Molecular and immunohistochemical expression of apoptotic proteins Bax, Bcl-2 and Caspase 3 in infantile hemangioma tissues as an effect of propranolol treatment

Wnęk, Aneta; Andrzejewska, Ewa; Kobos, Józef; Taran, Katarzyna; Przewratil, Przemysław

doi:10.1016/j.imlet.2017.03.005

Cited by 32 publications

(17 citation statements)

References 30 publications

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“…When administrated with LEN prior to hypoxia treatment, the viability of PNCM and H9c2 cells was enhanced by LEN in a dosedependent manner while apoptosis was inhibited to some extent, which indicated that LEN inhibited hypoxia-induced cell injury in cardiomyocytes PNCM and H9c2 cells. The ratio of Bax to Bcl-2 and the cleavage of caspase-3 are two important apoptosis-related indications [24,25]. The decreased ratio of Bax to Bcl-2 and suppressive cleavage of caspase-3 by LEN in hypoxia-treated cell indicated that LEN inhibited cell apoptosis to some extent.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Lentinan protects cardiomyocytes against hypoxia-induced injury by regulation of microRNA-22/Sirt1

Zhang

Zhao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Myocardial ischemia is a serious disease which threatens human's life. Lentinan (LEN) possesses multiple biological properties: anticancer, antibacterial, antiviral and antioxidant effects. Our study investigated the effects of LEN on hypoxia-stimulated cardiomyocytes and the underlying mechanism. Primary neonatal rat ventricular cardiomyocytes (PNCM) were isolated from neonate rat pups. PNCM and H9c2 cells were stimulated by hypoxia and treated by LEN. Cell viability and apoptosis were detected by cell counting kit-8 and flow cytometry, respectively. Moreover, apoptotic factors were examined by western blot. Phosphatidylinositol 3'-kinase (PI3K)/protein kinase B (AKT) and b-catenin pathways related proteins were analyzed by western blot. Furthermore, the expression of microRNA-22 (miR-22) was detected by qRT-PCR. Altered expression of miR-22 and silenced information regulator 1 (Sirt1) was achieved by transfection. The relationship between miR-22 and Sirt1 was verified by luciferase assay. We found that LEN promoted cell viability and decreased apoptosis which led to the contrary results with what hypoxia induced. Moreover, LEN decreased the ratio of Bax to Bcl-2 and the level of cleaved caspase-3, as well as activated PI3K/AKT and b-catenin. LEN decreased the expression of miR-22 which was upregulated by hypoxia. miR-22 overexpression broken the promoting effects led by LEN. Moreover, Sirt1 was verified to be a target of miR-22. Silence of Sirt1 led to the opposite results with LEN. In conclusion, LEN relieved hypoxia-induced cellular injuries evidenced by increasing viability and decreasing apoptosis via down-regulation of miR-22, which was accompanied by activation of PI3K/AKT and b-catenin pathways. HIGHLIGHTS Lentinan alleviates hypoxia-induced injuries of PNCM and H9c2 cells; microRNA-22 expression is decreased by lentinan; Lentinan reduces hypoxia-induced injury by microRNA-22 downregulation; Lentinan regulates PI3K/AKT and Wnt/b-catenin by regulation of microRNA-22/Sirt1.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Lentinan protects cardiomyocytes against hypoxia-induced injury by regulation of microRNA-22/Sirt1

Zhang

Zhao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Although an inverse relation and important decreased ratio of PEDF/VEGF has been reported to explain retinal neovascularization, 13 our findings point to an effect of propranolol on MPs-released PEDF independent of that on VEGF. These data are consistent with that documented by others which fail to show changes in VEGF in microglia unless following adrenergic prestimulation.…”

Section: Discussioncontrasting

confidence: 58%

“…More recently, the antiangiogenic properties of propranolol have been demonstrated in a model of CNV. [8][9][10] Although these studies pointed to an effect of propranolol in reducing VEGF, others have questioned this mechanism to fully explain the effects of propranolol, 11,12 while proposing concomitant respective activation of prodeath and suppression of prosurvival factors 5,13 in b-adrenoceptor-bearing vascular cells, 7 suggesting that antiangiogenic mechanisms for propranolol may differ depending on the type of environment and tissue/cell incurring vasoproliferation. In this context, CNV as observed in various clinical conditions as well as in the laser-induced photocoagulation model, is associated with an inflammatory component.…”

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confidence: 99%

Propranolol Attenuates Proangiogenic Activity of Mononuclear Phagocytes: Implication in Choroidal Neovascularization

