Tranziens receptor potenciál ankyrin 1 és vanilloid 1 ioncsatornák, valamint a hipofízis adenilát-cikláz aktiváló polipeptid előfordulása és expressziós változásai endometriumban és emlőben
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The Transient Receptor Potential Ankyrin 1 (TRPA1) and Vanilloid 1 (TRPV1) are non-selective cation channels predominantly localized on capsaicin-sensitive peptidergic sensory neurons and mediate pain and inflammation. TRPV1 or „capsaicin receptor” is activated by noxious heat (>43°C), protons (pH>5.5), bradykinin, lipoxygenase products and anandamide produced during inflammation and tissue injury. TRPV1 is also expressed in the central nervous system (CNS) and on several non-neuronal cells in the skin, kidney, lung, testis, pancreas, spleen, cornea, and the uterus. TRPA1 is also activated by various chemical and physical stimuli, such as noxious cold (<17C°), allyl-isothiocyanate, cinnamaldehyde, as well as endogenous ligands like hydrogen peroxide, formaldehyde, methylglyoxal and acrolein produced during inflammation and tissue damage. The pathophysiological relevance of TRPA1 has been shown in inflammatory diseases of the respiratory, cardiovascular and gastrointestinal tracts. Similarly to TRPV1, functional TRPA1 was also described on enterochromaffin cells, synoviocytes, fibroblasts, melanocytes, pancreatic beta cells, epidermal keratinocytes, intestinal epithelial cells, and macrophages, as well as human endometrium cells besides sensory neurons. Although the physiological/pathophysiological relevance of non-neuronal TRP is unknown, a cross-talk has been proposed between non-neuronal and neuronal TRP channels. The expression of TRPV1 at protein level has been shown in the intact human endometrium at both neuronal and non-neuronal sites. Although the non-neuronal receptor expression was steady during the menstrual cycle, neuronal TRPV1 expression presumably has an estrogen-dependent regulation The consistent upregulation of TRPV1 in the peritoneal and endometrial tissues of women with chronic pelvic pain suggests its potential significance in various gynecological pain symptoms. Further research revealed increased TRPV1 expression at both neuronal and non-neuronal sites in the peritoneal endometriosis lesions and endometrioma. Despite these data on TRPV1 expression in the human endometrium and association with constant severe pelvic pain, there are no data about its expression in DIE. Furthermore, there is no information about TRPA1 expression in the human endometrium at all.