Within‐day variation and influence of physical exercise on circulating Galectin‐3 in patients with rheumatoid arthritis and healthy individuals

Abstract

Galectin‐3 has been suggested as a pro‐inflammatory mediator in rheumatoid arthritis (RA). Previous studies have reported overexpression of Galectin‐3 in RA synovitis and increased levels in synovial fluid and serum in long‐standing RA compared with osteoarthritis and healthy controls. Our objectives were to study whether serum Galectin‐3 (1) exhibits circadian variation and/or (2) responds to exercise in RA and controls. The study on circadian patterns (1) comprised eleven patients with newly diagnosed RA, disease duration less than 6 months (ERA), 10 patients with long‐standing RA [5–15 years (LRA)] and 16 self‐reportedly healthy control subjects. During 24 h, 7 blood samples were drawn at 3‐h intervals starting at 10 a.m. through 10 p.m. and at 7 and 10 a.m. on the following day. The study on the effect of physical activity (2) included 10 patients with ERA, 10 with LRA and 14 controls. The participants underwent a standardized exercise programme and four blood samples were drawn before, during and after exercise. Serum Galectin‐3 was quantified by ELISA (R&D systems). (1) Galectin‐3 was increased at baseline in both RA subsets (P = 0.08). There were no diurnal oscillations (P = 0.85). Day‐to‐day variation amounted to 3%. (2) Baseline Galectin‐3 was increased in LRA versus controls and ERA (P < 0.01 and 0.05). Physical exercise induced 10–15% Galectin‐3 increments in RA and controls (P < 0.001) peaking after 1–3 h. To conclude, Galectin‐3 did not exhibit circadian variation. Day‐to‐day variation was 3%. Exercise elicited comparable increments in patients with RA of short and long duration and controls, approaching normal after 1–3 h.

Galectin-3 and Cardiovascular Biomarkers Reflect Adaptation Response to Scuba Diving

“…It could be ascribed to the release from cardiomyocytes due to the increased permeability, but also to the secretion from resident macrophages due to their activation. The observed Gal-3 increase immediately after diving is in agreement with the previous studies, which described Gal-3 increase 1 and 3 h after the exercise and the decrease to the baseline 24 h after half-marathon [25,34,35]. However, these studies cannot be fully compared with this research since immersion and elevated pressure additionally contributes myocardial stretching and changes preload and afterload [36].…”

“…Recently, Gal-3 has been shown as a helpful tool for better management of heart dysfunction [16], because its plasma level is strongly associated with changes in left ventricular structure and function. Its level also increases after different forms of physical activity [17][18][19], but there is no data on the effect of SCUBA diving on Gal-3 plasma concentration.…”

Galectin-3 as a novel biomarker for disease diagnosis and a target for therapy (Review)

“…Furthermore, galectin-3 is a stable biomarker and is not associated with age, body mass index or sex ( 19 , 20 ). Furthermore, galectin-3 does not exhibit circadian variation and increases marginally following exercise, returning to normal levels after 1–3 h ( 21 ). Therefore, galectin-3 may be used in the diagnosis and prognosis of various types of disease, and therefore may also serve as a therapeutic target for treating disease.…”

Prognostic value of plasma galectin‐3 levels after aneurysmal subarachnoid hemorrhage

“…It is involved in cell adhesion, proliferation, clearance, apoptosis, cell activation, cell migration, and phagocytosis (Argüeso, Mauris, & Uchino, ; Chen, Hou, Zhang, Chen, & He, ; Li, Li, & Gao, ; de Oliveira et al., ). Gla‐3 was recently identified as a proinflammatory protein and correlated with the occurrence and progression of cancer, systemic lupus erythematosus, rheumatoid arthritis, chronic heart failure, and systemic sclerosis (Issa et al., ; Koca et al., ; Nielsen et al., ; Piper, de Courcey, Sherwood, Amin‐Youssef, & McDonagh, ; Zeinali, Adelinik, Papian, Khorramdelazad, & Abedinzadeh, ). Interestingly, activated glia can express Gal‐3 (Jaquenod De Giusti et al., ); moreover, Gal‐3 is required for resident microglia activation and proliferation in response to ischemic injury (Lalancette‐Hébert et al., ).…”