Delineating the hormonal signaling alterations that occur across lifespan and exploring possible remedial interventions could possibly help us improve the quality of life of the elderly and promote longevity.Īging and the quest for the ‘fountain of youth’ have intrigued the interest and the curiosity of scientific society throughout the history of mankind. As hypothalamic–pituitary unit is the central regulator of crucial body functions, these alterations can be translated in significant clinical sequelae that can impair the quality of life and promote frailty and disease. Specifically, alterations in hormonal networks and concomitant hormonal deficits/excess, augmented by poor sensitivity of tissues to their action, take place. Endocrine function undergoes major changes during aging, as well. The ability of an organism to adjust to these alterations, in conjunction with the dynamic effect of various environmental stimuli across lifespan, promotes longevity, frailty or disease. Defined as the gradual, time-dependent, heterogeneous decline of physiological functions, aging is orchestrated by a plethora of molecular mechanisms, which vividly interact to alter body homeostasis. | 17 Department of Endocrinology, Diabetes and Metabolism, ‘Red Cross Hospital’, Athens, GreeceĪging and its underlying pathophysiological background has always attracted the attention of the scientific society.| 16 Endocrine Unit, 2nd Department of Internal Medicine, Attikon University Hospital, Athens, Greece.| 15 Evangelismos Hospital, Athens, Greece.| 14 Second Department of Internal Medicine Propaedeutic, Research Institute and Diabetes Center, National and Kapodistrian University of Athens, Attikon University Hospital, Athens, Greece.Orsola-Malpighi Hospital of Bologna, Bologna, Italy | 12 Department of Internal Medicine, Mc Goven Medical School, The University of Texas, Houston, Texas, USA.| 11 Endocrine Division, Internal Medicine Department, University Hospital of Patras, Patras, Greece.| 10 2nd Department of Obstetrics and Gynecology, University of Athens, Aretaieio Hospital, Athens, Greece.| 9 Endocrine Department, Elena Venizelou Hospital, Athens, Greece.| 8 First Department of Pediatrics Medical School, Aghia Sophia Children’s Hospital, National and Kapodistrian University of Athens, Athens, Greece.| 7 First Department of Obstetrics & Gynecology, Medical School, Aristotle University of Thessaloniki, Unit of Reproductive Endocrinology, Thessaloniki, Greece.| 6 National Hellenic Research Foundation, Institute of Biology, Medicinal Chemistry and Biotechnology, Athens, Greece.| 5 Endocrine Clinic, Evgenidion Hospital, University of Athens, Athens, Greece.
Our results show that neuroendocrine cells derived from the neuroectoderm lack CD44 immunoreactivity. Furthermore, double immunolabeling for CD44 and a variety of peptide hormones was applied to characterize the different neuroendocrine cell types. Since little is known about the distribution of CD44 in non-neoplastic neuroendocrine cell types, we systematically investigated 42 samples of tissue from different organs, including the pituitary gland, thyroid, parathyroid, adrenal gland, lung, pancreas, stomach, duodenum, jejunum, ileum, appendix, and colon, immunohistochemically for the expression of CD44 standard and variant exon-encoded gene products (CD44v3, v4, v5, v6, v9). Isoforms of the transmembrane glycoprotein CD44, which are generated by alternative splicing of nine variant exons, have been implicated in tumor cell adhesion, invasion and metastatic spread and may be indicators of the degree of tumor differentiation.