Bone Marrow Derived Kit-positive Cells Colonize the Gut but Fail to Restore Pacemaker Function in Intestines Lacking Interstitial Cells of Cajal

McCann, Conor J.; Hwang, Sung-Jin; Hennig, Grant W.; Ward, Sean M.; Sanders, Kenton M.

doi:10.5056/jnm14026

Cited by 8 publications

(7 citation statements)

References 48 publications

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“…Similar findings were also reported along with improved gastric emptying in W/W v mutant mice [ 108 ]. However, McCann et al [ 109 ] found that when GFP + Kit + bone-marrow-derived cells (from Kit +/copGFP mice) were transplanted into the small intestine of W/W v mutant mice, they did not observe these cells differentiate into network-forming ICC-like cells. These contradictory findings indicate more detailed molecular and functional characterisation of the transplanted cells is needed before the potential utility of this approach can be properly assessed.…”

Section: Icc and Gi Therapymentioning

confidence: 99%

Understanding the Biology of Human Interstitial Cells of Cajal in Gastrointestinal Motility

Foong

Zhou

Zarrouk

et al. 2020

IJMS

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Millions of patients worldwide suffer from gastrointestinal (GI) motility disorders such as gastroparesis. These disorders typically include debilitating symptoms, such as chronic nausea and vomiting. As no cures are currently available, clinical care is limited to symptom management, while the underlying causes of impaired GI motility remain unaddressed. The efficient movement of contents through the GI tract is facilitated by peristalsis. These rhythmic slow waves of GI muscle contraction are mediated by several cell types, including smooth muscle cells, enteric neurons, telocytes, and specialised gut pacemaker cells called interstitial cells of Cajal (ICC). As ICC dysfunction or loss has been implicated in several GI motility disorders, ICC represent a potentially valuable therapeutic target. Due to their availability, murine ICC have been extensively studied at the molecular level using both normal and diseased GI tissue. In contrast, relatively little is known about the biology of human ICC or their involvement in GI disease pathogenesis. Here, we demonstrate human gastric tissue as a source of primary human cells with ICC phenotype. Further characterisation of these cells will provide new insights into human GI biology, with the potential for developing novel therapies to address the fundamental causes of GI dysmotility.

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Section: Icc and Gi Therapymentioning

confidence: 99%

Understanding the Biology of Human Interstitial Cells of Cajal in Gastrointestinal Motility

Foong

Zhou

Zarrouk

et al. 2020

IJMS

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“…However, it is not clear whether increased unitary potential but no slow wave observed in this study 23 is sufficient to accelerate intestinal transit observed in Ishii's study, 22 since electrophysiological study was not performed in Ishii's study. 22 Further study is required.…”

mentioning

confidence: 64%

Is This the Era of Interstitial Cells of Cajal Transplantation?

Park

2014

J Neurogastroenterol Motil

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“…Western blot analysis was performed using standard techniques and as previously described ( 27 ). Details are provided in the Supplementary Data .…”

Section: Methodsmentioning

confidence: 99%

The Role of Prostaglandins in Disrupted Gastric Motor Activity Associated With Type 2 Diabetes

et al. 2019

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Patients with diabetes often develop gastrointestinal motor problems, including gastroparesis. Previous studies have suggested this gastric motor disorder was a consequence of an enteric neuropathy. Disruptions in interstitial cells of Cajal (ICC) have also been reported. A thorough examination of functional changes in gastric motor activity during diabetes has not yet been performed. We comprehensively examined the gastric antrums of Lep ob mice using functional, morphological, and molecular techniques to determine the pathophysiological consequences in this type 2 diabetic animal model. Video analysis and isometric force measurements revealed higher frequency and less robust antral contractions in Lep ob mice compared with controls. Electrical pacemaker activity was reduced in amplitude and increased in frequency. Populations of enteric neurons, ICC, and platelet-derived growth factor receptor α + cells were unchanged. Analysis of components of the prostaglandin pathway revealed upregulation of multiple enzymes and receptors. Prostaglandin-endoperoxide synthase-2 inhibition increased slow wave amplitudes and reduced frequency of diabetic antrums. In conclusion, gastric pacemaker and contractile activity is disordered in type 2 diabetic mice, and this appears to be a consequence of excessive prostaglandin signaling. Inhibition of prostaglandin synthesis may provide a novel treatment for diabetic gastric motility disorders.

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Bone Marrow Derived Kit-positive Cells Colonize the Gut but Fail to Restore Pacemaker Function in Intestines Lacking Interstitial Cells of Cajal

Cited by 8 publications

References 48 publications

Understanding the Biology of Human Interstitial Cells of Cajal in Gastrointestinal Motility

Understanding the Biology of Human Interstitial Cells of Cajal in Gastrointestinal Motility

Is This the Era of Interstitial Cells of Cajal Transplantation?

The Role of Prostaglandins in Disrupted Gastric Motor Activity Associated With Type 2 Diabetes

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