Late Embryonic and Postnatal Development of Interstitial Cells of Cajal in Mouse Esophagus: Distribution, Proliferation and Kit Dependence

Xiao, He; Yang, Wen-cui; Wen, X; Tang, Di; Xiao, Lan; Han, Juan; Yu, Bin; Zhang, Wei; Mei, Feng

doi:10.1159/000332381

Cited by 7 publications

(5 citation statements)

References 112 publications

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“…ICLCs were first described in the gastrointestinal tract by Santiago Ramón y Cajal in 1893 [14,15]. In the last century, several studies have found that ICLCs exist in the gut of both human beings and animals, and they have been detected in the esophagus, stomach, small intestine, large bowel, ileum, and colon [16][17][18]. More recently, studies have found that ICLCs are distributed in the gallbladder and extrahepatic biliary duct of both guinea-pigs and humans [18][19][20][21].…”

Section: Discussionmentioning

confidence: 99%

Effect of Neutrophils on Gallbladder Interstitial Cajal-Like Cells in Guinea Pig Model of Acute Cholecystitis

Huang

Qiu

Yang

et al. 2016

Cell Physiol Biochem

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Background: Acute cholecystitis is a common condition in gallbladder motility disorder. Interstitial Cajal-like cells (ICLCs) in the gallbladder are known as one of the players in the complex motility mechanisms affecting gallbladder motility. Aim: This study explored morphological symptoms and molecular mechanisms underlying gallbladder ICLC changes induced by acute cholecystitis. Materials and Methods: Fifteen adult guinea pigs were randomly divided into 3 groups: sham-operated group (healthy controls) and 2 experimental groups wherein these guinea pigs were subjected to common bile duct ligation to induce acute cholecystitis. Neutrophils were isolated from the peripheral blood of sham-operated animals and from the experimental animals at 24 and 48 h after surgery, and co-cultured with gallbladder ICLCs. The morphology of gallbladder ICLCs was examined by laser confocal immunofluorescence microscopy, TUNEL assay was used to detect apoptosis, and western blot and real-time PCR were performed to detect stem cell factor (SCF) and c-kit protein and mRNA expression, respectively. Results: No morphological differences in the gallbladder ICLCs were observed between single-culture and co-culture with healthy control neutrophil groups. However, the ICLCs in all co-culture groups with acute inflammation were impaired. In the co-culture groups, the rate of ICLC apoptosis was significantly higher than that in the single-culture group. SCF and c-kit protein and mRNA expression levels decreased in all co-culture groups as well. Conclusion: We demonstrated that the neutrophils are involved in gallbladder ICLC injury in acute cholecystitis cases and associated with gallbladder motility disorder.

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Section: Discussionmentioning

confidence: 99%

Effect of Neutrophils on Gallbladder Interstitial Cajal-Like Cells in Guinea Pig Model of Acute Cholecystitis

Huang

Qiu

Yang

et al. 2016

Cell Physiol Biochem

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“…It is known that Cajal cell proliferation persists throughout the postnatal period. KIT and Ki-67 signal are observed in the proliferation and development of this kind of cell [27]. Ki-67 protein is associated with cellular proliferation and it can be detected in the cell nucleus during the active phases of the cell cycle [28].…”

Section: Discussionmentioning

confidence: 99%

Concomitant Gastrointestinal Stromal Tumor of the Stomach and Gastric Adenocarcinoma in a Patient with Billroth 2 Resection

Sista

Abruzzese

Schietroma

et al. 2013

Case Reports in Surgery

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Background. With this study we focus on the etiopathogenesis and on the therapy of the simultaneous occurrence of Gastric gastrointestinal stromal tumor (gGIST) and adenocarcinoma of the stomach in a patient with Billroth II gastric resection (BIIGR). We report the first case of this event and a review of the literature. Methods. A 70-year-old man with a BIIGR, affected by adenocarcinoma of the stomach, was successfully treated with total gastrectomy. The histological examination showed a gastric adenocarcinoma with a synchronous GIST sized 2 cm and S-100, CD117, and CD34 positive. The mutation of PDGFR gene was detected. Discussion. This tumor is a rare mesenchymal neoplasm of the gastrointestinal tract. Few cases of synchronous gastric adenocarcinoma and GIST are observed in the literature and no case in patients with BIIGR. Various hypotheses have been proposed to explain this occurrence. It is frequently attributed to Metallothioneins genes mutations or embryological abnormalities, but this has not been proven yet. We suggest a hypothesis about the etiopathogenesis of this event in a BIIGR patient. Conclusion. GIST may occur synchronously with gastric adenocarcinoma. This simultaneous occurrence needs more studies to be proven. The study of Cajal cells' proliferation signalling is crucial to demonstrate our hypotesis.

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“…ANO1, also known as transmembrane member 16A, is a voltage-sensitive calcium chloride channel that is highly expressed in ICCs throughout the GI tract. However, ANO1 expression is downregulated along with Kit when ICCs are undergoing a phenotypic change [He et al, 2012]. CD44 has been identified as an ICC-specific cell-surface glycoprotein in the GI tract.…”

Section: Introductionmentioning

confidence: 99%

Identification of CD44 as a Cell-Surface Marker for Kit Negative Interstitial Cells of Cajal in Adult Mouse Colon

Han

Zhang

et al. 2020

Cells Tissues Organs

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Loss of Kit protein expression is proven to influence the plasticity of interstitial cells of Cajal (ICCs) and may contribute to gastrointestinal (GI) dysfunctions. The role and fate of Kit negative ICCs are unclear, and cell-specific markers for the Kit ICCs are unknown. In this study, we treated adult mice with imatinib (a Kit signaling blocker) for 8 or 16 days and investigated whether CD44 is a specific marker for the Kit negative ICCs in the adult mouse colon. We aimed at examining the protein and mRNA level of CD44 and Kit by using Western blot and real-time RT-PCR, respectively. Our results indicated that Kit expression was downregulated for both protein and mRNA levels after imatinib treatment for 8 or 16 days as compared to the vehicle-treated mice. Interestingly, CD44 expression remained unchanged throughout the treatment. Immunostaining on whole-mount preparations for Kit and CD44 showed that CD44 was exclusively co-localized with Kit in the ICCs of the vehicle-treated mouse colon. After imatinib treatment, a number of CD44+/Kit– cells with elaborated processes were observed with an evident decrease of Kit+ cell number within the muscular layers (ICC-IM) and around the myenteric nerve plexus (ICC-MY) as compared to vehicle-treated mice. After discontinuing imatinib for 16 days, Kit+ ICC-MY and ICC-IM were completely co-localized with normalization of CD44 and Kit+ cell numbers. Overall, our results identify CD44 as a cell-specific surface marker for Kit–ICCs and may be useful to understand the role and fate of Kit– ICCs in GI disorders.

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Late Embryonic and Postnatal Development of Interstitial Cells of Cajal in Mouse Esophagus: Distribution, Proliferation and Kit Dependence

Cited by 7 publications

References 112 publications

Effect of Neutrophils on Gallbladder Interstitial Cajal-Like Cells in Guinea Pig Model of Acute Cholecystitis

Effect of Neutrophils on Gallbladder Interstitial Cajal-Like Cells in Guinea Pig Model of Acute Cholecystitis

Concomitant Gastrointestinal Stromal Tumor of the Stomach and Gastric Adenocarcinoma in a Patient with Billroth 2 Resection

Identification of CD44 as a Cell-Surface Marker for Kit Negative Interstitial Cells of Cajal in Adult Mouse Colon

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