Hedgehog signaling activation induces stem cell proliferation and hormone release in the adult pituitary gland.
نویسندگان
چکیده
Hedgehog (HH) signaling is known to be essential during the embryonal development of the pituitary gland but the knowledge about its role in the adult pituitary and in associated tumors is sparse. In this report we investigated the effect of excess Hh signaling activation in murine pituitary explants and analyzed the HH signaling status of human adenopituitary lobes and a large cohort of pituitary adenomas. Our data show that excess Hh signaling led to increased proliferation of Sox2(+) and Sox9(+) adult pituitary stem cells and to elevated expression levels of adrenocorticotropic hormone (Acth), growth hormone (Gh) and prolactin (Prl) in the adult gland. Inhibition of the pathway by cyclopamine reversed these effects indicating that active Hh signaling positively regulates proliferative processes of adult pituitary stem cells and hormone production in the anterior pituitary. Since hormone producing cells of the adenohypophysis as well as ACTH-, GH- and PRL-immunopositive adenomas express SHH and its target GLI1, we furthermore propose that excess HH signaling is involved in the development/maintenance of hormone-producing pituitary adenomas. These findings advance the understanding of physiological hormone regulation and may open new treatment options for pituitary tumors.
منابع مشابه
Pituitary stem cells: review of the literature and current understanding.
BACKGROUND The existence of pituitary stem cells in the adult pituitary gland is supported by such findings as postnatal proliferation, differentiation based on environmental alterations, and development of hormone-producing cells after specific lesions in the pituitary. OBJECTIVE We discuss which cells in the adult pituitary gland might play a role as pituitary stem cells, the potential for ...
متن کاملFgf3 signaling from the ventral diencephalon is required for early specification and subsequent survival of the zebrafish adenohypophysis.
The pituitary gland consists of two major parts: the neurohypophysis, which is of neural origin; and the adenohypophysis, which is of non-neural ectodermal origin. Development of the adenohypophysis is governed by signaling proteins from the infundibulum, a ventral structure of the diencephalon that gives rise to the neurohypophysis. In mouse, the fibroblast growth factors Fgf8, Fgf10 and Fgf18...
متن کاملInteraction of PACAP with Sonic hedgehog reveals complex regulation of the hedgehog pathway by PKA.
Sonic hedgehog (Shh) signaling is essential for proliferation of cerebellar granule cell progenitors (cGCPs) and its aberrant activation causes a cerebellar cancer medulloblastoma. Pituitary adenylate cyclase activating polypeptide (PACAP) inhibits Shh-driven proliferation of cGCPs and acts as tumor suppressor in murine medulloblastoma. We show that PACAP blocks canonical Shh signaling by a mec...
متن کاملInvestigating the role of signaling pathways and cancer stem cells in esophageal cancer with a therapeutic approach
Esophageal cancer (EC) is the sixth main cause of cancer death worldwide. Important genes associated with esophageal cancer include FOXO3, AKT, and GSK3β. Excessive FOXO3 expression inhibits the proliferation of cancer cells. The expression of AKT is involved in controlling cell growth in tumors. GSK3β activity is higher in cancer tissues. Given the effective role of cancer stem cells (CSCs) in...
متن کاملNotch signaling in stomach epithelial stem cell homeostasis
The mammalian adult gastric epithelium self-renews continually through the activity of stem cells located in the isthmus of individual gland units. Mechanisms facilitating stomach stem and progenitor cell homeostasis are unknown. Here, we show that Notch signaling occurs in the mouse stomach epithelium during development and becomes restricted mainly to the isthmus in adult glands, akin to its ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Scientific reports
دوره 6 شماره
صفحات -
تاریخ انتشار 2016