A possible interaction o TIMP-1 and TSP-1 with familial mediterranean fever


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YILDIRIM M. E. , KÜÇÜK KURTULGAN H. , KILIÇGÜN H., BAKIR D., Ersan S.

JOURNAL OF CLINICAL AND ANALYTICAL MEDICINE, cilt.10, ss.104-108, 2019 (ESCI İndekslerine Giren Dergi) identifier

  • Cilt numarası: 10 Konu: 1
  • Basım Tarihi: 2019
  • Doi Numarası: 10.4328/jcam.5959
  • Dergi Adı: JOURNAL OF CLINICAL AND ANALYTICAL MEDICINE
  • Sayfa Sayıları: ss.104-108

Özet

Aim: Matrix metalloproteinases (MMPs) may influence many biological and pathological processes including inflammatory responses. Thrombospondins (TSP) are a glycoprotein group of the extracellular matrix. In this study, we aimed to investigate a possible association of TIMP-1 (an inhibitor of metalloproteinases) and TSP-1 (an adhesive protein involved in cell-matrix interactions) with familial Mediterranean fever. Material and Method: Thirty FMF patients who had compound heterozygous or homozygous MEFV mutations and thirty healthy controls were included in this study. The patients were selected after screening by reverse hybridization procedure. TIMP-1 and TSP-1 levels of the patients and controls were measured by ELIZA. Results: TIMP-1 and TSP-1 levels of the patients who had homozygous or compound heterozygous MEFV mutation were compared with 30 healthy controls. The levels of TIMP-1 in the patients were statistically higher than those in the control group (p < 0.001). There was no significant difference between the patients and controls in terms of TSP-1 levels (p = 0.84). Discussion: IL-1 beta has an important role in FMF disease and it may stimulate expression of TIMP-1. TIMP-1 levels are increased in FMF patients on the basis of inflammation and higher TIMP-1 levels in patients may be associated with the self-limited nature of FMF. TSP-1 level can be modulated by proinflammatory cytokines but there was no any significant difference between TSP-1 levels of FMF patients and the control group in our study. It can be thought that there is no interaction between TSP-1 and the pathogenesis of FMF.