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Clinical relevance of thyroid dysfunction in human haematopoiesis: biochemical and molecular studies

Miosz Piotr Kawa^1,, Katarzyna Grymua^1,, Edyta Paczkowska², Magdalena Bakiewicz-Masiuk², Elbieta Dbkowska², Monika Kozioek³, Maciej Tarnowski⁴, Patrycja Kos², Violetta Dziedziejko⁵, Magdalena Kucia⁴, Anhelli Syrenicz³ and Bogusaw Machaliski²

Departments of
¹ Physiology,
² General Pathology
³ Endocrinology, Arterial Hypertension, and Metabolic Diseases, Pomeranian Medical University, 72 Powstancow Wlkp Street, 70-111 Szczecin, Poland
⁴ Stem Cell Institute, University of Louisville, Louisville, 40202 Kentucky, USA
⁵ Department of Biochemistry and Chemistry, Pomeranian Medical University, 72 Powstancow Wlkp Street, 70-111 Szczecin, Poland

(Correspondence should be addressed to B Machaliski; Email: machalin{at}sci.pam.szczecin.pl)

(M P Kawa and K Grymua contributed equally to this work)

Objective: Abnormalities in haematological parameters have been noted in patients with thyroid diseases. Nevertheless, the exact mechanism of thyroid hormones' (THs) action on human haematopoiesis is still not entirely clear.

Design: The influence of THs through TH receptors (TR-1 and TRβ-1) on haematopoiesis in patients with hypo- and hyperthyroidism was analysed.

Methods: TR gene expression at the mRNA and protein levels in human CD34⁺-enriched haematopoietic progenitor cells (HPCs) obtained from the peripheral blood of patients with thyroid disorders and healthy volunteers was analysed. The cell populations were also investigated for clonogenic growth of granulocyte macrophage-colony forming units and erythrocyte-burst forming units (BFU-E). The level of apoptosis was determined by annexin V/propidium iodide staining and quantitative RT-PCR.

Results: The studies revealed that hypo- and hyperthyroidism modify TR gene expression in HPCs in vivo. TH deficiency resulted in a decrease in total blood counts and clonogenic potential of BFU-E. In contrast, hyperthyroid patients presented increased clonogenic growth and BFU-E number and significantly higher expressions of cell cycle-regulating genes such as those for PCNA and cyclin D1. Finally, an increase in the frequency of apoptotic CD34⁺-enriched HPCs in hypo- and hyperthyroidism with a modulation of apoptosis-related genes was detected.

Conclusions: The following conclusions were derived: i) TR expression in human haematopoietic cells depends on TH status, ii) both hypo- and hyperthyroidism significantly influence clonogenicity and induce apoptosis in CD34⁺-enriched HPCs and iii) the molecular mechanism by which THs influence haematopoiesis might provide a basis for designing novel therapeutic interventions in thyroid diseases.