Bone Marrow-Derived Stem Cell Populations Are Differentially Regulated by Thyroid or/and Ovarian Hormone Loss

Abstract

Bone marrow-derived stem cells (BMDSCs) play an essential role in organ repair and regeneration. The molecular mechanisms by which hormones control BMDSCs proliferation and differentiation are unclear. Our aim in this study was to investigate how a lack of ovarian or/and thyroid hormones affects stem cell number in bone marrow lineage. To examine the effect of thyroid or/and ovarian hormones on the proliferative activity of BMDSCs, we removed the thyroid or/and the ovaries of adult female rats. An absence of ovarian and thyroid hormones was confirmed by Pap staining and Thyroid Stimulating Hormone (TSH) measurement, respectively. To obtain the stem cells from the bone marrow, we punctured the iliac crest, and aspirated and isolated cells by using a density gradient. Specific markers were used by cytometry to identify the different BMDSCs types: endothelial progenitor cells (EPCs), precursor B cells/pro-B cells, and mesenchymal stem cells (MSCs). Interestingly, our results showed that hypothyroidism caused a significant increase in the percentage of EPCs, whereas a lack of ovarian hormones significantly increased the precursor B cells/pro-B cells. Moreover, the removal of both glands led to increased MSCs. In conclusion, both ovarian and thyroid hormones appear to have key and diverse roles in regulating the proliferation of cells populations of the bone marrow.

Influence of height on endothelial maintenance activity: a narrative review

“…In addition, thyroid hormones are also known to be associated with growth rate [ 108 ]. Thyroid hormones regulate bone marrow-derived hematopoietic stem cells [ 109 ]. In our previous study, the absence of thyroid cysts was shown to be associated with latent thyroid damage [ 110 – 112 ].…”

Bone-Marrow Stem Cells and Acellular Human Amniotic Membrane in a Rat Model of Heart Failure

“…The animals were again anesthetized (50 mg/kg Ketamine and 10 mg/kg Xylazine) and subjected to median transsternal sternotomy. The BMSC group received 5 × 10 6 mononuclear stem cells injected in multiple sites directly on the infarcted area and transition zone, as previously described [ 27 ], and the hAM group received a patch of hAM, measuring approximately 2 cm × 3 cm, on the anterior left ventricle surface; this patch was sutured with 7-0 polypropylene over the ischemic area identified under direct visualization. The control group received only saline solution by transsternal sternotomy.…”

The Role of Endothelial Progenitor Cells in Atherosclerosis and Impact of Anti-Lipemic Treatments on Endothelial Repair

“…The entire process of vascular repair mediated through EPCs consists of several distinct events like progenitor cell mobilization from their organ of origin, circulation in the blood stream, harbouring at the place of damaged endothelium (“homing”) and finally, further differentiation and cell maturation [ 10 ]. Different substances are involved in the mobilization of progenitor cells from their place of origin into the blood stream, like NO, but also growth factors and cytokines, including vascular endothelial growth factor (VEGF), stromal-cell-derived factor-1α (SDF-1α), impaired glucose metabolism, erythropoietin, thyroid hormones and estrogens [ 44 , 45 , 46 ]. Once in the blood stream, EPCs migrate towards damaged endothelial regions where they adhere to the damaged vessel surface.…”

“…The concentration of SDF-1α is upregulated in the damaged endothelium due to tissue hypoxia. SDF-1α interacts with CX chemokine receptor 4 (CXCR4) on the endothelial surface [ 46 ]. After being embedded in the injured endothelium, progenitor cells proliferate and maturate and thus physically replace damaged mature endothelial cells.…”