We studied cell cultures isolated from the pulp of third molar germ of an adult human and from the skin of a human fetus on gestation day 10. Both cultures expressed similar repertoire of surface markers typical of multipotent mesenchymal cells (CD44, CD90, and CD105). Under in vitro conditions, dental pulp cells were more susceptible to factors inducing their differentiation into adipogenic, chondrogenic, and osteogenic lineage cells.
Preeclampsia (PE) is a multisystem pathologic state that clinically manifests
itself after the 20th week of pregnancy. It is characterized by high maternal
and perinatal morbidity and mortality. According to modern concepts, the
impairment of trophoblast invasion into maternal spiral arteries, leading to
the development of ischemia in placenta, is considered to be the major
pathogenetic factor of PE development. Ischemic lesions initiate the
development of a systemic inflammatory response (SIR) and endothelial
dysfunction, which is the main cause of the multiple organ failure in PE. Some
data has appear indicating the importance of a glycans-forming endothelial
glycocalyx and extracellular matrix (ECM) for placenta morphogenesis, as well
as their role in the regulation of vascular permeability and vascular tone in
hypertension disorders and, in particular, PE. Since intact glycocalyx and ECM
are considered to be the major factors that maintain the physiological vascular
tone and adequate intercellular interactions, their value in PE pathogenesis is
underestimated. This review is focused on hyaluronic acid (HA) as the key
glycan providing the organization and stabilization of the ECM and glycocalyx,
its distribution in tissues in the case of presence or absence of placental
pathology, as well as on the regulatory function of hyaluronic acids of various
molecular weights in different physiological and pathophysiological processes.
The summarized data will provide a better understanding of the PE pathogenesis,
with the main focus on glycopathology.
Today pre-eclampsia (PE) is considered as a disease of various theories; still all of them agree that endothelial dysfunction is the leading pathogenic factor. Endothelial dysfunction is a sequence of permanent immune activation, resulting in the change of both the phenotype and the functions of an endothelial cell and of the extracellular layer associated with the cell membrane—endothelial glycocalyx (eGC). Numerous studies demonstrate that eGC mediates and regulates the key functions of endothelial cells including regulation of vascular tone and thromboresistance; and these functions are disrupted during PE. Taking into account that eGC and its components undergo alterations under pathological conditions leading to endothelial activation, it is supposed that eGC plays a certain role in pathogenesis of PE. Envisaging the eGC damage as a key factor of PE, might be a new approach to prevention, treatment, and rehabilitation of patients with PE. This approach could include the development of drugs protecting eGC and promoting regeneration of this structure. Since the issue of PE is far from being solved, any effort in this direction might be valuable.
A new cell type, interstitial Cajal-like cell (ICLC), was recently described in different organs. The name was recently changed to telocytes (TCs), and their typical thin, long processes have been named telopodes (Tp). TCs regulate the contractile activity of smooth muscle cells and play a role in regulating vessel contractions. Although the placenta is not an innervated organ, we believe that TCs are present in the placenta. We studied placenta samples from physiological pregnancies and in different variants of preeclampsia (PE). We examined these samples using light microscopy of semi-thin sections, transmission electron microscopy, and immunohistochemistry. Immunohistochemical examination was performed with primary antibodies to CD34, CD117, SMA, and vimentin, and TMEM16a (DOG-1), the latter was used for the diagnosis of gastrointestinal stromal tumours (GIST) consisting of TCs. We have identified a heterogenetic population of ТСs in term placentas, as these cell types differed in their localization, immunophenotype and ultrastructural characteristics. We assume TMEM16a could be used as the marker for identification of TCs. In PE we have revealed telocyte-like cells with ultrastructural signs of fibrocytes (significant process thickening and the granular endoplasmic reticulum content was increased) and a loss of TMEM16a immunohistochemical staining.
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