scholarly journals Autophagy Involvement in the Postnatal Development of the Rat Retina

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 177
Author(s):  
Noemi Anna Pesce ◽  
Alessio Canovai ◽  
Emma Lardner ◽  
Maurizio Cammalleri ◽  
Anders Kvanta ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Environmental Changes ◽  
Retinal Development ◽  
Post Partum ◽  
Endothelial Cell Proliferation ◽  
Cellular Adaptation ◽  
Rat Retina ◽  
Rat Pups ◽  
Evolutionarily Conserved

During retinal development, a physiologic hypoxia stimulates endothelial cell proliferation. The hypoxic milieu warrants retina vascularization and promotes the activation of several mechanisms aimed to ensure homeostasis and energy balance of both endothelial and retinal cells. Autophagy is an evolutionarily conserved catabolic system that contributes to cellular adaptation to a variety of environmental changes and stresses. In association with the physiologic hypoxia, autophagy plays a crucial role during development. Autophagy expression profile was evaluated in the developing retina from birth to post-natal day 18 of rat pups, using qPCR, western blotting and immunostaining methodologies. The rat post-partum developing retina displayed increased active autophagy during the first postnatal days, correlating to the hypoxic phase. In latter stages of development, rat retinal autophagy decreases, reaching a normalization between post-natal days 14-18, when the retina is fully vascularized and mature. Collectively, the present study elaborates on the link between hypoxia and autophagy, and contributes to further elucidate the role of autophagy during retinal development.

scholarly journals Cell proliferation controls body size growth, tentacle morphogenesis, and regeneration in hydrozoan jellyfish Cladonema pacificum

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7579 ◽  
Author(s):  
Sosuke Fujita ◽  
Erina Kuranaga ◽  
Yu-ichiro Nakajima
Keyword(s):  
Cell Proliferation ◽  
Body Size ◽  
Environmental Changes ◽  
Size Control ◽  
Cellular Mechanisms ◽  
Proliferating Cells ◽  
Size Growth ◽  
Local Cell ◽  
Proliferating Cell

Jellyfish have existed on the earth for around 600 million years and have evolved in response to environmental changes. Hydrozoan jellyfish, members of phylum Cnidaria, exist in multiple life stages, including planula larvae, vegetatively-propagating polyps, and sexually-reproducing medusae. Although free-swimming medusae display complex morphology and exhibit increase in body size and regenerative ability, their underlying cellular mechanisms are poorly understood. Here, we investigate the roles of cell proliferation in body-size growth, appendage morphogenesis, and regeneration using Cladonema pacificum as a hydrozoan jellyfish model. By examining the distribution of S phase cells and mitotic cells, we revealed spatially distinct proliferating cell populations in medusae, uniform cell proliferation in the umbrella, and clustered cell proliferation in tentacles. Blocking cell proliferation by hydroxyurea caused inhibition of body size growth and defects in tentacle branching, nematocyte differentiation, and regeneration. Local cell proliferation in tentacle bulbs is observed in medusae of two other hydrozoan species, Cytaeis uchidae and Rathkea octopunctata, indicating that it may be a conserved feature among hydrozoan jellyfish. Altogether, our results suggest that hydrozoan medusae possess actively proliferating cells and provide experimental evidence regarding the role of cell proliferation in body-size control, tentacle morphogenesis, and regeneration.

Kallistatin Inhibits Endothelial Cell Proliferation, Migration and Adhesion in Vitro and Angiogenesis in the Ischemic Hindlimb of Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 706-707
Author(s):  
Robert Q Miao ◽  
Jun Agata ◽  
Lee Chao ◽  
Julie Chao
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Gene Delivery ◽  
Fluorescent Protein ◽  
Regional Blood Flow ◽  
Endothelial Cell Proliferation ◽  
Hek 293

