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Studies on the molecular mechanisms involved in apoptosis triggered by Canine Distemper Virus (CDV)

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Title Studies on the molecular mechanisms involved in apoptosis triggered by Canine Distemper Virus (CDV)
 
Creator Singh, Sarabjot
Deka, Dipak
Ramneek
 
Subject Apoptosis
Cancer cells
CDV
HCT-15 cell line
Infection
IPA
 
Description 525-544
Apoptosis is a form of natural or stress induced cell death that plays a pivotal role in many cellular processes. Virus
induced apoptosis is of significant importance since many viruses/viral proteins have been reported to induces apoptosis in
different cell types. The present study was carried out to identify genes and pathways to explain the mechanisms involved in
CDV induced apoptosis. For this, HCT-15 cells were infected with CDV-SH, a Snyder Hill strain of canine distemper virus,
at different time points. Viability and apoptosis studies were performed using MTT and TUNEL assays, respectively. The
qPCR arrays were custom designed to study the expression profile of apoptotic genes in HCT-15 cells after 6, 12, 24 and
48 h of CDV infection. Results showed viability of cells as 100%, 88.18%, 78.34% and 74.62% at 6, 12, 24 and 48 h after
infection. Expression studies revealed increased expression of TNF-, TRAIL, Calpain, IFN- and RIG-1 genes and downregulation
of 21 genes in all the groups. Ingenuity Pathway Analysis (IPA) showed activation of apoptosis signaling
pathway in CDV infected HCT-15 cells. Immuno-cytochemistry studies using antibodies against apoptotic protein (caspase-
8, caspase-9, caspase-3, MAVS, IRF-3, cytochrome C, MKK7) showed only basal level of expression indicating no
dysregulation in the expression of these genes which was in consistence with the qPCR array results. In qPCR & IPA
analysis, although up-regulation of caspase 8, 9 and 3 was not observed, we hypothesized that CDV induced apoptosis in
HCT-15 cell line might have occurred through caspase independent pathways (like Calpain or other molecule mediated)
 
Date 2023-08-03T07:14:27Z
2023-08-03T07:14:27Z
2023-08
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://nopr.niscpr.res.in/handle/123456789/62401
https://doi.org/10.56042/ijbb.v60i7.1296
 
Language en
 
Publisher NIScPR-CSIR,India
 
Source IJBB Vol.60(07) [July 2023]