Month: June 2024

Prolonged inflammatory stimulation of fibroblasts promotes the formation of type III collagen and fibronectin in response to TGF-β1

Introduction

Inflammation is associated with tissue damage and the concomitant induction of wound healing responses. Pro-inflammatory cytokines such as TNF-α initiate wound healing by promoting the activation and proliferation of fibroblasts. Growth factors such as TGF-β1 drive granulation tissue formation, a type of new connective tissue formed by fibroblasts during wound healing. Fibroblast activation protein (FAP) and α-smooth muscle actin (α-SMA) identify distinct fibroblast phenotypes associated with distinct ECM remodeling.

In this study we investigated whether prolonged inflammatory stimulation of fibroblasts would augment the fibrogenic response to TGF-β1, and the fibroblast phenotype resulting from fibro-inflammation.

Poster

Conclusion

TNF-α shifts TGF-β1 stimulated α-SMA+ fibroblasts towards a fibro-inflammatory FAP+ phenotype. The TGF-β1 + TNF-α stimulation is characterized by increased type III collagen and fibronectin formation, while type I and VI collagen are reduced, compared to TGF-β1 stimulation only. In conclusion, the soluble nordicPRO-C3™ and FBN-C biomarkers may be used to identify FAP + fibroblast activity, associated with fibrogenesis.

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Biomarkers quantifying changes in the hair follicular extracellular matrix are elevated in patients with alopecia

Introduction

Alterations in the extracellular matrix (ECM) within the hair follicle microenvironment may contribute to the development and progression of non-scarring alopecia. Various ECM proteins such as type III collagen
and elastin are present within the hair follicle ECM. During wound healing, there is an increase in type III
collagen, while elastin is responsible for the elasticity of connective tissue, and its degradation might affect hair follicle function. There is also an increased immune cell infiltration, such as neutrophils, which target the hair bulb and disrupt the normal ECM architecture within the follicle leading to hair loss.

We aimed to investigate if biomarkers reflecting ECM remodeling could separate patients with non-scarring alopecia from healthy controls.

Poster

Conclusion

Patients with alopecia had an increase in type III collagen formation and elastin degradation, indicating the wound healing processes as well as the loss of elasticity within the surrounding ECM of the hair follicle. Objective biomarkers quantifying changes the hair follicle and its surrounding tissues could serve as potential biomarkers of diagnosis and disease monitoring in alopecia.

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PRO-C22 – A novel serological biomarker of tissue damage is associated with disease severity, disease activity, and systemic inflammation in patients with hidradenitis suppurativa

Introduction

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease that has a substantial diagnostic delay, in part due to diagnostic challenges with lesions mimicking abscesses. Utilizing robust serological biomarkers could aid in earlier diagnosis and better monitoring of disease severity. One such potential biomarker is type XXII collagen, a fibrillar collagen located at the interface between the anagen hair follicle and the dermis in the skin.

In this study we aimed to evaluate a novel serological biomarker reflecting type XXII collagen turnover, in patients with HS to test its association with disease severity, disease activity, and systemic inflammation.

Poster

Conclusion

We developed and evaluated the novel biomarker PRO-C22 reflecting tissue damage, which was associated to disease severity, activity and correlated with systemic inflammation in patients with HS. Such biomarker may be useful in early patient stratification and efficacy of treatment marker.

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The activity of fibroblast activation protein (FAP) is reflected by a specific fragment of type III collagen that can be serologically assessed and serve as a non-invasive biomarker

Introduction

Non-small cell lung cancers (NSCLC) are associated with both inflammatory and fibrotic tumor microenvironments (TME). The inflammatory component involves an influx of macrophages, which release matrix metalloproteinases (MMPs) that cleave extracellular matrix proteins, including type III collagen, leading to the release of the C3M fragment into circulation. In parallel, tumor fibrosis is marked by the accumulation of fibroblasts and high expression of Fibroblast Activation Protein (FAP), which is typically low or absent in benign tissue. FAP possesses unique proteolytic activity and has been shown to cleave various ECM proteins, including collagens.