P76 Kallistatin is a serine proteinase inhibitor (serpin) which has multifunctions including regulation of tissue kallikrein activity, blood pressure, inflammation and neointima hyperplasia. In this study, we investigated the potential role of kallistatin in vascular biology by studying its effects on the proliferation, migration and adhesion of cultured primary human endothelial cells in vitro, and angiogenesis in the ischemic hindlimb of rats. Purified kallistatin significantly inhibits cultured endothelial cell proliferation, migration and adhesion induced by VEGF or bFGF. To further investigate the role of kallistatin in vascular growth in vivo, we prepared adenovirus carrying the human kallistatin gene under the control of the cytomegalovirus promoter/enhancer (Ad.CMV-cHKBP). Expression of recombinant human kallistatin in HEK 293 cells transfected with Ad.CMV-cHKBP was identified by a specific ELISA. The effect of adenovirus-mediated kallistatin gene delivery on angiogenesis was evaluated in a rat model of hindlimb ischemia. Adenovirus carrying the human kallistatin or green fluorescent protein (GFP) gene were injected locally into the ischemic adductor at the time of surgery. Histological and morphometric analysis at 14 days post injection showed that adenovirus-mediated kallistatin gene delivery significantly reduced capillary density in the ischemic muscle as compared to that of control rats injected with GFP. The anti-angiogenic effect of kallistatin was associated with reduced regional blood flow in the ischemic hindlimb measured by microsphere assays. Expression of human kallistatin was identified in the injected muscle and immunoreactive human kallistatin levels were measured in the muscle and in the circulation of rats following kallistatin gene delivery. These results demonstrate a novel role of kallistatin in the inhibition of angiogenesis and in vascular remodeling.

Role of ephrin B2 in human retinal endothelial cell proliferation and migration

2003 ◽  
Vol 15 (11) ◽  
pp. 1011-1017 ◽  
Author(s):  
Jena J. Steinle ◽  
Cynthia J. Meininger ◽  
Usha Chowdhury ◽  
Guoyao Wu ◽  
Harris J. Granger
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
Retinal Endothelial Cell ◽  
And Migration ◽  
Proliferation And Migration

Role of Amblyomin-X on angiogenesis and endothelial cell proliferation

2010 ◽  
Vol 196 ◽  
pp. S179
Author(s):  
C.C. Drewes ◽  
R.Y.S. Dias ◽  
C.B. Hebeda ◽  
S.M. Simons ◽  
A.M. Chudzinski-Tavassi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Endothelial Cell Proliferation

scholarly journals Intravascular neutrophils partially mediate the endometrial endothelial cell proliferative response to oestrogen in ovariectomised mice

Reproduction ◽  
2004 ◽  
Vol 127 (5) ◽  
pp. 613-620 ◽  
Author(s):  
B Heryanto ◽  
J E Girling ◽  
P A W Rogers
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Proliferative Response ◽  
Endothelial Cell Proliferation ◽  
Vascular Endothelial ◽  
Proliferating Cells ◽  
Oestrogen Treatment ◽  
Neutrophil Depletion ◽  
Endothelial Growth Factor

The aim of this study was to investigate the role of intravascular neutrophils in initiating endothelial cell proliferation following oestrogen treatment in ovariectomised mouse endometrium. Uterine tissues were collected from ovariectomised C57/CBA female mice 24 h after oestrogen treatment with or without systemic neutrophil depletion. Neutropenia was achieved with either an in-house anti-neutrophil serum (ANS) or Gr-1 monoclonal antibody. All mice received an i.p. injection of bromodeoxyuridine (BrdU) 4 h prior to dissection to allow visualisation of proliferating cells using immunocytochemistry. Endometrial sections were immunostained for BrdU, vascular endothelial growth factor (VEGF), and neutrophils (using ANS). Oestrogen treatment of ovariectomised mice significantly increased the number of intravascular neutrophils, whereas induction of neutropenia with either ANS or Gr-1 in conjunction with oestrogen treatment prevented this increase. Oestrogen treatment of ovariectomised mice also significantly increased the number of intravascular VEGF-positive cells; however, whereas induction of neutropenia with ANS significantly reduced this increase, Gr-1 did not. In both studies, neutropenia significantly reduced, but did not eliminate, the amount of endometrial endothelial cell proliferation. These results suggest a role for neutrophils in endometrial angiogenesis following acute oestrogen treatment; however, the presence of VEGF-positive cells even after induction of neutropenia suggests that more than one type of leukocyte may be involved.

