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.
- 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
|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|
|Collagen Biosynthesis & Modification||27||27|
|De Novo Lipogenesis||20||20|
|Fatty Acid Metabolism||55||57|
|Focal Adhesion Kinase||49||49|
|Internal Reference Gene||10||10|
|MAPK Cell Stress||67||67|
|MHC Class II Antigen Presentation||16||15|
|Phagocytic Cell Function||27||27|
|Programmed Cell Death||41||41|
|Type I Interferon||24||31|
|Type II Interferon||30||37|
|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.|
|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)|
- 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.
- Vukmirovic, M and Kaminski, N. Impact of Transcriptomics on Our Understanding of Pulmonary Fibrosis. Front Med (Lausanne). 2018;5:87.
- Mora, AL et al. Emerging therapies for idiopathic pulmonary fibrosis, a progressive age-related disease. Nat Rev Drug Discov. 2017;16(11):755-772.
- Rosenbloom, J et al. Human Fibrotic Diseases: Current Challenges in Fibrosis Research. Methods Mol Biol. 2017;1627:1-23.
- Musso, G et al. Non-alcoholic steatohepatitis: emerging molecular targets and therapeutic strategies. Nat Rev Drug Discov. 2016;15(4):249-274.
- 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.
- Meng, XM et al. TGF-β: the master regulator of fibrosis. Nat Rev Nephrol. 2016;12(6):325-338.
- Szabo, G and Petrasek, J. Inflammasome activation and function in liver disease. Nat Rev Gastroenterol Hepatol. 2015;12(7):387-400.
- Nanthakumar, CB et al. Dissecting fibrosis: therapeutic insights from the small-molecule toolbox. Nat Rev Drug Discov. 2015;14(10):693-720.
- 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.
- 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.