CILP

Last update 08 May 2025

Basic Info

Synonyms

cartilage intermediate layer protein, Cartilage intermediate layer protein 1, Cartilage intermediate layer protein 1 C1

+ [5]

Introduction

Probably plays a role in cartilage scaffolding. May act by antagonizing TGF-beta1 (TGFB1) and IGF1 functions. Has the ability to suppress IGF1-induced proliferation and sulfated proteoglycan synthesis, and inhibits ligand-induced IGF1R autophosphorylation. May inhibit TGFB1-mediated induction of cartilage matrix genes via its interaction with TGFB1. Overexpression may lead to impair chondrocyte growth and matrix repair and indirectly promote inorganic pyrophosphate (PPi) supersaturation in aging and osteoarthritis cartilage.

100 Clinical Results associated with CILP

100 Translational Medicine associated with CILP

0 Patents (Medical) associated with CILP

104

Literatures (Medical) associated with CILP

01 Mar 2025·Journal of Cellular and Molecular Medicine

Cartilage Intermediate Layer Protein‐1 Promotes Extracellular Matrix Degeneration via Interacting With CD47

Article

Author: Zhang, Zehua ; Yang, Yusheng ; He, Jinyue ; Xiang, Yu ; Xu, Jianzhong ; Deng, Jiezhong ; Luo, Fei

ABSTRACTIntervertebral Disc Degeneration (IDD) is a multifactorial result contributing to Low Back Pain (LBP) while Cartilage Intermediate Layer Protein‐1 (CILP‐1) is gradually up‐regulated along with IDD. Whether CILP‐1 acts in a direct role promoting IDD via regulating matrix metabolism remains to be elucidated. Herein, we firstly detected the expression level of matrix‐related phenotypes in nucleus pulposus (NP) cells treated with CILP‐1, including ADAMTS, MMPs, IL‐6, Collagens, Aggrecan (ACAN) and SOX9. Meanwhile, the phosphorylation levels of MAPKs and NF‐κB were detected to explore the involved signalling pathways, which were further validated by inhibition experiments. Furthermore, molecular docking analysis was employed to evaluate the possibility of CD47 acting as the direct receptor mediating CILP's regulation above, which was further validated by immunoprecipitation and inhibition experiment. Our findings have made a comprehensive investigation into the regulatory effect of CILP‐1 on the matrix metabolism of NP cells and explored the underlying mechanism.

01 Dec 2024·Journal of Cellular and Molecular Medicine

Regulation of Clusterin in the Heart and Plasma of Mice After Transverse Aortic Constriction

Article

Author: Chwastyniak, Maggy ; Weber, Lukas ; Ernst, Matthias ; Turkieh, Annie ; Pinet, Florence ; Beseme, Olivia ; Kiss, Attila ; Ye, Quianling ; Podesser, Bruno K. ; Amouyel, Philippe ; Baydar, Simge

ABSTRACTChronic pressure overload induces adverse cardiac remodelling characterised by left ventricular (LV) hypertrophy and fibrosis, leading to heart failure (HF). Identification of new biomarkers for adverse cardiac remodelling enables us to better understand this process and, consequently, to prevent HF. We recently identified clusterin (CLU) as a biomarker of cardiac remodelling and HF after myocardial infarction. The aim of this study was to investigate whether CLU expression is regulated in the heart and could be used as an indicator of adverse cardiac remodelling in response to pressure overload. We quantified CLU in the LV of mice subjected to transverse aortic constriction (TAC) and observed increased CLU mRNA levels and its mature protein form (m‐CLU) compared to the sham. Interestingly, CLU mRNA levels were positively correlated with pro‐hypertrophic (ANP, BNP, B‐MHC), pro‐ and anti‐fibrotic (TGFb, ColI and CILP) genes. In addition, m‐CLU was positively correlated with LV hypertrophy, LV end diastolic and systolic diameters, and negatively correlated with LV ejection fraction. Finally, we observed that m‐CLU levels only increased in TAC mice with severe cardiac remodelling and dysfunction without any significant difference in plasma CLU levels. This is the first study to demonstrate that cardiac expression of CLU is induced in the LV of TAC mice during adverse cardiac remodelling. However, plasma CLU levels could not be used as biomarkers of TAC‐induced cardiac remodelling and dysfunction.

01 Dec 2024·Molecular Biology Reports

Cholesterol associated genetic risk score and acute coronary syndrome in Czech males

Article

Author: Kettner, Jiri ; Adamkova, Vera ; Mrázková, Jolana ; Lanska, Vera ; Pitha, Jan ; Kautzner, Josef ; Staněk, Vladimir ; Gebauerová, Marie ; Hubacek, Jaroslav A

AbstractBackgroundDespite a general decline in mean levels across populations, LDL-cholesterol levels remain a major risk factor for acute coronary syndrome (ACS). The APOB, LDL-R, CILP, and SORT-1 genes have been shown to contain variants that have significant effects on plasma cholesterol levels.Methods and resultsWe examined polymorphisms within these genes in 1191 controls and 929 patients with ACS. Only rs646776 within SORT-1 was significantly associated with a risk of ACS (P < 0.05, AA vs. + G comparison; OR 1.21; 95% CI 1.01–1.45). With regard to genetic risk score (GRS), the presence of at least 7 alleles associated with elevated cholesterol levels was connected with increased risk (P < 0.01) of ACS (OR 1.26; 95% CI 1.06–1.52). Neither total mortality nor CVD mortality in ACS subjects (follow up—9.84 ± 3.82 years) was associated with the SNPs analysed or cholesterol-associated GRS.ConclusionsWe conclude that, based on only a few potent SNPs known to affect plasma cholesterol, GRS has the potential to predict ACS risk, but not ACS associated mortality.

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CILP

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