Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.

Dates of Funding: 2025-2027

Project Title: "Placental Proteins as a Novel Intervention to Prevent Adult Metabolic Liver Disease in Prematurity"

Prematurity and its complications are the number one cause of death of babies in the US and despite improvement in care, babies who survive premature birth often have long-term health problems, including cerebral palsy, intellectual disabilities and chronic lung disease. In addition, prematurity is associated with increased hepatic lipid accumulation, contributing to the development of metabolic dysfunction-associated steatotic liver disease (MASLD) in children who were born prematurely. Emerging evidence supports a critical role of the placenta in secreting factors that are essential for normal fetal organ development. One key difference between fetal and postnatal life is the abrupt cessation of the umbilical circulation at birth, which deprives premature infants of essential placental factors, including proteins, needed for organ development. We identified 434 proteins secreted by the human placenta into the fetal circulation before 32 weeks of gestation. Notably, many of these proteins have been associated with developmental processes such as neurogenesis, lung development and angiogenesis, suggesting that these proteins play important roles in normal fetal development. In this pilot project we will test the hypothesis that administration of proteins secreted by the human preterm placenta into the fetal circulation prevents neonatal and adult metabolic liver disease in premature guinea pigs.