Conclusion Of Biology Project On Gastrointestinal Disorder.
Answers
Answer:
he mammalian gut epithelium is a rapidly self-renewing tissue in the body, and its homeostasis is preserved through strict regulation of epithelial cell proliferation, growth arrest, and apoptosis. Unlike other tissues of the body, the GI mucosa is exposed to dietary constituents and its own secretions that contain a variety of molecules and factors modulating the growth of the mucosa. In addition, the food ingestion and presence of food within the digestive tract cause the release of a number of hormones, particularly gut hormones and peptide growth factors that have effects specific to the GI mucosa. Although this wide variety of growth regulators has complicated our understanding of the overall regulation of GI mucosal growth, the humoral factors have the potential to affect all cells along the GI tract equally, whereas those in the lumen lose effectiveness distally as they move down the GI tract. It is both the humoral mechanism and gradient-oriented mechanism that explain the varied growth responses to feeding, development, surgery, and disease.
An increasing body of evidence indicates that polyamines are necessary for normal intestinal mucosal growth and that decreasing cellular polyamines inhibits cell proliferation and disrupts epithelial integrity. Polyamines are shown to regulate intestinal epithelial cell renewal by virtue of their ability to modulate expression of various genes. Increasing the levels of cellular polyamines stimulates GI mucosal growth and cell proliferation by increasing expression of growth-promoting genes through enhancement of their gene transcription and translation, whereas growth inhibition following polyamine depletion results primarily from the activation of growth-inhibiting genes by stabilizing their mRNAs via the RBP HuR. In addition, polyamines also modulate apoptosis of intestinal epithelial cells through multiple signaling pathways including alterations in expression of apoptosis-associated signaling proteins.
However, there are still many critical issues that remain to be addressed regarding the roles of polyamines in maintenance of gut epithelial integrity. For example, studies to define the molecular process responsible for regulation of RNA-binding proteins by polyamines and how polyamine depletion-induced growth-inhibiting proteins interact with their downstream target signals are needed and will lead to a better understanding of the biological functions of cellular polyamines and the mechanism of polyamine depletion-induced growth arrest under physiological and various pathological conditions. It is very interesting to determine if polyamines are involved in the regulation of microRNA biogenesis in the GI tissues and how polyamine-modulated microRNAs affect expression of growth-associated genes during GI mucosal growth inhibition under various pathological conditions.
Explanation:
Summary and Conclusions
Publication Details
The mammalian gut epithelium is a rapidly self-renewing tissue in the body, and its homeostasis is preserved through strict regulation of epithelial cell proliferation, growth arrest, and apoptosis. Unlike other tissues of the body, the GI mucosa is exposed to dietary constituents and its own secretions that contain a variety of molecules and factors modulating the growth of the mucosa. In addition, the food ingestion and presence of food within the digestive tract cause the release of a number of hormones, particularly gut hormones and peptide growth factors that have effects specific to the GI mucosa. Although this wide variety of growth regulators has complicated our understanding of the overall regulation of GI mucosal growth, the humoral factors have the potential to affect all cells along the GI tract equally, whereas those in the lumen lose effectiveness distally as they move down the GI tract. It is both the humoral mechanism and gradient-oriented mechanism that explain the varied growth responses to feeding, development, surgery, and disease.
An increasing body of evidence indicates that polyamines are necessary for normal intestinal mucosal growth and that decreasing cellular polyamines inhibits cell proliferation and disrupts epithelial integrity. Polyamines are shown to regulate intestinal epithelial cell renewal by virtue of their ability to modulate expression of various genes. Increasing the levels of cellular polyamines stimulates GI mucosal growth and cell proliferation by increasing expression of growth-promoting genes through enhancement of their gene transcription and translation, whereas growth inhibition following polyamine depletion results primarily from the activation of growth-inhibiting genes by stabilizing their mRNAs via the RBP HuR. In addition, polyamines also modulate apoptosis of intestinal epithelial cells through multiple signaling pathways including alterations in expression of apoptosis-associated signaling proteins.
However, there are still many critical issues that remain to be addressed regarding the roles of polyamines in maintenance of gut epithelial integrity. For example, studies to define the molecular process responsible for regulation of RNA-binding proteins by polyamines and how polyamine depletion-induced growth-inhibiting proteins interact with their downstream target signals are needed and will lead to a better understanding of the biological functions of cellular polyamines and the mechanism of polyamine depletion-induced growth arrest under physiological and various pathological conditions. It is very interesting to determine if polyamines are involved in the regulation of microRNA biogenesis in the GI tissues and how polyamine-modulated microRNAs affect expression of growth-associated genes during GI mucosal growth inhibition under various pathological conditions.