Laminin receptor mediates anti-inflammatory and anti-thrombogenic effects of pigment epithelium-derived factor in myeloma cells

2014 ◽  
Vol 443 (3) ◽  
pp. 847-851 ◽  
Author(s):  
Takanori Matsui ◽  
Yuichiro Higashimoto ◽  
Sho-ichi Yamagishi
Keyword(s):  
Pigment Epithelium ◽  
Laminin Receptor ◽  
Myeloma Cells ◽  
Pigment Epithelium Derived Factor ◽  
Anti Inflammatory

scholarly journals Laminin Receptor Involvement in the Anti-angiogenic Activity of Pigment Epithelium-derived Factor

2009 ◽  
Vol 284 (16) ◽  
pp. 10480-10490 ◽  
Author(s):  
Adrien Bernard ◽  
Jacqueline Gao-Li ◽  
Claudio-Areias Franco ◽  
Tahar Bouceba ◽  
Alexis Huet ◽  
...  
Keyword(s):  
Pigment Epithelium ◽  
Laminin Receptor ◽  
Angiogenic Activity ◽  
Pigment Epithelium Derived Factor

Decreased expression of pigment epithelium-derived factor within the penile tissues contributes to erectile dysfunction in diabetic rats

2018 ◽  
Vol 132 (20) ◽  
pp. 2175-2188 ◽  
Author(s):  
Hongjie Qiao ◽  
Yuanyuan Zhang ◽  
Wenwen Lin ◽  
Yu-Feng Wang ◽  
Cristina M. Furdui ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Erectile Dysfunction ◽  
Pigment Epithelium ◽  
Diabetic Rats ◽  
No Synthase ◽  
Inflammatory Factor ◽  
Potential Implication ◽  
Pigment Epithelium Derived Factor ◽  
Tnf Α ◽  
Anti Inflammatory

Increased production of reactive oxygen species (ROS) and inflammation are major contributors to the development and progression of diabetes-associated erectile dysfunction (DMED). As an endogenous antioxidant and anti-inflammatory factor, the potential implication of pigment epithelium-derived factor (PEDF) in DMED has not been revealed. To assess the potential antioxidant and anti-inflammatory functions of PEDF in DMED, we first demonstrated that PEDF was significantly decreased at the levels of the mRNA and protein in the penis of diabetic rats compared with normal controls. To test the hypothesis that decreased the penile levels of PEDF are associated with oxidative stress and inflammation in DMED, an adenovirus expressing PEDF (Ad-PEDF) or the same titer of control virus (Ad-GFP) was intracavernously administered at 2 weeks after diabetic onset. After 6 weeks of treatment, we found that administration of Ad-PEDF could significantly increase erectile response to cavernosal nerve stimulation in the diabetic rats by restoring the endothelial NO synthase (eNOS), P-eNOS, and neuronal NO synthase (nNOS) protein levels to the standard levels represented in normal rats and by suppressing the levels of tumor necrosis factor-α (TNF-α) and oxidative stress. In conclusion, the present data indicated that the antioxidant and anti-inflammatory potential of PEDF plays important role in restoring erectile function by the inhibition of oxidative stress and TNF-α production.

scholarly journals Pigment Epithelium-Derived Factor (PEDF) Receptors Are Involved in Survival of Retinal Neurons

2020 ◽  
Vol 22 (1) ◽  
pp. 369
Author(s):  
Susanne Bürger ◽  
Jie Meng ◽  
Annette Zwanzig ◽  
Mike Beck ◽  
Maik Pankonin ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Pigment Epithelium ◽  
Laminin Receptor ◽  
Retinal Ganglion ◽  
Retinal Neurons ◽  
Differential Survival ◽  
Hypoxic Conditions ◽  
Pigment Epithelium Derived Factor ◽  
Inhibition Of Angiogenesis

The demise of retinal ganglion cells (RGCs) is characteristic of diseases of the retina such as glaucoma and diabetic or ischemic retinopathies. Pigment epithelium-derived factor (PEDF) is a multifunctional secreted protein that mediates neuroprotection and inhibition of angiogenesis in the retina. We have studied expression and regulation of two of several receptors for PEDF, patatin-like phospholipase 2 gene product/PEDF-R and laminin receptor (LR), in serum-starved RGC under normoxia and hypoxia and investigated their involvement in the survival of retinal neuronal cells. We show that PEDF-R and LR are co-expressed in RGC and R28 retinal precursor cells. Expression of both receptors was enhanced in the presence of complex secretions from retinal glial (Müller) cells and upregulated by VEGF and under hypoxic conditions. PEDF-R- and LR-knocked-down cells demonstrated a markedly attenuated expression of anti-apoptotic Bcl-2 family members (Bcl-2, Bcl-xL) and neuroprotective mediators (PEDF, VEGF, BDNF) suggesting that both PEDF-R and LR mediate pro-survival effects of PEDF on RGC. While this study does not provide evidence for a differential survival-promoting influence of either PEDF-R or LR, it nevertheless highlights the importance of both PEDF receptors for the viability of retinal neurons.

