C. Betsholtz

Postnatal FGFR-signalling establishes gradients of cell identities along the proximal-distal axis of the lung airways

The paper identifies gene-expression gradients along the lung airway axis and shows FGFR-signaling establishes these gradients postnatally.

Immunoregulatory subtype of dermal lymphatic endothelial cells at capillary terminals drives lymphatic malformations

The paper identifies an immunoregulatory subtype of lymphatic endothelial cells that drives lymphatic malformations through pro-inflammatory signaling and immune cell interactions.

Claudin5 protects the peripheral endothelial barrier in an organ and vessel type-specific manner

The paper identifies Claudin5's organ- and vessel-type-specific role in maintaining endothelial barrier integrity through single-cell RNAseq analysis and functional studies in mice.

Semaphorin 3G exacerbates joint inflammation through the accumulation and proliferation of macrophages in the synovium

This study identifies Semaphorin 3G as a factor that worsens joint inflammation by promoting macrophage accumulation and proliferation in RA synovium.

Multimodal characterization of the murine neurovascular niche using a novel microvascular isolation protocol

This paper introduces a method to isolate murine brain microvasculature without transgenic lines or FACS sorting, validated through scRNA-seq, WB, and primary culture.

Emerging single cell endothelial heterogeneity supports sprouting tumour angiogenesis and growth

The paper identifies a novel endothelial cell population in tumors that contributes to vascularization and growth.

Lack of evidence of ACE2 expression and replicative infection by SARS-CoV-2 in human endothelial cells

The paper investigates ACE2 expression and SARS-CoV-2 infection in human endothelial cells, finding low or absent ACE2 expression and no viral replication.

Pericyte-specific vascular expression of SARS-CoV-2 receptor ACE2 - implications for microvascular inflammation and hypercoagulopathy in COVID-19

The paper shows that pericytes, not endothelial cells, express ACE2 in microvessels, suggesting they may be infected in COVID-19 and contribute to microvascular inflammation and hypercoagulopathy.