Omri

Tahiri

Pierre

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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Targeting b-adrenergic receptor signaling with propranolol has emerged as a potential candidate to counteract choroidal neovascularization (CNV). Little is known of its effect on macrophages, which play a critical role in CNV. We investigated the effect of propranolol on angiogenic response of mononuclear phagocytes (MPs). METHODS. The angiogenic effect of propranolol was evaluated in laser-induced CNV model. Mice received intraperitoneal injections of propranolol (6 mg/kg/d) or vehicle. CNV area and inflammatory cells were determined respectively by using lectin staining and an anti-IBA-1 antibody on RPE/choroid flat mounts. Inflammatory gene expression was evaluated by quantitative (q) PCR analysis. Mechanisms of propranolol was studied in MP cell lines J774 and RAW264.7 and in primary peritoneal macrophages. Expression of pro-and antiangiogenic mediators was studied. In addition, effects of propranolol treatment of MPs was assessed on choroidal explant. RESULTS. CNV was attenuated by propranolol and concomitantly associated with decreased inflammatory mediators IL-6 and TNFa, albeit with accumulation of (b-adrenoceptor harboring) MPs in the CNV area. Conditioned media from MPs preincubated with propranolol exerted antiangiogenic effects. Treatment of J774 confirmed the attenuation of inflammatory response to propranolol and increased cleaved caspase-3 on choroidal explant. We found that propranolol increased pigment epithelium-derived factor (PEDF) expression in MPs. Trapping of PEDF with an antibody abrogated antiangiogenic effects of propranolol. PEDF was also detected in CNV-associated MPs. CONCLUSIONS. We hereby show that propranolol confers on MPs antiangiogenic properties by increasing PEDF expression, which complements its effects on vascular tissue resulting in inhibition of choroidal vasoproliferation in inflammatory conditions. The study supports possible use of propranolol as a therapeutic modality for CNV.

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“…BCL2, an anti-apoptotic BCL2 family member, mainly locates on the outer member of mitochondria [ 30 ]. It is known that BCL2 plays crucial roles in the prevention of apoptosis in response to a variety of stimuli by blocking release of cytochrome c from mitochondria, and followed by inactivation of caspase cascades [ 31 ]. Previous research has revealed an elevation of BCL2 in cancerous cells exposed to IR, implying these cells have the potential to adapt to radiotherapy [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-153-3p enhances cell radiosensitivity by targeting BCL2 in human glioma

Sun

Piao

2018

Biol Res

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BackgroundGlioma is the most prevalent malignant tumor in human central nervous systems. Recently, the development of resistance to radiotherapy in glioma patients markedly vitiates the therapy outcome. MiR-153-3p has been reported to be closely correlated with tumor progression, but its effect and molecular mechanism underlying radioresistance remains unclear in glioma.MethodsThe expression of miR-153-3p was determined in radioresistant glioma clinical specimens as well as glioma cell lines exposed to irradiation (IR) using quantitative real-time PCR. Cell viability, proliferation and apoptosis were then evaluated by MTT assay, colony formation assay, Flow cytometry analysis and caspase-3 activity assay in glioma cells (U87 and U251). Tumor forming was evaluated by nude mice model in vivo. TUNEL staining was used to detect cell apoptosis in nude mice model. The target genes of miR-153-3p were predicted and validated using integrated bioinformatics analysis and a luciferase reporter assay.ResultsHere, we found that miR-153-3p was down-regulated in radioresistant glioma clinical specimens as well as glioma cell lines (U87 and U251) exposed to IR. Enhanced expression of miR-153-3p promoted the radiosensitivity, promoted apoptosis and elevated caspase-3 activity in glioma cells in vitro, as well as the radiosensitivity in U251 cell mouse xenografs in vivo. Mechanically, B cell lymphoma-2 gene (BCL2) was identified as the direct and functional target of miR-153-3p. Moreover, restoration of BCL2 expression reversed miR-153-3p-induced increase of radiosensitivity, apoptosis and caspase-3 activity in U251 cells in vitro. In addition, clinical data indicated that the expression of miR-153-3p was significantly negatively associated with BCL2 in radioresistance of glioma samples.ConclusionsOur findings suggest that miR-153-3p is a potential target to enhance the effect of radiosensitivity on glioma cells, thus representing a new potential therapeutic target for glioma.

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Molecular and immunohistochemical expression of apoptotic proteins Bax, Bcl-2 and Caspase 3 in infantile hemangioma tissues as an effect of propranolol treatment

Cited by 32 publications

References 30 publications

RETRACTED ARTICLE: Lentinan protects cardiomyocytes against hypoxia-induced injury by regulation of microRNA-22/Sirt1

RETRACTED ARTICLE: Lentinan protects cardiomyocytes against hypoxia-induced injury by regulation of microRNA-22/Sirt1

Propranolol Attenuates Proangiogenic Activity of Mononuclear Phagocytes: Implication in Choroidal Neovascularization

MicroRNA-153-3p enhances cell radiosensitivity by targeting BCL2 in human glioma

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