Ultrastructural changes in the interstitial cells of Cajal and gastric dysrhythmias in mice lacking full‐length dystrophin (<i>mdx</i> mice)

Vannucchi, Maria Giuliana; Zizzo, Maria Grazia; Zardo, Claudio; Pieri, Laura; Serio, Rosa; Mulè, Flavia; Faussone–Pellegrini, Maria Simonetta

doi:10.1002/jcp.10470

Cited by 21 publications

(38 citation statements)

References 57 publications

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“…Interestingly, a functional impairment and altered ultrastructural features were found for all gastric ICC populations [40]. ICC-DMP were seen to maintain an intense NK1r-IR (personal observation), but whether NK1r-IR is present or absent on the other ICC sub-types of these animals is not known.…”

Section: Muscular Dystrophy (Mdx Mice)mentioning

confidence: 97%

“…The ICC-MP, which are distributed throughout the entire gut, and the colonic ICC-SMP are responsible for pacemaker activity [9,38,40]. The presence of nerve endings close to ICC-MP has been interpreted as a neural control of the slow-wave activity [41].…”

Section: Roles Of the Icc Sub-typesmentioning

confidence: 99%

“…ICC-IM, which show a large number of nerve ending contacts, have been proposed to be intermediaries in neurotransmission [9, 30-32, 35, 39, 42-47]. Functional investigations performed on the stomach of mutant mouse strains lacking one or more ICC sub-types and of dystrophic mice (mdx mice) showed that the ICC-SEP generate the secondary regenerative component of slow waves [40,[48][49][50][51]. ICC-DMP have been suggested to be involved in mediation of NO-dependent neurotransmission [52] and were also seen to produce slow waves, which, however, are of a different character from those produced by the ICC-MP [53].…”

Section: Roles Of the Icc Sub-typesmentioning

confidence: 99%

“…In a mouse strain used to study muscular dystrophy, the mdx mice, ICC do not express dystrophin, a molecule usually present on their plasma membrane in normal animals [91], but still express c-kit [40]. Interestingly, a functional impairment and altered ultrastructural features were found for all gastric ICC populations [40].…”

Section: Muscular Dystrophy (Mdx Mice)mentioning

confidence: 99%

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Relationships between neurokinin receptor‐expressing interstitial cells of Cajal and tachykininergic nerves in the gut

Faussone–Pellegrini

2006

J Cellular Molecular Medi

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The so-called interstitial cells of Cajal (ICC) are distributed throughout the muscle coat of the alimentary tract with characteristic intramural location and species-variations in structure and staining. Several ICC sub-types have been identified: ICC-DMP, ICC-MP, ICC-IM, ICC-SM. Gut motility is regulated by ICC and each sub-type is responsible for the electrical activities typical of each gut region and/or muscle layer. The interstitial position of the ICC between nerve endings and smooth muscle cells has been extensively considered. Some of these nerve endings contain tachykinins. Three distinct tachykinin receptors (NK1r, NK2r and NK3r) have been demonstrated by molecular biology. Each of them binds with different affinities to a series of tachykinins (SP, NKA and NKB). In the ileum, SP-immunoreactive (SP-IR) nerve fibers form a rich plexus at the deep muscular plexus (DMP), distributed around SP-negative cells, and ICC-DMP intensely express the SP-preferred receptor NK1r; conversely a faint NK1r-IR is detected on the ICC-MP and mainly after receptor internalization was induced by agonists. ICC-IM are never stained in laboratory mammals, while those of the human antrum are NK1r-IR. RT-PCR conducted on isolated ileal ICC-MP and gastric ICC-IM showed that these cells express NK1r and NK3r. Colonic ICC, except those in humans, do not express NK1r-IR, at least in resting conditions. Outside the gut, NK1r-IR cells were seen in the arterial wall and exocrine pancreas. In the mouse gut only, NK1r-IR is present in non-neuronal cells located within the intestinal villi, so-called myoid cells, which are c-kit-negative and α-smooth muscle actin-positive. Immunohistochemistry and functional studies confirmed that ICC receive input from SP-IR terminals, with differences between ICC sub-types. In the rat, very early after birth, NK1r is expressed by the ICC-DMP and SP by the related nerve varicosities. Studies on pathological conditions are few and those on mutant strains practically absent. It has only been reported that in the inflamed ileum of rats the NK1r-IR ICC-DMP disappear and that at the peak of inflammatory conditions ICC-MP are NK1r-IR. In the ileum of mice with a mutation in the W locus, ICC-DMP were seen to express c-kit-IR but not NK1-IR, and SP-IR innervation seems unchanged. In summary, there are distinct ICC populations, each of them under a different tachykininergic control and, likely, having different functions. Further studies are recommended at the aim of understanding ICC involvement in modulating/transmitting tachykininergic inputs.

