Study of bone factor expression in murine model in the absence of pleiotrophin and its changes in the inflammatory situation

Pleiotrophin (PTN) is a peptide involved in the development and maintenance of bone tissue with important functions in inflammatory processes. However, the deletion of PTN in murine models does not produce a significant bone deterioration, but the mechanisms that compensate for its loss have not been studied to date. Our study was aimed at verifying how the deletion of PTN and acute inflammation affect the expression of bone factors. To this end, we used three-month-old female mice deficient for PTN (PTNKo) to which we induced acute inflammation by administration of lipopolysaccharide (LPS). Vertebrae and tibiae were isolated to measure gene expression and carry out an osteocyte count. In cell cultures, we checked whether PTN could protect MC3T3 (osteoblast) and MLOY4 (osteocyte) cells from the induction of cell death caused by etoposide. Our results show that the expression of osteocalcin is increased in the vertebrae of PTNKo mice, and that inflammation increased the expression of podhalanin (E11), connexin 43 (Cox43) and the parathormone-related peptide (PTHrP) in the PTNKo mice treated with LPS. Administering PTN significantly reduced etoposide-induced death in MC3T3 and MLOY4 cell cultures. Thus, PTN deficiency induced increased expression of OCN, and acute inflammation produced overexpression of E11, PTHrP, and Cox43 in PTNKo mice. PTN increased the viability of osteoblastic cells and osteocytes compared to etoposide treatment.