Modulation of Multidrug Resistance-Associated Protein 2 (Mrp2) and Mrp3 Expression and Function with Small Interfering RNA in Sandwich-Cultured Rat Hepatocytes

2004 ◽  
Vol 66 (4) ◽  
pp. 1004-1010 ◽  
Author(s):  
Xianbin Tian ◽  
Maciej J. Zamek-Gliszczynski ◽  
Peijin Zhang ◽  
Kim L. R. Brouwer
Keyword(s):  
Multidrug Resistance ◽  
Small Interfering Rna ◽  
Rat Hepatocytes ◽  
Cultured Rat Hepatocytes ◽  
And Function ◽  
Interfering Rna

scholarly journals Inducible proteolytic inactivation of OPA1 mediated by the OMA1 protease in mammalian cells

2009 ◽  
Vol 187 (7) ◽  
pp. 959-966 ◽  
Author(s):  
Brian Head ◽  
Lorena Griparic ◽  
Mandana Amiri ◽  
Shilpa Gandre-Babbe ◽  
Alexander M. van der Bliek
Keyword(s):  
Membrane Potential ◽  
Mammalian Cells ◽  
Small Interfering Rna ◽  
Mitochondrial Network ◽  
Membrane Fusion Protein ◽  
Zinc Metalloprotease ◽  
Mitochondrial Inner Membrane ◽  
Proteolytic Cascade ◽  
And Function ◽  
Interfering Rna

The mammalian mitochondrial inner membrane fusion protein OPA1 is controlled by complex patterns of alternative splicing and proteolysis. A subset of OPA1 isoforms is constitutively cleaved by YME1L. Other isoforms are not cleaved by YME1L, but they are cleaved when mitochondria lose membrane potential or adenosine triphosphate. In this study, we show that this inducible cleavage is mediated by a zinc metalloprotease called OMA1. We find that OMA1 small interfering RNA inhibits inducible cleavage, helps retain fusion competence, and slows the onset of apoptosis, showing that OMA1 controls OPA1 cleavage and function. We also find that OMA1 is normally cleaved from 60 to 40 kD by another as of yet unidentified protease. Loss of membrane potential causes 60-kD protein to accumulate, suggesting that OMA1 is attenuated by proteolytic degradation. We conclude that a proteolytic cascade controls OPA1. Inducible cleavage provides a mechanism for quality control because proteolytic inactivation of OPA1 promotes selective removal of defective mitochondrial fragments by preventing their fusion with the mitochondrial network.

scholarly journals Long Non-coding RNA Uc.48+ Small Interfering RNA Alleviates Neuroinflammatory Hyperalgesia in Gp120-Treated Rats via the P2Y12 Receptor

2021 ◽  
Vol 15 ◽  
Author(s):  
Lichao Peng ◽  
Bing Wu ◽  
Liran Shi ◽  
Lifang Zou ◽  
Lin Li ◽  
...  
Keyword(s):  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Small Interfering Rna ◽  
P2y12 Receptor ◽  
Virus Envelope ◽  
Protein Coding ◽  
Non Coding Rna ◽  
And Function ◽  
Interfering Rna ◽  
Long Non Coding Rna

Human immunodeficiency virus envelope glycoprotein 120 (gp120) leads to hyperalgesia. Long non-coding RNAs are characterized by the lack of a protein-coding sequence and may contribute to the development and maintenance of inflammatory and neuroinflammatory pain. Rats with neuroinflammatory pain were established by gp120 treatment, which is featured by intensified pain behaviors. Long non-coding RNA uc.48+ was increased in the dorsal root ganglia of gp120-treated rats, and small interfering RNA that targets uc.48+ markedly alleviated hyperalgesia in gp120-treated rats. Notably, uc.48+ overexpression increased P2Y12 expression in control rats dorsal root ganglia and induced hyperalgesia. Uc.48+ small interfering RNA inhibited P2Y12 expression in gp120-treated rats. Uc.48+ potentiated P2Y12 receptor functions in the neurons and heterologous cells. Therefore, uc.48+ siRNA treatment reduced the upregulation of P2Y12 expression and function in DRG neurons, and, hence, alleviated hyperalgesia in gp120-treated rats.

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