Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.

Dates of Funding: 2025-2027

Project Title: "Modeling Maternal Obesity Effects on Offspring Stellate Cell Activation Using Umbilical Cord Mesenchymal Stem Cells"

Metabolic dysfunction-associated steatotic liver disease (MASLD) has risen alongside childhood obesity. The intrauterine environment may prime the development of MASLD and obesity in offspring. Umbilical cord mesenchymal stem cells (UC-MSCs), a fetal tissue, robustly predict adiposity and hepatic fat in childhood. Further investigation using UC-MSCs represents a unique opportunity to understand the underlying mechanisms of MASLD progression. Hepatic stellate cells are of mesodermal origin and are critical in the response to liver injury. Current models of liver fibrosis derive stellate cells from induced pluripotent stem cells but are limited in studying the developmental origins of MASLD. We propose differentiating UC-MSCs to stellate cells to produce a new model in studying pathways contributing to liver fibrosis and to characterize the differences in response of these stellate cells to activation based on in utero exposure to maternal obesity.