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Is LPAR5 agonist a new treatment for microvilli inclusion disease?
Am J Physiol Gastrointest Liver Physiol
January 2025
Division of Digestive Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, United States.
Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation.
Am J Physiol Gastrointest Liver Physiol
December 2024
Section of Surgical Sciences, Vanderbilt University Medical Center, Nashville, Tennessee, United States.
Functional loss of the motor protein myosin Vb (MYO5B) induces various defects in intestinal epithelial function and causes a congenital diarrheal disorder, namely, microvillus inclusion disease (MVID). Utilizing the MVID model mice (MYO5BΔIEC) and [MYO5B(G519R)], we previously reported that functional MYO5B loss disrupts progenitor cell differentiation and enterocyte maturation that result in villus blunting and deadly malabsorption symptoms. In this study, we determined that both absence and a point mutation of MYO5B impair lipid metabolism and alter mitochondrial structure, which may underlie the progenitor cell malfunction observed in the MVID intestine.
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- - Functional loss of the motor protein MYO5B leads to serious intestinal issues, including microvillus inclusion disease (MVID), characterized by progenitor cell dysfunction and malabsorption symptoms.
- - Research using MVID model mice showed that both the absence and mutation of MYO5B disrupt lipid metabolism and mitochondrial structure, resulting in reduced fatty acid oxidation and altered energy metabolism.
- - Treatment with Compound-1, which targets LPAR5, was found to improve intestinal function and weight loss in mice with MYO5B mutations, suggesting a potential therapeutic approach for treating MVID.
The role of LPA receptor signaling in modulating cellular responses of colon cancer cells co-cultured with lymphoid endothelial cells under hypoxic stress.
Tissue Cell
December 2024
Division of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka 577-8502, Japan. Electronic address:
Solid tumors are formed by cancer cells and the surrounding non-cancer stromal cells under hypoxic conditions, collectively referred to as the tumor microenvironment (TME). Lysophosphatidic acid (LPA) receptor (LPA to LPA) signaling is crucial in regulating tumor progression. This study investigated the impact of LPA receptor signaling on the biological behaviors of colon cancer DLD-1 cells co-cultured with lymphatic endothelial SVEC4-10 cells under hypoxic conditions.
View Article and Find Full Text PDFCrosstalk between cannabinoid receptor 2 and lysophosphatidic acid receptor 5.
Biochem Biophys Res Commun
July 2023
Department of Life Science, Kyonggi University, Suwon, 16227, Republic of Korea. Electronic address:
Cannabinoid receptor 2 (CB) and lysophosphatidic acid receptor 5 (LPA) are both classified as G-protein coupled receptors (GPCRs) activated by bioactive lipids and are highly expressed in colon cancer cells. However, crosstalk between two receptors and its potential effects on cancer cell physiology have not been fully elucidated. In the present study, the results of bioluminescence resonance energy transfer analysis showed that, among the LPA receptors, CB strongly and specifically interacted with LPA.
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