Browsing by Subject "Interstitial cells of Cajal"

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    Distribution of interstitial cells of Cajal in Meriones unguiculatus and alterations in the development of incomplete intestinal obstruction
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2013) Bo, Wu; Li, Liu; Hengyu, Gao; Haimei, Sun; Hong, Xue; Xiaoshuang, Li; Guoquan, Zhang; Deshan, Zhou
    The interstitial cells of Cajal (ICCs) act as pacemaker cells that are involved in gastrointestinal (GI) motility disorders, although the pathogenesis of these disorders is still unclear. The GI tract of Mongolian gerbils shares similar anatomical features with that of humans, but no investigation of ICCs has been reported in the GI tracts of this animal. In the present study, we first observed the distribution and morphological features of ICCs in the Mongolian gerbil GI tract. The ICCs were mainly distributed within the smooth muscle layers (ICC-IM), the myenteric plexus (ICC-MY), the deep muscular plexus in the small intestine (ICC-DMP) and the submucosal surface of the circular muscle layer in the colon (ICC-SM). The density of the ICC-IM gradually decreased from the stomach to the colon, whereas the density of the ICC-MY gradually increased. Second, we compared differences in the ICCs between the control and obstructed intestines, and no significant difference was observed in the number of ICCs after 7 days of obstruction. However, the numbers were reduced by approximately day 14 of obstruction. The pattern of immunoreactivity also partly differed from that of the control group, i.e., a scattered and interrupted network of ICCs was often observed. Western blotting revealed that p-Kit and SCF were significantly reduced in the dilated intestines by day 14. Our results indicate that the Mongolian gerbil may be a good animal model for studying changes in ICCs that may contribute to the pathogenesis of GI motility disorders.
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    Ultrastructural changes of the human enteric nervous system and interstitial cells of Cajal in diverticular disease.
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2020) Alaburda, Paulius; Lukosiene, Jaune I.; Pauza, Audrys G.; Kyguoliene, Kristina Rysevaite; Kupcinskas, Juozas; Saladzinskas, Zilvinas; Pauziene, Neringa
    Background. In spite of numerous advances in understanding diverticular disease, its pathogenesis remains one of the main problems to be solved. We aimed to investigate the ultrastructural changes of the enteric nervous system in unaffected individuals, in asymptomatic patients with diverticulosis and in patients with diverticular disease. Methods. Transmission electron microscopy was used to analyse samples of the myenteric, outer submucosal and inner submucosal plexuses from patients without diverticula (n=9), asymptomatic patients with diverticulosis (n=7) and in patients with complicated diverticular disease (n=9). We described the structure of ganglia, interstitial cells of Cajal and enteric nerves, as well as their relationship with each other. The distribution and size of nerve processes were analysed quantitatively. Results. In complicated diverticular disease, neurons exhibited larger lipofuscin-like inclusions, their membranous organelles had larger cisterns and the nucleus showed deeper indentations. Nerve remodeling occurred in every plexus, characterised by an increased percentage of swollen and fine neurites. Interstitial cells of Cajal had looser contacts with the surrounding cells and showed cytoplasmic depletion and proliferation of the rough endoplasmic reticulum. In asymptomatic patients with diverticulosis, alterations of enteric nerves and ICC were less pronounced. Conclusions. In conclusion, the present findings suggest that most ultrastructural changes of the enteric nervous system occur in complicated diverticular disease. The changes are compatible with damage to the enteric nervous system and reactive remodeling of enteric ganglia, nerves and interstitial cells of Cajal. Disrupted architecture of enteric plexuses might explain clinical and pathophysiological changes associated with diverticular disease