Role of Unmodified Low Generation - PAMAM Dendrimers in Efficient Non-Toxic Gene Transfection

2016 ◽  
Vol 1 (16) ◽  
pp. 5206-5217 ◽  
Author(s):  
Hema Kumari Alajangi ◽  
Poornemaa Natarajan ◽  
Manika Vij ◽  
Munia Ganguli ◽  
Deenan Santhiya
Keyword(s):  
Gene Transfection ◽  
Pamam Dendrimers ◽  
Toxic Gene

Geldanamycin inhibits hemorrhage-induced increases in caspase-3 activity: role of inducible nitric oxide synthase

2007 ◽  
Vol 103 (3) ◽  
pp. 1045-1055 ◽  
Author(s):  
Juliann G. Kiang ◽  
Phillip D. Bowman ◽  
Xinyue Lu ◽  
Yansong Li ◽  
Brian W. Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Caspase 3 ◽  
Gene Transfection ◽  
Organ Injury ◽  
Molecular Events ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Hemorrhage has been shown to increase inducible nitric oxide synthase (iNOS) and deplete ATP levels in tissues and geldanamycin limits both processes. Moreover, it is evident that inhibition of iNOS reduces caspase-3 and increases survival. Thus we sought to identify the molecular events responsible for the beneficial effect of geldanamycin. Hemorrhage in mice significantly increased caspase-3 activity and protein while treatment with geldanamycin significantly limited these increases. Similarly, geldanamycin inhibited increases in proteins forming the apoptosome (a complex of caspase-9, cytochrome c, and Apaf-1). Modulation of the expression of iNOS by iNOS gene transfection or siRNA treatment demonstrated that the level of iNOS correlates with caspase-3 activity. Our data indicate that geldanamycin limits caspase-3 expression and protects from organ injury by suppressing iNOS expression and apoptosome formation. Geldanamycin, therefore, may prove useful as an adjuvant in fluids used to treat patients suffering blood loss.

Cationic lipids derived from glycine betaine promote efficient and non-toxic gene transfection in cultured hepatocytes

2002 ◽  
Vol 4 (4) ◽  
pp. 415-427 ◽  
Author(s):  
David Gilot ◽  
Marie-Laure Miramon ◽  
Thierry Benvegnu ◽  
Vincent Ferrieres ◽  
Olivier Loreal ◽  
...  
Keyword(s):  
Glycine Betaine ◽  
Gene Transfection ◽  
Cationic Lipids ◽  
Cultured Hepatocytes ◽  
Toxic Gene

The Deficiency of Maged1 Attenuates Parkinson's Disease Progression by Inhibiting Apoptosis and Enhancing Autophagy in Mice

2020 ◽  
Author(s):  
Jie Wang ◽  
Wei-Yan You ◽  
Qing Ye ◽  
Jia-Qi Zhang ◽  
Chuan He ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Signaling Pathway ◽  
Knockout Mice ◽  
Gene Transfection ◽  
Motor Deficits ◽  
Mice Model

Abstract Background: Melanoma-associated antigen D1 (Maged1) is expressed in most adult tissues, predominantly in the brain, and has critical functions in the central nervous system in both developmental and adult stages. Loss of Maged1 in mice has been linked to depression, cognitive disorder, circadian rhythm, and drug addiction. However, the role of Maged1 in Parkinson’s disease (PD) remains unclear.Methods: Immunostaining was performed to investigate the expression of Maged1 in the samples from mice and human. To make the acute mice model of PD, C57BL/6 mice and Maged1 knockout mice were injected with 20 mg/kg 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) four times, every 2-hour intervals. SY5Y cells were treated by 200 μM 1-Methyl-4-phenylpyridinium iodide (MPP+). To examine motor balance and coordination, the rotarod test and pole test were used. Then we further investigated the role of Maged1 deficiency in DA neurons by high-performance liquid chromatography, immunohistochemistry, western blot, CCK8 assay, and gene transfection in vivo or in vitro.Results: Maged1 was expressed in DA neurons of samples from mice and human. And the expression of Maged1 was time-dependently upregulated by the treatment with MPTP or MPP+ in vivo or in vitro. Knockout of Maged1 in mice partly rescued the motor deficits and the reduced levels of striatal dopamine and its metabolites by MPTP treatment. Moreover, Maged1 deficiency protected primary DA neurons and differentiated ReNcell VM cells from MPP+ toxicity. Furthermore, along with the overexpression or downregulation of Maged1 in cultured SH-SY5Y cells, the reduced the cell viability by MPP+ treatment was relatively aggerated or attenuated. The effect of Maged1 deficiency may be attributed to the upregulated Akt signaling pathway and the downregulated mTOR signaling pathway, which further attenuated the MPTP or MPP+ -induced cell apoptosis and impairment of autophagy. Consistent with the above data, the degeneration of midbrain and striatum among 15-m Maged1 knockout mice was relatively mild compared to those in 15-m wild-type mice under physiological conditions.Conclusions: Maged1 deficiency-mediated apoptosis inhibition and autophagy enhancement may be a potential pro-survival mechanism during the progression of PD.

Mechanism of gene transfection by polyamidoamine (PAMAM) dendrimers modified with ornithine residues

2011 ◽  
Vol 19 (9) ◽  
pp. 770-780 ◽  
Author(s):  
Ajay Kumar ◽  
Venkata K. Yellepeddi ◽  
Kiran K. Vangara ◽  
Kevin B. Strychar ◽  
Srinath Palakurthi
Keyword(s):  
Gene Transfection ◽  
Pamam Dendrimers

scholarly journals Investigation of the role of ABC proteins in the resistance to paromomycin in Leishmania amazonensis

2019 ◽  
Author(s):  
Tabata Rodrigues Costa ◽  
Adriano Cappellazzo Coelho
Keyword(s):  
Visceral Leishmaniasis ◽  
Southeast Asia ◽  
Amphotericin B ◽  
Mechanism Of Action ◽  
Urban Areas ◽  
Gene Transfection ◽  
Leishmania Amazonensis ◽  
Parasitic Disease ◽  
Wide Geographic Distribution

Leishmaniasis is a parasitic disease with wide geographic distribution in tropical and subtropical areas, including Brazil where an increased number of cases in urban areas has been reported in the recent years. No vaccines are available for control of the disease and chemotherapy is restricted to some drugs like antimony and amphotericin B. Although not yet approved for the treatment of leishmaniasis in Brazil, paromomycin has been used in the treatment of visceral leishmaniasis in Southeast Asia with effectiveness of approximately 90%. To understand the mechanism of action and resistance of this drug in Leishmania, we aim to investigate the role of a subfamily of ABC (ATP binding cassette) proteins in the mechanisms of paromomycin resistance by gene transfection and overexpression of these genes in Leishmania amazonensis.

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