Low concentration of oxidant and nitric oxide donors stimulate proliferation of human endothelial cells in vitro

Łuczak, Katarzyna; Balcerczyk, Aneta; Soszyński, Mirosław; Bartosz, Grzegorz

doi:10.1016/j.cellbi.2004.03.004

Cited by 64 publications

(50 citation statements)

References 22 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been demonstrated that NO has either an antiproliferative or a proproliferative action, depending on cell type or on NO concentration (Du et al 1997;Hajri et al 1998;Krischel et al 1998;Ulibarri et al 1999;Frank et al 2000;Kim et al 2002;Packer et al 2003;Luczak et al 2004;Cayre et al 2005;Matarredona et al 2005;Bal-Price et al 2006;Magalhaes et al 2006;Tao et al 2006;Villalobo 2006;Zhu et al 2006;Mejia-Garcia and Paes-de-Carvalho 2007). In retinal cells, the increase in cell proliferation induced by NPY was abolished by the NOS inhibitor, L-NAME, and by the sGC inhibitor, ODQ, suggesting that the NO-GC pathway mediates retinal cell proliferation induced by NPY.…”

Section: Discussionmentioning

confidence: 87%

Neuropeptide Y stimulates retinal neural cell proliferation – involvement of nitric oxide

Álvaro

Martins

Araújo

et al. 2008

Journal of Neurochemistry

View full text Add to dashboard Cite

Neuropeptide Y (NPY) is a 36 amino acid peptide widely present in the CNS, including the retina. Previous studies have demonstrated that NPY promotes cell proliferation of rat post‐natal hippocampal and olfactory epithelium precursor cells. The aim of this work was to investigate the role of NPY on cell proliferation of rat retinal neural cells. For this purpose, primary retinal cell cultures expressing NPY, and NPY Y1, Y2, Y4 and Y5 receptors [Álvaro et al., (2007) Neurochem. Int., 50, 757] were used. NPY (10–1000 nM) stimulated cell proliferation through the activation of NPY Y1, Y2 and Y5 receptors. NPY also increased the number of proliferating neuronal progenitor cells (BrdU+/nestin+ cells). The intracellular mechanisms coupled to NPY receptors activation that mediate the increase in cell proliferation were also investigated. The stimulatory effect of NPY on cell proliferation was reduced by l‐nitroarginine‐methyl‐esther (l‐NAME; 500 μM), a nitric oxide synthase inhibitor, 1H‐[1,2,4]oxadiazolo‐[4, 3‐a]quinoxalin‐1‐one (ODQ; 20 μM), a soluble guanylyl cyclase inhibitor or U0126 (1 μM), an inhibitor of the extracellular signal‐regulated kinase 1/2 (ERK 1/2). In conclusion, NPY stimulates retinal neural cell proliferation, and this effect is mediated through nitric oxide–cyclic GMP and ERK 1/2 pathways.

show abstract

Section: Discussionmentioning

confidence: 87%

Neuropeptide Y stimulates retinal neural cell proliferation – involvement of nitric oxide

Álvaro

Martins

Araújo

et al. 2008

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…Endothelial cells generate ROS, which may play a physiologic or pathologic role depending on the level of ROS. Low levels of ROS act as signaling molecules that induce endothelial cell proliferation and migration in response to a variety of stimuli, such as ischemia and angiogenic factors (26,27). In pathologic conditions in which ROS already are generated at high levels (e.g., in the penis of diabetic mice, as shown in the present study), the high levels of ROS induce apoptosis and cell death (28).…”

Section: Discussionmentioning

confidence: 88%

Inhibition of Ninjurin 1 restores erectile function through dual angiogenic and neurotrophic effects in the diabetic mouse

