Association between Leukocyte Cell-Derived Chemotaxin 2 and Metabolic and Renal Diseases in a Geriatric Population: A Pilot Study

Author:

Kuzan Aleksandra1ORCID,Maksymowicz Krzysztof2,Królewicz Emilia1,Lindner-Pawłowicz Karolina3,Zatyka Piotr4,Wojnicz Piotr4,Nowaczyński Maciej4,Słomczyński Adam4,Sobieszczańska Małgorzata3ORCID

Affiliation:

1. Department of Medical Biochemistry, Wroclaw Medical University, 50-368 Wroclaw, Poland

2. Department of Forensic Medicine, Faculty of Medicine, Wroclaw Medical University, 50-345 Wroclaw, Poland

3. Clinical Department of Geriatrics, Wroclaw Medical University, 50-368 Wroclaw, Poland

4. Faculty of Medicine, Wroclaw Medical University, 50-367 Wroclaw, Poland

Abstract

LECT2 is not a routine diagnostic marker for any disease, but it has been associated with many pathologies, including systemic amyloidosis, rheumatoid arthritis, diabetes, atherosclerosis, and metabolic syndrome. With human aortic sections (n = 22) and sera from geriatric subjects (n = 79), we analyzed the relationships that could be observed between this protein and other parameters related to metabolic diseases. As a result, we observed a relatively high (r~0.8, p < 0.05) positive correlation between SRA and LECT2 and a negative correlation between EGFR and LECT2 (r~−0.4, p < 0.05). We observed LECT2 expression in macrophages, myocytes, and other aortic cells, with a tendency to be overexpressed in developed atherosclerotic plaques. We conclude that LECT2 exerts its chemotactic effects not only as a protein synthesized in the liver and secreted and circulating in the blood but also as a locally expressed protein within atherosclerotic plaque development. The LECT2-EGFR correlation suggests an association of this protein with loss of normal renal function. This fact can be associated with LECT2 amyloidosis, although it should be verified whether in the geriatric population there is indeed a widespread accumulation of LECT2 with the progression of aging or whether it is rather a marker of general deterioration of renal function.

Publisher

MDPI AG

Subject

General Medicine

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