Based on this, we hypothesized that FAP-mediated cleavage of type III collagen would generate a distinct fragment, C3F, that could enter the circulation and serve as a potential marker of FAP activity within the TME.

Poster

Conclusion

FAP activity can be assessed by targeting a FAP-cleaved fragment of type III collagen, C3F and function as a non-invasive biomarker for patients with NSCLC. By showing that this fragment differs from the MMP-generated fragment C3M, this study supports the notion that different biological processes are reflected in the proteolytic degradation of the ECM and can be reflected by specific circulating protein fragments.

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Serum type XII collagen is elevated in patients with solid tumors and is upregulated in cancer associated fibroblasts (CAFs) and normal fibroblasts (NFs) upon TGFb treatment

Introduction

Understanding the tumor microenvironment (TME) and extracellular matrix (ECM) is crucial in cancer research due to their impact on tumor progression. Collagens, major ECM components, regulate cell signaling and behavior, with type XII collagen being particularly vital for ECM organization. This collagen type is often overproduced by cancer-associated fibroblasts (CAFs), and its upregulation has been linked to poor survival outcomes in various cancers. In light of these findings, this study aimed to develop an ELISA for quantifying circulating type XII collagen as a potential cancer biomarker.

Poster

Conclusion

This study unveils a promising avenue for harnessing PRO-C12 as a non-invasive serum biomarker, enabling the quantification of type XII collagen fragments in cancer patients. Further investigations are warranted to explore the potential of PRO-C12 across different cancer types and disease stages, shedding light on its multifaceted role in cancer development.

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The non-invasive fibrosis biomarker measuring type III collagen synthesis (PRO-C3) is elevated in patients with myeloproliferative neoplasms and associate with disease severity and allele burden – lessons learned from the DALIAH trial

Introduction

Myeloproliferative neoplasms (MPNs) are chronic blood cancers characterized by elevated blood cell counts. MPNs arise due to acquired somatic driver mutations in stem cells (JAK2V617F, CALR and MPL) and develop over decades from the earliest stages of essential thrombocythemia (ET) and polycythemia vera (PV) towards advanced primary myelofibrosis (PMF) with bone marrow failure. MPNs are driven by chronic inflammation and characterized by persistent connective tissue remodeling leading to organ
dysfunction due to excessive accumulation of collagens (fibrosis) in the bone marrow. Reduction or stabilization of bone marrow fibrosis is considered a significant therapeutic goal in MPNs, hence monitoring and quantitating fibrosis non-invasively is ideally suited for patients with MPNs.

The aim of this study was to investigate the relevance of non-invasive serological biomarkers of type I collagen synthesis (PRO-C1) and type III collagen synthesis (nordicPRO-C3™) in patients with MPNs.

Poster

Conclusion

The non-invasive fibrosis associated biomarker nordicPRO-C3™, that reflects type III collagen synthesis, is elevated in MPN patients and associate with the severity of the disease and with the JAK2V617F allele burden. NordicPRO-C3™ has potential as a non-invasive bone marrow fibrosis biomarker to stratify and monitor patients with MPNs.

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Variations in fibrotic activity of cancer-associated fibroblasts from different tissues measured using noninvasive, clinically validated biomarkers

Introduction

Cancer-associated fibroblasts (CAFs) are pivotal orchestrators of tumor progression through their modulation of the extracellular matrix (ECM), particularly via the deposition of collagens. Different stimuli (e.g. TGF-β, PDGF-AB, IL-1α) can activate fibroblasts and induce phenotypic alterations in CAFs, promoting a pro-tumorigenic microenvironment characterized by enhanced ECM synthesis and remodeling. Consequently, targeting CAFs and their related pathways presents a promising therapeutic strategy for cancer treatment. However, numerous studies have revealed that CAFs exhibit heterogeneity both within and between individual tissues. Despite this, the specific patterns of collagen deposition by different CAFs remain insufficiently characterized.

