Background: Diabetic cataract extraction can be frequently complicated by macular oedema, progression of retinopathy, or development of iris neovascularisation. The pathogenesis of these complications may be the result of changes in the concentration of angiogenic and anti-angiogenic cytokines in the immediate postoperative period. The study aims to prospectively analyse this. Methods: Uneventful phacoemulsification with intraocular lens implant was performed in seven eyes of six patients with diabetic retinopathy ranging from severe non-proliferative to quiescent proliferative. Patients were reviewed 1 day, 1 week, 1 month, and 3 months after surgery with fundus fluorescein angiography (FFA) and aqueous sampling. Each sample was analysed for VEGF, HGF, Il-1 β (pg/ml), and PEDF (μg/ml) by sandwich ELISA. Results: Clinically significant macular oedema (CSMO) occurred in one patient although increased macular hyperfluorescence occurred in three patients on FFA at 1 month. VEGF 165 concentration increased 1 day after surgery from a median baseline of 68 pg/ml (range 22–87 pg/ml) to 723 pg/ml (range 336–2071) at day 1. By 1 month it had decreased to 179 (range 66–811 pg/ml). HGF concentrations steadily increased over the month while IL-1 β and PEDF concentrations demonstrated an acute rise on day 1 after surgery and then IL-1β returned to baseline concentrations while PEDF decreased to below baseline. Conclusion: These results confirm altered concentrations of angiogenic and antiangiogenic growth factors after cataract surgery, which may induce subclinical and clinical worsening of diabetic maculopathy.

/pdf/diabetic-cataract-removal-postoperative-progression-of-2fnurr0end.pdf

Diabetic cataract removal: postoperative progression of maculopathy—growth factor and clinical analysis

Recent advances in the understanding of lipid metabolism suggest a critical role of endoplasmic reticulum (ER) stress in obesity-induced kidney injury. Hepatocyte growth factor (HGF) is a pleiotropic cytokine frequently featured in stem cell therapy with distinct renotropic benefits. This study aims to define the potential link between human induced pluripotent stem cell-derived mesenchymal stem cells (iPS-MSCs)/bone marrow-derived MSCs (BM-MSCs) and ER stress in lipotoxic kidney injury induced by palmitic acid (PA) in renal tubular cells and by high-fat diet (HFD) in mice. iPS-MSCs or BM-MSCs alleviated ER stress (by preventing induction of Bip, chop, and unfolded protein response), inflammation (Il6, Cxcl1, and Cxcl2), and apoptosis (Bax/Bcl2 and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling-positive cells) in renal cortex of animals exposed to HFD thus mitigating histologic damage and albuminuria, via activating HGF/c-Met paracrine signaling that resulted in enhanced HGF secretion in the glomerular compartment and c-Met expression in the tubules. Coculture experiments identified glomerular endothelial cells (GECs) to be the exclusive source of glomerular HGF when incubated with either iPS-MSCs or BM-MSCs in the presence of PA. Furthermore, both GEC-derived HGF and exogenous recombinant HGF attenuated PA-induced ER stress in cultured tubular cells, and this effect was abrogated by a neutralizing anti-HGF antibody. Taken together, this study is the first to demonstrate that MSCs ameliorate lipotoxic kidney injury via a novel microenvironment-dependent paracrine HGF/c-Met signaling mechanism to suppress ER stress and its downstream pro-inflammatory and pro-apoptotic consequences. Stem Cells Translational Medicine 2019;8:898&910.

https://stemcellsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/sctm.18-0265

Amelioration of Endoplasmic Reticulum Stress by Mesenchymal Stem Cells via Hepatocyte Growth Factor/c-Met Signaling in Obesity-Associated Kidney Injury.

Tomoregulin ectodomain shedding by proinflammatory cytokines.

The microvasculature is principally composed of two cell types: endothelium and mural support cells Multiple sources are available for human endothelial cells (ECs) but sources for human microvascular mural cells (MCs) are limited We derived multipotent mesenchymal progenitor cells from human embryonic stem cells (hES-MC) that can function as an MC and stabilize human EC networks in three-dimensional (3D) collagen-fibronectin culture by paracrine mechanisms Here, we have investigated the basis for hES-MC-mediated stabilization and identified the pleiotropic growth factor hepatocyte growth factor/scatter factor (HGF/SF) as a putative hES-MC-derived regulator of EC network stabilization in 3D in vitro culture Pharmacological inhibition of the HGF receptor (Met) (1 μm SU11274) inhibits EC network formation in the presence of hES-MC hES-MC produce and release HGF while human umbilical vein endothelial cells (HUVEC) do not When HUVEC are cultured alone the networks collapse, but in the presence of recomb

Dissecting the role of human embryonic stem cell-derived mesenchymal cells in human umbilical vein endothelial cell network stabilization in three-dimensional environments.

Hepatocyte growth factor-regulated genes in differentiated RAW 264.7 osteoclast and undifferentiated cells.

To investigate the possible role of hepatocyte growth factor (HGF) in the reconstruction process following inflammatory damage in lung tissue, we compared HGF production of human lung microvascular endothelial cells (HLWECs) and human umbilical vein endothelial cells (HUVECs) after stimulation by interleukin(IL)-1beta. In an HLMEC-conditioned medium, large amounts of total (single and 2-chain) HGF were detected, and were 26- to 28-fold higher than those in HUVECs or human lung fibroblasts. The production of total HGF increased in a dose-dependent manner (4.7 to 9.2 times) with IL-1beta. In contrast, the amount of HGF in an HUVEC-conditioned medium was unaffected by IL-1beta treatment. The amount of cell-associated HGF also showed a dose-related increase (140% to 160%) in HLMECs, but not in HUVECs with IL1beta. In addition, HGF and c-met (HGF receptor) mRNAs in HLMECs and HUVECs were examined by the RT-PCR method. HGF and c-met mRNAs were clearly detected in HLMECs before and after treatment with IL-1beta, but not in HUVECs. These results suggest that increases in HGF production from HLMECs may play a role in the reconstruction process following inflammatory damage in lung tissue.

PRODUCTION OF HEPATOCYTE GROWTH FACTOR FROM HUMAN LUNG MICROVASCULAR ENDOTHELIAL CELLS INDUCED BY INTERLEUKIN-1β

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PRODUCTION OF HEPATOCYTE GROWTH FACTOR FROM HUMAN LUNG MICROVASCULAR ENDOTHELIAL CELLS INDUCED BY INTERLEUKIN-1β