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Section: Muscular Dystrophy (Mdx Mice)mentioning

confidence: 97%

Section: Roles Of the Icc Sub-typesmentioning

confidence: 99%

Section: Roles Of the Icc Sub-typesmentioning

confidence: 99%

Section: Muscular Dystrophy (Mdx Mice)mentioning

confidence: 99%

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Relationships between neurokinin receptor‐expressing interstitial cells of Cajal and tachykininergic nerves in the gut

Faussone–Pellegrini

2006

J Cellular Molecular Medi

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“…Interstitial cells of Cajal are localised between the two muscular layers of the gastrointestinal tract and are involved in the regulation of peristaltic movements [10]. Primary cilia were observed on the surface of the interstitial cells of Cajal in the rabbit [11], rat duodenum [12] and mouse stomach [13]. The presence of primary cilia in 4 patients with human gastric GIST cells has been already observed in a ultrastructure study [14].…”

mentioning

confidence: 93%

Primary cilia in gastrointestinal stromal tumors

Dvořák¹,

Sitorová²,

Nikolov³

et al. 2014

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The primary cilium is a solitary, sensory, non-motile microtubule-based structure that arises from the centrosome and is projected from the surface of most human cells. The objective of the current pilot study was to conduct an investigation of presence and frequency of cilia in gastrointestinal stromal tumors (GIST).The presence of primary cilia in GIST was evaluated in 9 patients, including 8 primary tumors and 1 liver metastasis. In 2 patients the presence of primary cilia was evaluated not only in the primary tumor, but also in recurrence: in 1 patient in recurrence without previous treatment with imatinib and in 1 patient in recurrence after treatment with imatinib. The primary cilia of GIST cells were immunofluorescently stained with primary monoclonal anti-acetylated tubulin alpha antibody and cell nuclei with DAPI.We observed 9985 nuclei of cells of GISTs and 425 primary cilia in total. The median of frequency of primary cilia in cells of GISTs in all examined samples was 4.26%, in primary tumors was 4.32% and in metastases was 3.64%, respectively.This pilot study provides the evidence of the presence of primary cilia in GISTs in different organs. Primary cilia were identified in all examined cases of GIST, including primary tumors, metastases and recurrent lesions without and with previous treatment with imatinib.

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Actin Microfilament Involved in Regulation of Pacemaking Activity in Cultured Interstitial Cells of Cajal from Murine Intestine

et al. 2010

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The present study investigated the effect of actin microfilament structure on pacemaker currents and calcium oscillation in cultured murine intestinal interstitial cells of Cajal (ICCs) by whole-cell patch-clamp technique and calcium imaging technique. Cytochalasin B, a disruptor of actin microfilaments, decreased the amplitude and frequency of pacemaker currents from 491.32 +/- 160.33 pA and 11.73 +/- 0.79 cycles/min to 233.12 +/- 92.00 pA and 10.29 +/- 0.76 cycles/min. Cytochalasin B also decreased the amplitude and frequency of calcium oscillation from 0.32 +/- 0.08 (DeltaF/F0) and 2.75 +/- 0.17 cycles/min to 0.02 +/- 0.01 (DeltaF/F0) and 1.20 +/- 0.08 cycles/min. Phalloidin, a stabilizer of actin microfilaments, increased the amplitude and frequency of pacemaker currents from 751.79 +/- 282.82 pA and 13.93 +/- 1.00 cycles/min to 1234.34 +/- 607.83 pA and 14.68 +/- 1.00 cycles/min. Phalloidin also increased the amplitude and frequency of calcium oscillation from 0.26 +/- 0.01 (DeltaF/F0) and 2.27 +/- 0.18 cycles/min to 0.43 +/- 0.03 (DeltaF/F0) and 2.87 +/- 0.07 cycles/min. 2-Aminoethoxydiphenyl borane (2-APB), an IP(3) receptor blocker, suppressed both pacemaker currents and calcium oscillations. 2-APB also blocked the phalloidin-induced increase in pacemaker currents and calcium oscillation. Ryanodine, an inhibitor of calcium-induced calcium release, did not affect pacemaker current but suppressed calcium oscillations. Ryanodine had no effect on altering phalloidin-induced increases in pacemaker current and calcium oscillation. These results suggest that actin microfilaments regulate pacemaker activity via the IP(3)-induced calcium release signaling pathway.

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Ultrastructural changes in the interstitial cells of Cajal and gastric dysrhythmias in mice lacking full‐length dystrophin (mdx mice)

Cited by 21 publications

References 57 publications

Relationships between neurokinin receptor‐expressing interstitial cells of Cajal and tachykininergic nerves in the gut

Relationships between neurokinin receptor‐expressing interstitial cells of Cajal and tachykininergic nerves in the gut

Primary cilia in gastrointestinal stromal tumors

Actin Microfilament Involved in Regulation of Pacemaking Activity in Cultured Interstitial Cells of Cajal from Murine Intestine

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