Primitive macrophages induce sarcomeric maturation and functional enhancement of developing human cardiac microtissues via efferocytic pathways.

Yolk sac macrophages are the first to seed the developing heart, however we have no understanding of their roles in human heart development and function due to a lack of accessible tissue. Here, we bridge this gap by differentiating human embryonic stem cells (hESCs) into primitive LYVE1 macrophages (hESC-macrophages) that stably engraft within contractile cardiac microtissues composed of hESC-cardiomyocytes and fibroblasts. Engraftment induces a human fetal cardiac macrophage gene program enriched in efferocytic pathways.

Two distinct mechanisms mediate the involvement of bone marrow cells in islet remodeling: neogenesis of insulin-producing cells and support of islet recovery.

We have recently reported that small-sized bone marrow cells (BMCs) isolated by counterflow centrifugal elutriation and depleted of lineage markers (Fr25lin(-)) have the capacity to differentiate and contribute to regeneration of injured islets. In this study, we assess some of the characteristics of these cells compared to elutriated hematopoietic progenitors (R/O) and whole BMCs in a murine model of streptozotocin-induced chemical diabetes. The GFP(bright)CD45(+) progeny of whole BMCs and R/O progenitors progressively infiltrate the pancreas with evolution of donor chimerism; are found at islet perimeter, vascular, and ductal walls; and have a modest impact on islet recovery from injury.

Effect of coadministration of neuronal growth factors on neuroglial differentiation of bone marrow-derived stem cells in the ischemic retina.

Purpose: Brain-derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF) have limited and transient supportive effects on retinal recovery from ischemia. The aim of this study was to investigate their effect on engrafted adult bone marrow-derived stem cells in a rodent model of anterior ischemic optic neuropathy (rAION).

Methods: Small cells were isolated from the bone marrow of green fluorescent protein expressing mice by counterflow centrifugal elutriation, depleted of cells expressing lineage markers, and grafted in conjunction with growth factors into the vitreous body of mice with unilateral rAION.

VEGF induces neuroglial differentiation in bone marrow-derived stem cells and promotes microglia conversion following mobilization with GM-CSF.

Purpose: Evaluation of potential tropic effects of vascular endothelial growth factor (VEGF) on the incorporation and differentiation of bone-marrow-derived stem cells (BMSCs) in a murine model of anterior ischemic optic neuropathy (AION).

Methods: In the first approach, small-sized subset of BMCs were isolated from GFP donors mice by counterflow centrifugal elutriation and depleted of hematopoietic lineages (Fr25lin(-)). These cells were injected into a peripheral vein (1 × 10(6) in 0.

C1824T mutation in the LMNA gene has no association with senile cataract.

Mutations in the LMNA gene encoding lamins A/C are responsible for Hutchinson-Gilford syndrome (HGS), a disorder of premature aging. Cataract is 1 of the main manifestations. The most prevalent mutation in Hutchinson-Gilford syndrome is C1824T, which activates a cryptic splice donor site to produce an abnormal lamin A protein.