
Phagocytic Cell Function 27 27
PI3K-Akt 89 89
Platelet Degranulation 33 34
PPAR Signaling 28 33
Programmed Cell Death 41 41
Proteotoxic Stress 43 43
SASP 15 15
TGF-beta 38 38
Th1 Differentiation 13 13
Th17 Differentiation 24 24
Th2 Differentiation 13 13
TLR Signaling 63 63
Type I Interferon 24 31
Type II Interferon 30 37
Wnt 38 38

 

Cell Type Description
B Cells B cells are the primary mediators of the humoral immune response, bearing antigen-specific B cell receptors and producing antibodies that can enable the immune system to respond to a broad variety of antigens. B cells can also function as MHC class II antigen presenting cells to stimulate T cell immunity.
T Cells T-cells mediate cell-based immunity by recognizing primarily peptide antigens displayed on MHC class I or class II and either producing cytokines or directly killing the presenting cell.
TH1 CD4+ T cell subset that produces IL2 and Interferon-gamma to promote cellular immunity by acting on CD8+ T Cells, NK Cells and Macrophages.
Regulatory T Cells (Tregs) CD4+ T Cells that suppress effector B and T Cells and play a central role in suppression of the immune response and tolerance to self-antigens.
CD8+ T Cells A subset of T cells that are capable of binding cognate-antigen expressing cells via class I MHC and directly lysing them via perforin and granzymes.
Exhausted CD8+ T Cells T-cells overstimulated by antigen can develop an "exhausted" phenotype, in which they are no longer effective in targeting antigen-bearing cells.
Cytotoxic Cells All cells capable of cytotoxic activity, which can include T, NKT, and NK-cells.
Dendritic Cells Professional antigen presenting cells that internalize, process, and present antigens to lymphocytes via MHC class I and class II along with costimulatory signals to initiate cellular immune responses.
Macrophages Pluripotent cells with critical roles in initiating innate and adaptive immune responses, phagocytosing abnormal cells, and regulating wound healing and tissue repair.
Mast Cells Mast cells release histamine containing granules and other signals in order to promote inflammation and regulate allergic responses.
Neutrophils Neutrophils are highly abundant cells that respond early to sites of infection or inflammation, phagocytose cellular debris, and promote downstream immunity.
Natural Killer (NK) Cells Cytotoxic cells of the innate immune system that are a significant source of interferon-gamma and are capable of directly killing targeted cells via detection of a loss in MHC surface expression.
NK CD56dim cells The amount of CD56 present on an NK cell is indicative of its age and differentiation state; CD56 dim cells are mature NK cells, more commonly found in peripheral blood than secondary lymphoid tissues, and have the greatest cytolytic activity.
Feature Specifications
Number of Targets 770 (Human), 770 (Mouse), including internal reference genes
Sample Input - Standard (No amplification required) 25-300 ng
Sample Input - Low Input As little as 1 ng with nCounter Low Input Kit (sold separately)
Sample Type(s) Cultured cells/cell lysates, sorted cells, FFPE-derived RNA, total RNA, fragmented RNA, PBMCs, and whole blood/plasma
Customizable Add up to 30 unique genes with Panel-Plus and up to 10 custom protein targets
Time to Results Approximately 24 hours
Data Analysis nSolver™ Analysis Software (RUO)

 

  1. Kazankov, K et al. The role of macrophages in nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Nat Rev Gastroenterol Hepatol. 2018;16(3):145-159.
  2. Vukmirovic, M and Kaminski, N. Impact of Transcriptomics on Our Understanding of Pulmonary Fibrosis. Front Med (Lausanne). 2018;5:87.
  3. Mora, AL et al. Emerging therapies for idiopathic pulmonary fibrosis, a progressive age-related disease. Nat Rev Drug Discov. 2017;16(11):755-772.
  4. Rosenbloom, J et al. Human Fibrotic Diseases: Current Challenges in Fibrosis Research. Methods Mol Biol. 2017;1627:1-23.
  5. Musso, G et al. Non-alcoholic steatohepatitis: emerging molecular targets and therapeutic strategies. Nat Rev Drug Discov. 2016;15(4):249-274.
  6. Sanders, FWB and Griffin, JL. De novo lipogenesis in the liver in health and disease: more than just a shunting yard for glucose. Biol Rev. 2016;91(2):452-468.
  7. Meng, XM et al. TGF-β: the master regulator of fibrosis. Nat Rev Nephrol. 2016;12(6):325-338.
  8. Szabo, G and Petrasek, J. Inflammasome activation and function in liver disease. Nat Rev Gastroenterol Hepatol. 2015;12(7):387-400.
  9. Nanthakumar, CB et al. Dissecting fibrosis: therapeutic insights from the small-molecule toolbox. Nat Rev Drug Discov. 2015;14(10):693-720.
  10. Selman, M and Pardo, A. Revealing the pathogenic and aging-related mechanisms of the enigmatic idiopathic pulmonary fibrosis. an integral model. Am J Repir Crit Care Med. 2014;189(10):1161-1172.
  11. Wick, G et al. The Immunology of Fibrosis. Annu Rev Immunol. 2013;31:107-135.
Product Product Description Quantity Catalog Number
nCounter Human Fibrosis V2 Panel Includes 760 genes;10 internal reference genes for data normalization 12 Reactions XT-CSO-HFIB2-12
nCounter Mouse Fibrosis V2 Panel Includes 760 genes;10 internal reference genes for data normalization 12 Reactions XT-CSO-MFIB2-12
nCounter Master Kit (MAX or FLEX Systems) Reagents and Cartridges Reagents, cartridges, and consumables necessary for sample processing on nCounter MAX and FLEX Systems 12 Reactions NAA-AKIT-012
nCounter SPRINT Cartridge 1 Cartridge, 12 lanes Reagents, cartridges, and consumables necessary for sample processing on nCounter MAX and FLEX Systems 12 Reactions SPRINT-CAR-1.0
nCounter SPRINT Reagent Pack nCounter SPRINT Reagent Pack containing Reagents A, B, C, and Hybridization Buffer 192 Reactions SPRINT-REAG-KIT

 

For Research Use Only. Not for use in diagnostic procedures.