STAT3-Ser/Hes3 Signaling: A New Molecular Component of the Neuroendocrine System?
The endocrine system involves communication among different tissues in distinct organs, includ- ing the pancreas and components of the Hypo- thalamic-Pituitary-Adrenal Axis. The molecular mechanisms underlying these complex interac- tions are a subject of intense study as they may hold clues for the progression and treatment of a variety of metabolic and degenerative diseases. A plethora of signaling pathways, activated by hor- mones and other endocrine factors have been implicated in this communication. Recent advances in the stem cell field introduce a new level of complexity: adult progenitor cells appear to utilize distinct signaling pathways than the more mature cells in the tissue they co-reside. It is therefore important to elucidate the signal transduction requirements of adult progenitor cells in addition to those of mature cells. Recent evidence suggests that a common non-canonical signaling pathway regulates adult progenitors in several different tissues, rendering it as a poten- tially valuable starting point to explore their biology. The STAT3-Ser/Hes3 Signaling Axis was first identified as a major regulator of neural stem cells and, subsequently, cancer stem cells. In the endocrine/neuroendocrine system, this path- way operates on several levels, regulating other types of plastic cells: (a) it regulates pancreatic islet cell function and insulin release; (b) insulin in turn activates the pathway in broadly distrib- uted neural progenitors and possibly also hypo- thalamic tanycytes, cells with important roles in the control of the adrenal gland; (c) adrenal pro- genitors themselves operate this pathway. The STAT3-Ser/Hes3 Signaling Axis therefore deserves additional research in the context of endocrinology.
P. Nikolakopoulou, S. W. Poser, J. Masjkur, M. Fernandez Rubin de Celis, L. Toutouna, C. L. Andoniadou, R. D. McKay, G. Chrousos, M. Ehrhart-Bornstein, S. R. Bornstein, A. Androutsellis-Theotokis.
Horm Metab Res. 2016 Jan 19. [Epub ahead of print]