Abstract
ABSTRACT The objective was to evaluate the in vitro effect of prolactin in osteogenic potential of adipose tissue-derived mesenchymal stem cells (ADSCs) in female rats. ADSCs were cultured in osteogenic medium with and without the addition of prolactin and distributed into three groups: 1) ADSCs (control), 2) ADSCs with addition of 100ng/mL of prolactin and 3) ADSCs with addition of 300ng/mL of prolactin. At 21 days of differentiation, the tests of MTT conversion into formazan crystals, percentage of mineralized nodules and cells per field and quantification of genic transcript for alkaline phosphatase, osteopontin, osteocalcin, bone sialoprotein, BMP-2 and collagen I by real-time RT-PCR were made. The addition of prolactin reduced the conversion of MTT in group 3 and increased the percentage of cells per field in the groups 2 and 3, however without significantly increasing the percentage of mineralized nodules and the expression of alkaline phosphatase, osteopontin, osteocalcin, bone sialoprotein, BMP-2 and collagen I. In conclusion, the addition of prolactin in concentrations of 100ng/mL and 300ng/mL does not change the osteogenic differentiation to the ADSCs of female rats despite increase in the cellularity of the culture.
Highlights
The physiological hyperprolactinemia that occurs during pregnancy and lactation has been associated to bone loss in women and animals
The objective of this study was to evaluate, under the osteogenic differentiation of ADSCs, two concentrations of prolactin that mimic the ones found in the blood of pregnant and lactanting female rats in order to infer on the isolated involvement of this hormone in the ADSCs
The cells extracted from the adipose tissue showed phenotypic characteristics compatible with mesenchymal stem cells, i.e. 90.26% of cells presented expression for CD90, 99.24% of cells presented expression for CD73, 91.90% of cells presented for CD54 expression and only 3.04% of cells presented for CD45 expression
Summary
The physiological hyperprolactinemia that occurs during pregnancy and lactation has been associated to bone loss in women and animals Some researchers demonstrate that the bone loss due to increased bone reabsorption, arising from hypersecretion of prolactin, is mediated by estrogen deficiency (Biller et al, 1992; Naliato et al, 2005). This assertion has already been refuted since women with hyperprolactinemia do not present improvement of bone changes after restoration of gonadal endocrine function (Klibanski et al, 1988; Schlechte et al, 1992). As the osteoblasts are originated from mesenchymal stem cells (MSC), the reduction of its number in the bones of female rats in lactation fosters the hypothesis of this study that the osteopenia, originated from the excess of prolactin, could be result of its effect on the osteogenic differentiation of mesenchymal stem cells
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