Significance of Stat3 Signaling in Epithelial Cell Differentiation of Fetal Mouse Lungs.

Significance of Stat3 Signaling in Epithelial Cell Differentiation of Fetal Mouse Lungs. Acta Histochem Cytochem. 2017 Feb 28;50(1):1-9 Authors: Kameyama H, Kudoh S, Hatakeyama J, Matuo A, Ito T Abstract To study the significance of signal transducer and activator of transcription (Stat) 3 in lung epithelial development of fetal mice, we examined fetal mouse lungs, focusing on the expression of Clara cell secretory protein (CCSP), Forkhead box protein J1 (Foxj1), calcitonin gene-related peptide (CGRP), phosphorylated Stat3 (Tyr705), and hairy/enhancer of split (Hes) 1, and observed cultured fetal lungs upon treatment with IL-6, a Stat3 activator, or cucurbitacin I, a Stat3 inhibitor. Moreover, the interaction of Stat3 signaling and Hes1 was studied using Hes1 gene-deficient mice. Phosphorylated Stat3 was detected in fetal lungs and, immunohistochemically, phosphorylated Stat3 was found to be co-localized in developing Clara cells, but not in ciliated cells. In the organ culture studies, upon treatment with IL-6, quantitative RT-PCR revealed that CCSP mRNA increased with increasing Stat3 phosphorylation, while cucurbitacin I decreased Hes1, CCSP, Foxj1 and CGRP mRNAs with decreasing Stat3 phosphorylation. In the lungs of Hes1 gene-deficient mice, Stat3 phosphorylation was not markedly different from wild-type mice, the expression of CCSP and CGRP was enhanced, and the treatment of IL-6 or cucurbitacin I induced similar effects on mous...
Source: Acta Histochemica et Cytochemica - Category: Biochemistry Authors: Tags: Acta Histochem Cytochem Source Type: research
More News: Biochemistry | Genetics | Study