John R. Greenland

Comparative molecular analysis of histopathologic subtypes reveals shared epithelial remodeling yet distinct fibroblast programs in scleroderma lung disease

This study compares molecular features of SSc-NSIP and SSc-UIP with IPF, finding shared epithelial changes and distinct fibroblast programs.

DLGAP5 promotes vascular cell proliferation and remodeling in pulmonary arterial hypertension

This study identifies DLGAP5 as a driver of pulmonary vascular remodeling in PAH by promoting cell proliferation and survival through cyclin A2 and DEPDC1 upregulation and BIM suppression.

Tracing cell communication programs across conditions at single cell resolution with CCC-RISE

The paper introduces CCC-RISE, a method to analyze cell-cell communication at single-cell resolution across conditions, identifying disease-relevant signaling programs and subpopulations.

Impaired complement regulation drives chronic lung allograft dysfunction after lung transplantation.

This study identifies a genetic variant linked to impaired complement regulation that worsens chronic lung allograft dysfunction-free survival by promoting B cell activation and donor-specific antibodies.

Lactate dehydrogenase-induced DNA Topoisomerase 1 is a novel regulator of smooth muscle cell proliferation and remodeling in pulmonary arterial hypertension

This study identifies LDHA-lactate-induced over-lactylation and TOP1 accumulation as drivers of PASMC hyper-proliferation and PAH, with TOP1 inhibition reversing these effects.

FcεR1γ-based Activating Chimeric Antigen Receptors enhanced Natural Killer cell function against HLA-E+ cells

This study modifies FcεR1γ with a 4-1BB co-stimulatory motif to enhance NK cell function against HLA-E+ cells, improving cytotoxicity in suppression-prone conditions.

Non-canonical HIPPO-MST1/2 promotes hyper-proliferation of pulmonary vascular cells through CDC20

The paper shows MST1/2 promotes hyper-proliferation and apoptosis resistance in PAH pulmonary vascular cells by up-regulating CDC20.

CITE-seq analysis reveals human cytomegalovirus and diabetes-associated adaptive NK cell alterations in cardiovascular disease.

The paper uses CITE-seq to analyze NK cell alterations in CAD patients, finding SPON2/IFNG ratio and adaptive NK cell signatures correlate with disease severity and inflammation.