Maria Venihaki, PhD
School of Medicine
University of Crete
The communication between the nervous, endocrine, and immune systems is required for the control of the immune/inflammatory response and is achieved via their common ligands and receptors. The hypothalamic-pituitary adrenal (HPA) axis is the major endocrine axis mediating the stress response, including immune-inflammatory processes. Wound healing, a process tightly related to inflammation, is a highly coordinated, dynamic, and interactive progression that results in the restoration of the functional integrity of the wounded tissue. Based on the above, the research interests of our team are to investigate the effects of hormones of the HPA axis as well as the role of other neuropeptides and stem cells on the process of wound healing and tissue repair and on the signaling pathways mediating their effects in these processes. Furthermore, we have recently started to investigate the role of the above mentioned neuropeptides on the inflammatory pain, a very common clinical problem.
1. A novel role of peripheral corticotropin-releasing hormone (CRH) on dermal fibroblasts. Rassouli O, Liapakis G, Lazaridis I, Sakellaris G, Gkountelias K, Gravanis A, Margioris AN, Karalis KP, Venihaki M. PLoS One. 2011; 6(7):e21654.
2. Members of CRF family and their receptors: from past to future. Liapakis G, Venihaki M, Margioris A, Grigoriadis D, Gkountelias K. Curr Med Chem. 2011;18(17):2583-600.
3. Urocortin III, a brain neuropeptide of the corticotropin-releasing hormone family: modulation by stress and attenuation of some anxiety-like behaviours. Venihaki M, Sakihara S, Subramanian S, Dikkes P, Weninger SC, Liapakis G, Graf T, Majzoub JA.J Neuroendocrinol. 2004 May;16(5):411-22.
4. NF-kappaB participates in the corticotropin-releasing, hormone-induced regulation of the pituitary proopiomelanocortin gene. Karalis KP, Venihaki M*, Zhao J*, vanVlerken LE, Chandras C. equally contributed authors. J Biol Chem. 2004, 279(12):10837-40.
5. Corticotropin-releasing hormone deficiency results in impaired splenocyte response to lipopolysaccharide. Venihaki M, Zhao J, and Karalis KP. J Neuroimmunol. 2003, 141(1-2): 3-9.