Open Journal of Rheumatology and Autoimmune Diseases

Volume 4, Issue 3 (August 2014)

ISSN Print: 2163-9914   ISSN Online: 2164-005X

Google-based Impact Factor: 0.47  Citations  

NF-κB Controls Resistance of Human Salivary Gland (HSG) Cells to Apoptosis in an in Vitro Model of Sjogren’s Syndrome

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DOI: 10.4236/ojra.2014.43025    3,084 Downloads   3,579 Views   Citations


Aim: To elucidate the anti-apoptotic properties of nuclear factor kappa light-chain-enhancer of activated B cells (NF-κB) and feedback regulation of NF-κB by nuclear factor of kappa light-chain-enhancer of activated B-cells inhibitor alpha (IκBα). Methods: We developed an in vitro model of Sjogren’s syndrome by transfecting human salivary gland (HSG) and acinar cells (NS-SV-AC) with a plasmid-encoding IκBαM (pCMV-IκBαM), a degradation-resistant IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha)-mutant, and examined TNF-induced apoptosis and anti-apoptotic properties of NF-κB. Apoptosis and induction of pro-apoptotic and anti-apoptotic genes were investigated by cDNA arrays, RT-PCR, electrophoretic mobility shift assays, and western blot. Results: In the presence of NF-κB inhibitors, TNF-induced apoptosis was markedly increased in both salivary gland and acinar cells. Increased caspase-3 activity was present in both HSG and NS-SV-AC cells. IκBαM-transfected salivary gland cells were more sensitive to TNF-induced apoptosis than IκBαM-transfected acinar cells. Transcription of pro-apoptotic genes was confirmed in both HSG and NS-SV-AC cells that were transfected with IκBαM. Results from caspase-3 activity assay confirmed previous experiments showing an apoptotic role for NF-κB. Conclusion: Data from gene expression arrays suggest that different mechanisms may operate during TNF-induced apoptosis in salivary gland ductal and acinar cells.

Cite this paper

Wang, Y. , Jamal, S. , Torres-Romero, L. , Molteni, A. , Shnyra, A. and McArthur, C. (2014) NF-κB Controls Resistance of Human Salivary Gland (HSG) Cells to Apoptosis in an in Vitro Model of Sjogren’s Syndrome. Open Journal of Rheumatology and Autoimmune Diseases, 4, 178-191. doi: 10.4236/ojra.2014.43025.

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