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.
Highlights
The transplantation of stem cells has been proposed as a novel approach for the treatment of patients with several diseases, including ischemic heart injury [1]
Various cells, including bone marrow derived as mononuclear cells, endothelial progenitor cells, mesenchymal stem cells (MSCs), and skeletal myoblasts, have been examined in ischemic heart models [1,2,3,4]
There are other cells that are recognized by the CD45− and CD34+ phenotypes, e.g., platelets and cells oferythroid lineage; the Endothelial progenitor cells (EPCs) can be differentiated by specific markers, such as CD31+
Summary
The transplantation of stem cells has been proposed as a novel approach for the treatment of patients with several diseases, including ischemic heart injury [1]. Various cells, including bone marrow derived as mononuclear cells, endothelial progenitor cells, mesenchymal stem cells (MSCs), and skeletal myoblasts, have been examined in ischemic heart models [1,2,3,4]. Endothelial progenitor cells (EPCs) of bone marrow have been proposed to have potential therapeutic applications for ischemic cardiovascular diseases [5,6,7,8]. Bone marrow-derived EPCs are known to circulate to neovascularization sites where they differentiate into endothelial cells and contribute to vasculogenesis [9,11,12] and the neovascularization of ischemic injuries [5,6,7,8]. There are other cells that are recognized by the CD45− and CD34+ phenotypes, e.g., platelets and cells oferythroid lineage; the EPCs can be differentiated by specific markers, such as CD31+
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