In this study, we investigated the fibrotic activity of CAFs from various cancer tissues by measuring the production of three specific collagen peptides in vitro using non-invasive, clinically validated biomarkers.

Poster

Conclusion

These findings underscore the heterogeneity in collagen production and fibrotic activity among CAFs from different indications, providing valuable insights into the ECM dynamics within distinct TMEs.
Collagen-based non-invasive biomarkers demonstrate the capability to differentiate between the fibrotic activity of CAFs isolated from different tissues. In conclusion, this model proves to be a useful tool for anti-fibrotic drug screening.

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Serum biochemical markers of synovial tissue turnover, but not cartilage markers, predict radiological progression in very early rheumatoid arthritis

Introduction

In early rheumatoid arthritis (RA), radiographic assessments are insensitive to identify patients at high risk of progression, because the extension of joint damage, especially cartilage degradation, is rather
limited. Biochemical markers reflecting dynamic processes of tissue remodeling may be more sensitive to predict progression in early RA. To investigate whether soluble markers of matrix-metalloprotease
(MMP) driven type I (C1M) and type II (C2M) collagen degradation as:

1. Indicators of synovial and cartilage tissues remodelling respectively
2. Predict progression of joint damage in a prospective longitudinal
   cohort of patients with early RA.

Poster

Conclusion

Increased baseline serum C1M is consistently associated with a higher risk of radiographic progression in patients with early RA. Synovial tissue remodeling may be a prominent determinant of progression in the early phase of the disease whereas cartilage turnover is likely to play a minor role at this stage.

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Detecting Extracellular Matrix Turnover in axSpA Patients with concomitant Inflammation on MRI and Normal CRP

Introduction

Many patients with axial spondyloarthritis (axSpA) present normal CRP levels despite ongoing inflammation in the axial skeleton. The disease is characterized by hallmark features such as erosions and new bone formation, as well as aberrant neutrophil activation. We hypothesize that mechanistic biomarkers reflecting inflammation directly within the axial skeleton may provide a more accurate assessment of disease activity than CRP.

This study aims to investigate the association between the soluble biomarkers nordicCpa9-HNE™, C3M, and nordicPRO-C3™ and MRI-detected inflammation in the sacroiliac joint (SIJ) and spine of axSpA patients.

Poster

Conclusion

NordicCPa9-HNE™, C3M, and CRP demonstrated significant correlations with spine MRI inflammation at baseline. Notably, CPa9-HNE and C3M exhibited superior sensitivity compared to CRP in detecting spine MRI inflammation at week 52. These findings suggest that nordicCPa9-HNE™ and C3M may serve as valuable biomarkers for monitoring disease activity changes in axial spondyloarthritis (AxSpA) with normal CRP.

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PRO-C3 determined active fibrogenesis is a predictor of liver-related outcomes in patients with chronic hepatitis C

Introduction

Patients with untreated chronic hepatitis C (CHC) infection are at increased risk of developing a liver related outcome. Despite the availability of simplified direct-acting antiviral therapy, the prevalence of CHC remains unchanged in many industrialized countries. Biomarkers that can predict which chronic liver disease patients with inflammatory injury are at greatest risk of developing a clinical outcome are required. In this study we aim to investigate the ability of nordicPRO-C3™ as a marker of active fibrogenesis to predict liver-related outcomes compared to METAVIR fibrosis stage on biopsy in patients with hepatitis C.

Poster

Conclusion

We conclude that fibrosis activity (nordicPRO-C3™) is associated with an increased risk of developing a liver-related outcome in patients with untreated HCV infection. NordicPRO-C3™ provides a higher risk predictor for outcomes than METAVIR fibrosis stage on biopsy. A pro-fibrogenic marker such as nordicPRO-C3™ could provide prognostic utility in other chronic liver disease patients with ongoing inflammatory injury.

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