Abstract
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.
Highlights
Gastrointestinal (GI) motility disorders can occur throughout the length of the gut—from the oesophagus to the colon
We examine gaps in the current understanding of human interstitial cells of Cajal (ICC)—their sources, molecular characterisation, and potential involvement in GI disorders and therapy—in order to propose a framework for better understanding the biology of human ICC in GI motility
Over the last few decades, an extensive body of work has established some fundamental molecular characteristics of murine ICC in both normal and diseased GI tissue. It is unclear how closely these findings can be translated to human GI physiology and disease treatment
Summary
Gastrointestinal (GI) motility disorders can occur throughout the length of the gut—from the oesophagus to the colon. The GI tract is an essential system for the digestion of food, absorption of nutrients and release of waste. These processes occur in different segments of the GI tract, requiring the movement of content between segments. While ICC are recognised as essential for normal GI motility, the fundamental molecular biology of human ICC in normal or diseased GI function is yet to be fully defined. We examine gaps in the current understanding of human ICC—their sources, molecular characterisation, and potential involvement in GI disorders and therapy—in order to propose a framework for better understanding the biology of human ICC in GI motility
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