272. Progesterone stimulates endothelial cell proliferation, but not stromal cell proliferation, in mouse endometrium

2005 ◽  
Vol 17 (9) ◽  
pp. 112
Author(s):  
L. M. Walter ◽  
P. A. W. Rogers ◽  
J. E. Girling
Keyword(s):  
Cell Proliferation ◽  
Stromal Cell ◽  
Cellular Proliferation ◽  
Previous Experiment ◽  
Single Injection ◽  
Endothelial Cell Proliferation ◽  
Treatment Groups ◽  
Brdu Injection ◽  
Significant Difference

Previous studies have suggested that progesterone stimulates stromal cell (SC) proliferation in the mouse endometrium1. However, these studies have not differentiated endothelial cells (EC) from other SC. In this study, we investigated the effects of progesterone on cellular proliferation in ovariectomised mouse endometrium. We hypothesised that progesterone would stimulate both SC and EC proliferation. One group of CBA × C57 mice (n = 6) were treated with a single injection of 100 ng of estradiol on day eight following ovariectomy, followed by a day with no treatment and three consecutive daily injections of 1 mg progesterone. Other groups were treated with either the vehicle (n = 5), estradiol (n = 4) or progesterone (n = 5) injections only. All groups were dissected on day 13 after ovariectomy, 4 h following a BrdU injection. CD31/BrdU double staining immunohistochemistry allowed proliferating EC to be differentiated from proliferating SC. Mice treated with progesterone only had significantly higher EC proliferation in comparison to females treated with progesterone following oestrogen priming (P = 0.05) or vehicle only (P = 0.01) (progesterone only: median=97.3 proliferating EC (PEC)/mm2 [range = 60.8–203.4]; oestrogen plus progesterone: 41.0 PEC/mm2 [8.9–86.9]; vehicle only: 0.0 PEC/mm2 [0.0–3.1]). Unexpectedly, there was no significant difference in SC proliferation among the treatment groups (progesterone only: 50.1 PSC/mm2 [39.2–102.6]; oestrogen plus progesterone: 46.1 PSC/mm2 [12.6–120.8]; vehicle only: 44.8 PSC/mm2 [17.3–68.4]). To determine if VEGF had a role in the progesterone-induced EC proliferation, the previous experiment was repeated with the inclusion of mice treated with VEGF anti-serum. The addition of VEGF anti-serum significantly inhibited progesterone-induced EC proliferation (46.8 PEC/mm2 [38.9–128.0]; P = 0.04], but had no effect on SC proliferation (P = 0.3). These results demonstrate that progesterone stimulates endometrial EC proliferation, but not SC proliferation as reported by earlier studies1. Studies are currently underway to further investigate the role of VEGF in mediating progesterone effects on endometrial EC. (1)Clarke, C.L. and Sutherland, R.L. (1990) Endocrine Reviews 11, 266–301.

Abstract P248: Novel Role of Axl Kinase in Endothelial Cell Proliferation and Pulmonary Arterial Hypertension