Anti-inflammatory effects of pigment epithelium-derived factor in diabetic nephropathy

2008 ◽  
Vol 294 (5) ◽  
pp. F1166-F1173 ◽  
Author(s):  
Joshua J. Wang ◽  
Sarah X. Zhang ◽  
Robert Mott ◽  
Ying Chen ◽  
Ryan R. Knapp ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
High Glucose ◽  
Matrix Protein ◽  
Pigment Epithelium ◽  
Diabetic Rats ◽  
Renoprotective Effect ◽  
Pigment Epithelium Derived Factor ◽  
Control Virus ◽  
Anti Inflammatory ◽  
Proinflammatory Factors

Previously, we have reported that pigment epithelium-derived factor (PEDF) ameliorates albuminuria and inhibits matrix protein deposition in the kidney of streptozotocin (STZ)-induced diabetic rats, suggesting a renoprotective effect of PEDF in early stages of diabetic nephropathy. As inflammation is a major contributor to the development and progression of diabetic nephropathy, we examined in the present study whether PEDF inhibits renal inflammation in diabetic kidney. Diabetic rats received an intravenous injection of an adenovirus expressing PEDF (Ad-PEDF) or the same titer of a control virus. Three wk after the injection, diabetic rats treated with the control virus showed significantly elevated renal levels of proinflammatory factors such as ICAM-1, MCP-1, TNF-α, and VEGF compared with age-matched nondiabetic controls. Ad-PEDF effectively suppressed the overexpression of these proinflammatory factors in diabetic kidneys. In cultured primary human renal mesangial cells (HMC), the high-glucose medium-induced upregulation of VEGF and MCP-1 was largely blocked by PEDF. Furthermore, PEDF inhibited high glucose-induced activation of NF-κB, a key transcription factor mediating inflammatory responses, and hypoxia-inducible factor-1, a major activator of VEGF expression in HMC. These results suggest that the renoprotective effect of PEDF against diabetic nephropathy may be partially through its anti-inflammatory activity, likely by blocking the NF-κB and HIF-1 pathways.

scholarly journals Pigment epithelium-derived factor (PEDF) negates hyperandrogenic PCOS features

2020 ◽  
Vol 245 (2) ◽  
pp. 291-300
Author(s):  
Irit Miller ◽  
Hadas Bar-Joseph ◽  
Luba Nemerovsky ◽  
Ido Ben-Ami ◽  
Ruth Shalgi
Keyword(s):  
Polycystic Ovary ◽  
Pigment Epithelium ◽  
Mrna Levels ◽  
Pigment Epithelium Derived Factor ◽  
Endogenous Protein ◽  
Anti Inflammatory ◽  
Stimulation Of ◽  
Inflammatory Effect

Polycystic ovary syndrome (PCOS), one of the most common female endocrine disorder, is a prevalent cause of infertility. Hyperandrogenism is a key feature in PCOS and is correlated with increased expression of VEGF and cytokines in the ovaries. We have previously shown that pigment epithelium-derived factor (PEDF), an endogenous protein, presents potent anti-angiogenic and anti-inflammatory activities in the ovary and negates the effects of cytokines and VEGF. Additionally, PEDF plays a role in both pathophysiology and treatment of ovarian-hyperstimulation syndrome (OHSS), frequently seen in PCOS patients. We established hyperandrogenic-PCOS models, both in vivo, using mice exposed prenatally to dihydrotestosterone (DHT) and, in vitro, using human primary granulosa cells (hpGCs) and human granulosa cell line (KGN). In PCOS-induced mice, the mRNA levels of I l-6, V egf and Amh were higher than those of control; yet, treatment with rPEDF decreased these levels. Moreover, treating OHSS-induced PCOS-mice with rPEDF alleviated all OHSS symptoms. Stimulation of hpGCs with DHT resulted in downregulation of PEDF mRNA expression, concomitantly with a significant increase in IL-6 and IL-8 mRNAs expression. However, co-stimulation of DHT with rPEDF attenuated the increase in cytokines expression. The anti-inflammatory effect of PEDF was found to be mediated via PPARγ pathway. Our findings suggest that rPEDF treatment may normalize the ovarian angiogenic-inflammatory imbalance, induced by PCOS-associated hyperandrogenism. Moreover, the therapeutic potency of PEDF in preventing OHSS symptomes offers a rationale for using PEDF as novel physiological treatment for PCOS sequels.

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