Yin

Choi

Kim

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Penile erection is a neurovascular phenomenon, and erectile dysfunction (ED) is caused mainly by vascular risk factors or diseases, neurologic abnormalities, and hormonal disturbances. Men with diabetic ED often have severe endothelial dysfunction and peripheral nerve damage, which result in poor response to oral phosphodiesterase-5 inhibitors. Nerve injury-induced protein 1 (Ninjurin 1, Ninj1) is known to be involved in neuroinflammatory processes and to be related to vascular regression during the embryonic period. Here, we demonstrate in streptozotocin-induced diabetic mice that inhibition of the Ninj1 pathway by administering Ninj1-neutralizing antibody (Ninj1-Ab) or by using Ninj1-knockout mice successfully restored erectile function through enhanced penile angiogenesis and neural regeneration. Angiopoietin-1 (Ang1) expression was down-regulated and angiopoietin-2 expression was up-regulated in the diabetic penis compared with that in controls, and these changes were reversed by treatment with Ninj1-Ab. Ninj1 blockade-mediated penile angiogenesis and neural regeneration as well as recovery of erectile function were abolished by inhibition of Ang1-Tie2 (tyrosine kinase with Ig and epidermal growth factor homology domain-2) signaling with soluble Tie2 antibody or Ang1 siRNA. The present results suggest that inhibition of the Ninj1 pathway will be a novel therapeutic strategy for treating ED.diabetes mellitus | male sexual dysfunction | peripheral neuropathy E rectile dysfunction (ED), which is defined as an inability to attain or maintain penile erection sufficient for satisfactory sexual intercourse (1), is caused by a variety of pathologic conditions including vascular risk factors or diseases, neurologic abnormalities, and hormonal disturbances (2, 3). Diabetes mellitus is one of the most common causes of ED, and about 50-75% of male diabetic patients have ED (4, 5). Multiple pathogenetic factors, such as endothelial dysfunction, atherosclerosis, autonomic neuropathy, inflammation, fibrosis, and hypogonadism, are involved in diabetic ED (4-6). The multiple factors causing diabetic ED contribute to reduced responsiveness to currently available oral phosphodiesterase-5 (PDE5) inhibitors, which enhance the nitric oxide (NO)-cGMP pathway by inhibiting the breakdown of cGMP (7). The severity of endothelial dysfunction and peripheral neuropathy are mainly responsible for the poor responsiveness of diabetic patients to PDE5 inhibitors (8, 9). Because the effects of PDE5 inhibitors depend on endogenous NO formation, PDE5 inhibitors fail to increase the cGMP level above the threshold required for penile erection if bioavailable NO is insufficient as the result of severe endothelial dysfunction or peripheral neuropathy (9). Therefore, a new treatment strategy that corrects both endothelial dysfunction and peripheral neuropathy is required for men with diabetic ED.A variety of strategies targeting therapeutic angiogenesis and neural regeneration have been introduced to restore erectile function at the preclinical lev...

show abstract

“…It is known that ROS at low levels induces the proliferation of different cell types and specifically endothelial cells [24]. Both psoriasin [13] and VEGF [25] are induced by ROS.…”

Section: Psoriasin Induces the Proliferation Of Endothelial Cells Thrmentioning

confidence: 99%

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Shubbar

Vegfors

Carlström

et al. 2011

Breast Cancer Res Treat

View full text Add to dashboard Cite

Psoriasin (S100A7), originally identified in psoriasis, is a calcium-binding protein belonging to the multigenic S100 family. In high-grade ductal carcinoma in situ (DCIS), psoriasin was identified as one of the most abundant transcripts. We have previously shown that psoriasin was induced by reactive oxygen species (ROS). Moreover, the downregulation of psoriasin by short hairpin RNA (shRNA) led to the reduced expression of VEGF and inhibited tumour Our data suggest that psoriasin expression in mammary epithelial cells leads to increased endothelial cell proliferation in a paracrine manner through RAGE. Psoriasin may therefore play a role in breast cancer progression by promoting oxidative stress response and angiogenesis.

show abstract

Low concentration of oxidant and nitric oxide donors stimulate proliferation of human endothelial cells in vitro

Cited by 64 publications

References 22 publications

Neuropeptide Y stimulates retinal neural cell proliferation – involvement of nitric oxide

Neuropeptide Y stimulates retinal neural cell proliferation – involvement of nitric oxide

Inhibition of Ninjurin 1 restores erectile function through dual angiogenic and neurotrophic effects in the diabetic mouse

Psoriasin (S100A7) increases the expression of ROS and VEGF and acts through RAGE to promote endothelial cell proliferation

Contact Info

Product

Resources

About