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Anastasia Gorelova ◽  
Sanghamitra Sahoo ◽  
Patrick J Pagano
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Endothelial Cell Proliferation ◽  
Vegf Receptor ◽  
Drug Bioavailability ◽  
Endothelial Proliferation ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is a poorly characterized disease of unclear etiology that affects individuals of all ages. Vascular remodeling and increase in pulmonary artery (PA) and right ventricle (RV) pressures are two major culprits in RV failure and death in PAH. Recent advances in the study of PAH suggest that endothelial cell proliferation is an early instigator of this hallmark remodeling. We postulated that Axl receptor tyrosine kinase (implicated in pro-proliferative and pro-survival signaling in cancerous cells) could mediate endothelial proliferation and thus hemodynamic changes occurring in PAH. Using immunofluorescent microscopy of lung microvessels of human PAH vs. non-PAH, we observed Axl expression on intimal endothelial cells but not medial smooth muscle cells. Furthermore, digitized microscopy revealed that Axl tended to increase on the endothelium of PAH vessels (1.65±0.15-fold vs. non-PAH; n=3-4; p=0.057 ). To address the role of Axl in vivo , an Axl inhibitor R428 was employed in a mouse model of pulmonary hypertension. C57Bl/6 mice were subjected to hypoxia at pO 2 =10% and VEGF receptor antagonist SU5416 (Su/Ch) or normoxia (Norm) for 3 wks. Indeed, Su/Ch caused a significant rise in lung Axl protein and mRNA (7.1±0.4- and 2.4±0.5-fold, Su/Ch vs. Norm, protein and mRNA, respectively; n=3-6; p<0.01). As predicted, RV pressure (RVP) rose from 27±0.5 to 43±1.8 mmHg (Norm vs. Su/Ch; n=6; p<0.01). However, we did not observe a decrease in RVP with twice-daily gavage of 75 mg/kg R428 (43±1.4 mmHg, Su/Ch + R428; n=6). A similar pattern was observed with mean PA pressure (18.4±0.3 and 28.7±1.2 mmHg, Norm vs. Su/Ch, p<0.01; 28.7±0.9 mmHg, Su/Ch + R428), RV resistance (1403±256 vs. 2703±464 Wood units, Norm vs. Su/Ch, n/s; vs. 3610±625 Wood units, Su/Ch + R428) and Fulton index (0.26±0.01 and 0.34±0.02, Norm vs. Su/Ch, p<0.05; 0.38±0.02, Su/Ch + R428). In conclusion, our preliminary results demonstrate upregulated Axl expression in the endothelium of PAH patients and in lungs of PH mice and suggest that Axl kinase may play a novel role in pulmonary vascular endothelial proliferation and remodeling in PAH. It remains to be determined whether drug bioavailability or severity of disease precluded an ameliorative effect of an Axl inhibitor.

Ascorbic Acid Blocks the Growth Inhibitory Effect of Tumor Necrosis Factor-α on Endothelial Cells

2003 ◽  
Vol 228 (7) ◽  
pp. 855-865 ◽  
Author(s):  
Rubina W. Saeed ◽  
Tina Peng ◽  
Christine N. Metz
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Tumor Necrosis ◽  
Endothelial Cell Proliferation ◽  
Cell Growth Inhibition ◽  
Tnf Α ◽  
Endothelial Cell Growth ◽  
Necrosis Factor

Impaired endothelial cell proliferation has been proposed to be an early, critical defect contributing to the development of atherosclerosis. Recent studies show that high plasma tumor necrosis factor (TNF)-α levels and low serum ascorbic acid (AA) levels correlate with atherosclerosis severity. Additionally, AA has been reported to have potential beneficial effects in preventing atherosclerosis. Based on these studies, we investigated the role of AA (≤ 1mM) on TNF-α-mediated vascular endothelial cell growth inhibition in vitro. In accordance with previous reports, we found that TNF-α alone inhibited endothelial cell proliferation. Further studies revealed that AA alone enhanced endothelial cell proliferation and that AA blocked endothelial cell growth inhibition induced by TNF-α. By contrast, we observed no effect of AA on endothelial cell activation or nuclear entry of nuclear factor-κB in response to TNF-α. The protective effect of AA on endothelial cell proliferation was not simply the result of its antioxidant activity but did correlate with collagen IV expression by endothelial cells. AA pre-treatment of proliferating endothelial cells promoted retinoblastoma protein (Rb) phosphorylation and decreased p53 levels when compared to untreated cells. Furthermore, the addition of AA to TNF-α-treated proliferating endothelial cells blocked both the inhibition of retinoblastoma protein phosphorylation and enhanced p53 expression induced by TNF-α. Consistent with these results, we found that AA protects endothelial cells against TNF-α-induced apoptosis. These studies highlight the potential therapeutic role of AA in promoting endothelial cell proliferation during inflammatory conditions, such as atherosclerosis and cardiovascular disease.

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