Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice after hyperoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- after hyperoxia treatment from P0-P3. For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.
Project description:Our previous data obtained by using immunohistochemistry showed, that Fgf10+/- (50% Fgf10 expression compared to WT) in hyperoxic condition at postnatal day 3 (P3) compared to WT has less vessel count in the lung and less muscularization of small capillaries in the lung. Furthermore, Fgf10+/- showed a drastic increase in mortality upon hyperoxic lung injury. Main question to be answer by this experiment is as followed: Does Fgf10+/- mice after hyperoxia from P0-P3 show different expression profiles at P3 compared to WT? To adress this question we harvest lungs at P3 from WT and Fgf10+/- after hyperoxia treatment from P0-P3. For this the mice were sacrificed by Ketamin/ Dormitor ip, lungs were perfused transcardiac with PBS and directly frozen in liquid nitrogen.
Project description:miR154-3p and -5p are mainly expressed in the lung epithelium pre- and postnatally in mice and are significantly higher expressed upon hyperoxia (BPD mouse model). In normoxia in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to increased Fgf10 signaling and Tgf- signaling. Furthermore, avleolar morphometry revealed increased MLI indicating interference with alveologenesis at P16. In hyperoxia (P0-P8) in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to decreased Fgf10 signaling and Tgf- signaling.
Project description:The aim of the study was to investigate whether the trefoil peptide genes, in concerted action with a miRNA regulatory network, were contributing to nutritional maintrenance. Using a Tff3 knock-out mouse model, 21 specific miRNAs were noted to be significantly deregulated when compared to the wild type strain. n = 6 mus musculus wild type samples and n = 6 knock-down experiments have been screened for a currently known mus musculus miRNAs and validated by TaqMan
Project description:The aim of the study was to investigate whether the trefoil peptide genes, in concerted action with a miRNA regulatory network, were contributing to nutritional maintrenance. Using a Tff2 knock-out mouse model, 48 specific miRNAs were noted to be significantly deregulated when compared to the wild type strain. n = 6 mus musculus wild type samples and n = 6 knock-down experiments have been screened for a currently known mus musculus miRNAs and validated by TaqMan