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<p>Endothelial cells lining the vessel network are indispensable for vascular transport but also provide paracrine signals controlling the behavior of nearby cell types. Pericytes are another essential component of the vessel wall, but little is known about their interactions with other cell populations during organ growth and patterning. Here, we use mouse genetics to address the function of three pericyte-derived factors in postnatal lung and brain. We find that inactivation of the gene for hepatocyte growth factor (HGF) or brain-derived neurotrophic factor (BDNF) in pericytes causes no overt alterations in postnatal brain but impairs lung development, which we attribute to defective interaction with AT2 epithelial cells and pulmonary endothelium, respectively. In contrast, pericyte expression of the growth factor Nodal is dispensable for lung morphogenesis but regulates vessel growth and barrier function in the postnatal brain through interactions with endothelial cells, astrocytes and microglia. Taken together, our findings establish that pericytes are a critical source of paracrine signals controlling morphogenetic processes in an organ-specific fashion.</p>

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Pericytes are organ-specific regulators of tissue morphogenesis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月12日

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  • Seyed Javad Rasouli,
  • Kai Kruse,
  • Rodrigo Diéguez-Hurtado,
  • Parisa Ghanbari,
  • Anusha Aravamudhan,
  • Mara E. Pitulescu,
  • Ralf H. Adams

摘要

Endothelial cells lining the vessel network are indispensable for vascular transport but also provide paracrine signals controlling the behavior of nearby cell types. Pericytes are another essential component of the vessel wall, but little is known about their interactions with other cell populations during organ growth and patterning. Here, we use mouse genetics to address the function of three pericyte-derived factors in postnatal lung and brain. We find that inactivation of the gene for hepatocyte growth factor (HGF) or brain-derived neurotrophic factor (BDNF) in pericytes causes no overt alterations in postnatal brain but impairs lung development, which we attribute to defective interaction with AT2 epithelial cells and pulmonary endothelium, respectively. In contrast, pericyte expression of the growth factor Nodal is dispensable for lung morphogenesis but regulates vessel growth and barrier function in the postnatal brain through interactions with endothelial cells, astrocytes and microglia. Taken together, our findings establish that pericytes are a critical source of paracrine signals controlling morphogenetic processes in an organ-specific fashion.