Open AccessUltrastructure damage of oviduct telocytes in rat model of acute salpingitis
Author(s) -
Yang Jian,
Chi Chi,
Liu Zhen,
Yang Gang,
Shen ZongJi,
Yang XiaoJun
Publication year - 2015
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12548
Subject(s) - oviduct , biology , fibrosis , paracrine signalling , salpingitis , microbiology and biotechnology , stromal cell , inflammation , pathology , immunology , cancer research , endocrinology , anatomy , medicine , biochemistry , receptor
Acute salpingitis ( AS ) is an inflammatory disease which causes severe damage to a subset of classically described cells lining in oviduct wall and contributes to interstitial fibrosis and fertility problems. Telocytes ( TC s), a newly discovered peculiar type of stromal cells, have been identified in many organs, including oviduct, with proposed multiple potential bio‐functions. However, with recent increasing reports regarding TC s alterations in disease‐affected tissues, there is still lack of evidence about TC s involvement in AS ‐affected oviduct tissues and potential pathophysiological roles. We presently identified normal TC s by their characteristic ultrastructural features and immunophenotype. However, in AS ‐affected oviduct tissues, TC s displayed multiple ultrastructural damage both in cellular body and prolongations, with obvious loss of TC s and development of tissue fibrosis. Furthermore, TC s lose their interstitial 3‐D network connected by homocellular or heterocellular junctions between TC s and adjacent cells. And especially, TC s connected to the activated immunocytes (mononuclear cells, eosinophils) and affected local immune state (repression or activation). Meanwhile, massive neutrophils infiltration and overproduced Inducible Nitric Oxide Synthase (iNOS), COX ‐2, suggested mechanism of inflammatory‐induced TC s damage. Consequently, TC s damage might contribute to AS ‐induced structural and reproductive functional abnormalities of oviduct, probably via : ( i ) substances, energy and functional insufficiency, presumably, e.g . TC ‐specific genetic material profiles, ion channels, cytoskeletal elements, Tps dynamics, etc ., ( ii ) impaired TC s‐mediated multicellular signalling, such as homeostasis/angiogenesis, tissue repair/regeneration, neurotransmission, ( iii ) derangement of 3‐D network and impaired mechanical support for TC s‐mediated multicellular signals within the stromal compartment, consequently induced interstitial fibrosis, ( iv ) involvement in local inflammatory process/ immunoregulation and possibly immune‐mediated early pregnancy failure.