Xuri Li

Expression of a novel PDGF isoform, PDGF-C, in normal and diseased rat kidney.

Angiogenesis stimulated by PDGF-CC, a novel member in the PDGF family, involves activation of PDGFR-alphaalpha and -alphabeta receptors.

PDGF-D is a potent transforming and angiogenic growth factor.

Novel PDGF family members: PDGF-C and PDGF-D.

Transgenic overexpression of platelet-derived growth factor-C in the mouse heart induces cardiac fibrosis, hypertrophy, and dilated cardiomyopathy.

Tissue plasminogen activator is a potent activator of PDGF-CC.

Revascularization of ischemic tissues by PDGF-CC via effects on endothelial cells and their progenitors.

VEGF-B inhibits apoptosis via VEGFR-1-mediated suppression of the expression of BH3-only protein genes in mice and rats.

Reevaluation of the role of VEGF-B suggests a restricted role in the revascularization of the ischemic myocardium.

Paracrine signaling by platelet-derived growth factor-CC promotes tumor growth by recruitment of cancer-associated fibroblasts.

A role for a CXCR2/phosphatidylinositol 3-kinase gamma signaling axis in acute and chronic vascular permeability.

VEGF-B is dispensable for blood vessel growth but critical for their survival, and VEGF-B targeting inhibits pathological angiogenesis.

VEGF-B: a survival, or an angiogenic factor?

Platelet-derived growth factor-DD targeting arrests pathological angiogenesis by modulating glycogen synthase kinase-3beta phosphorylation.

Survival effect of PDGF-CC rescues neurons from apoptosis in both brain and retina by regulating GSK3beta phosphorylation.

Semaphorin 3E initiates antiangiogenic signaling through plexin D1 by regulating Arf6 and R-Ras.

VEGF-B: a thing of beauty.

PDGF-CC blockade inhibits pathological angiogenesis by acting on multiple cellular and molecular targets.

Oligo-guanosine nucleotide induces neuropilin-1 internalization in endothelial cells and inhibits angiogenesis.

Complement-mediated inhibition of neovascularization reveals a point of convergence between innate immunity and angiogenesis.

VEGF-independent angiogenic pathways induced by PDGF-C.

Complicated life, complicated VEGF-B.

Targeting of junctional adhesion molecule-C (JAM-C) inhibits experimental choroidal neovascularization.